Endocrinology and Metabolism

Original Articles

Diabetes, obesity and metabolism Big Data Articles (National Health Insurance Service Database)
A Nomogram for End-Stage Renal Disease Prediction in Patients with Type 2 Diabetes Mellitus: A Nationwide Cohort Study in Korea: Inha Jung, Bong-Seong Kim, So Young Park, Da Young Lee, Ji Hee Yu, Ji A Seo, Kyung-Do Han, Nan Hee Kim; Endocrinol Metab. 2026;41(2):245-255. Published online November 12, 2025; DOI: https://doi.org/10.3803/EnM.2025.2570

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Abstract PDF Supplementary Material PubReader ePub: Background
Despite the rising incidence of end-stage renal disease (ESRD) among individuals with type 2 diabetes mellitus (T2DM) in Korea, no predictive model or nomogram has been developed using a nationwide cohort. In this study, we developed a nomogram to predict the long-term risk of ESRD in patients with T2DM using a large-scale, population-based Korean database.
Methods
Using the Korean National Health Insurance Database, patients with T2DM who underwent health examinations between 2015 and 2016 were assigned as development (n=1,744,277) and validation (n=747,407) cohorts. New ESRD cases were identified using codes for renal replacement therapy. A Cox proportional hazards regression model was used to derive a risk-scoring system, and 13 variables were selected. A risk score nomogram was then created to estimate the risk of ESRD.
Results
In the development cohort, 8,631 patients with T2DM developed ESRD during a follow-up period of 4.8±0.9 years. After multivariable adjustment, significant predictors of ESRD included male sex, current smoking, physical inactivity, low income, low body mass index, hypertension, low-density lipoprotein cholesterol ≥160 mg/dL, chronic kidney disease, insulin use, and longer duration of T2DM. A final nomogram incorporating 13 variables was developed to estimate the individual probability of ESRD. The concordance index for ESRD prediction in the validation cohort was 0.906 (95% confidence interval, 0.9 to 0.912).
Conclusion
This 13-variable nomogram provides a simple tool for identifying patients with T2DM at high risk of ESRD and may aid in early intervention.

Diabetes, obesity and metabolism
Irisin Attenuates Hepatic Stellate Cell Activation and Liver Fibrosis in Bile Duct Ligation Mice Model and Improves Mitochondrial Dysfunction: Thuy Linh Lai, So Young Park, Giang Nguyen, Phuc Thi Minh Pham, Seon Mee Kang, Jeana Hong, Jae-Ho Lee, Seung-Soon Im, Dae-Hee Choi, Eun-Hee Cho; Endocrinol Metab. 2024;39(6):908-920. Published online November 5, 2024; DOI: https://doi.org/10.3803/EnM.2024.1984

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Background
Liver fibrosis is a common outcome of chronic liver disease and is primarily driven by hepatic stellate cell (HSC) activation. Irisin, a myokine released during physical exercise, is beneficial for metabolic disorders and mitochondrial dysfunction. This study aimed to explore the effects of irisin on liver fibrosis in HSCs, a bile duct ligation (BDL) mouse model, and the associated mitochondrial dysfunction.
Methods
In vitro experiments utilized LX-2 cells, a human HSC line, stimulated with transforming growth factor-β1 (TGF-β1), a major regulator of HSC fibrosis, with or without irisin. Mitochondrial function was assessed using mitochondrial fission markers, transmission electron microscopy, mitochondrial membrane potential, and adenosine triphosphate (ATP) production. In vivo, liver fibrosis was induced in mice via BDL, followed by daily intraperitoneal injections of irisin (100 μg/kg/day) for 10 days.
Results
In vitro, irisin mitigated HSC activation and reduced reactive oxygen species associated with the TGF-β1/Smad signaling pathway. Irisin restored TGF-β1-induced increases in fission markers (Fis1, p-DRP1) and reversed the decreased expression of TFAM and SIRT3. Additionally, irisin restored mitochondrial membrane potential and ATP production lowered by TGF-β1 treatment. In vivo, irisin ameliorated the elevated liver-to-body weight ratio induced by BDL and alleviated liver fibrosis, as evidenced by Masson’s trichrome staining. Irisin also improved mitochondrial dysfunction induced by BDL surgery.
Conclusion
Irisin effectively attenuated HSC activation, ameliorated liver fibrosis in BDL mice, and improved associated mitochondrial dysfunction. These findings highlight the therapeutic potential of irisin for the treatment of liver fibrosis.

Citations

Citations to this article as recorded by

Targeting the Hepatic Stellate Cell Microenvironment: Nanomedicine Strategies for Liver Fibrosis Therapy
Lulu Pei, Xing Du, Zehao Mao, Kai Ding, Jiangyu Li, Tianqing Liu, Yongmei Zhao
Molecular Pharmaceutics.2026; 23(2): 662. CrossRef
From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis
Zhen Yang, Weizhao Tong, Kanglong Zhang, Guoxin Hu
Liver Research.2026; 10(2): 133. CrossRef
SREBP2 links ACSS2-dependent acetyl-CoA biosynthesis to metaboloepigenetic activation of hepatic stellate cells and liver fibrosis
Yu Wang, Aoqi Kang, Shunjie Wang, Zhen Yang, Hong Liu, Linbo Yue, Hao Li, Caiyi Wu, Wenjing Ren, Xiulian Miao, Zilong Li, Yong Xu, Zhiwen Fan
Metabolism.2026; 179: 156597. CrossRef
Synthesis and application of encapsulated Bifidobacterium Longum for mitigation of liver fibrosis via modulation of oxidative stress and inflammation in BDL rat model
Siavash Amiri, Mitra Motallebi, Mohsen Hemmati-Dinarvand, Merat Karimi, Maryam Akhavan Taheri, Sahar Ahmadi Asouri, Mohammad Esmaeil Shahaboddin
World Journal of Microbiology and Biotechnology.2026;[Epub] CrossRef
Circadian clock-driven inter-organ crosstalk in cardiovascular-kidney-metabolic (CKM) syndrome: Molecular mechanisms, pathological progression, and chronotherapeutic strategies
Yajie Cai, Yeyan Qin, Mengmeng Zhu, Xi Cheng, Yanfei Liu, Yue Liu
Metabolism.2026; 184: 156781. CrossRef
Irisin Attenuates Pulmonary Vascular Remodeling in Pulmonary Arterial Hypertension via Ubiquitin‐Mediated Regulation of ENO1
Na Sun, Yong‐Bing Wang, Jing Huang, Run‐Wei Deng, Hui‐Yu He, Lei Gao, Xuan Gao, You‐Li Fan, Yan Cong, Yao‐Lei Guo, Yi‐Qiang Chen, Gui‐Jia Wang, Shao‐Hong Fang, Xia Gu, Bo Yu, Bing‐Xiang Wu
Advanced Science.2025;[Epub] CrossRef
The Influence of Irisin on Selected Organs—The Liver, Kidneys, and Lungs: The Role of Physical Exercise
Maria Ciałowicz, Marek Woźniewski, Eugenia Murawska-Ciałowicz, Piotr Dzięgiel
Cells.2025; 14(16): 1228. CrossRef
Metabolic and immune links between sarcopenia and liver disease
Stanislav Nikolaevich Kotlyarov
World Journal of Hepatology.2025;[Epub] CrossRef
Irisin, the Myokine: Guardian and Mediator in Cardiovascular System
Tian Lan, Xueru Yan, Jie Li, Haoran Gu, Qi Hou, Enpeng He, Qingyuan Yang
Endocrinology, Diabetes & Metabolism.2025;[Epub] CrossRef
Inflammation—Insulin Resistance Crosstalk and the Central Role of Myokines
Maria-Zinaida Dobre, Bogdana Virgolici, Daciana Costina Andrada Dunca-Stefan, Ioana-Cristina Doicin, Iulia-Ioana Stanescu-Spinu
International Journal of Molecular Sciences.2025; 27(1): 60. CrossRef

Diabetes, obesity and metabolism
Impact of Chronic Kidney Disease and Gout on End-Stage Renal Disease in Type 2 Diabetes: Population-Based Cohort Study: Inha Jung, Da Young Lee, Seung Min Chung, So Young Park, Ji Hee Yu, Jun Sung Moon, Ji A Seo, Kyungdo Han, Nan Hee Kim; Endocrinol Metab. 2024;39(5):748-757. Published online August 30, 2024; DOI: https://doi.org/10.3803/EnM.2024.2020

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Background
We examined the impact of gout on the end-stage renal disease (ESRD) risk in patients with type 2 diabetes mellitus (T2DM) and determined whether this association differs according to chronic kidney disease (CKD) status.
Methods
Using the Korean National Health Insurance Service, this nationwide cohort study enrolled 847,884 patients with T2DM who underwent health checkups in 2009. Based on the presence of CKD (estimated glomerular filtration rate <60 mL/min/1.73 m²) and gout (two outpatient visits or one hospitalization within 5 years), patients were classified into four groups: CKD⁻Gout⁻, CKD⁻ Gout⁺, CKD⁺Gout⁻, and CKD⁺Gout⁺. Patients with incident ESRD were followed up until December 2018.
Results
Among 847,884 patients, 11,825 (1.4%) experienced progression to ESRD. ESRD incidence increased in the following order: 0.77 per 1,000 person-years (PY) in the CKD⁻Gout⁻ group, 1.34/1,000 PY in the CKD⁻Gout⁺ group, 8.20/1,000 PY in the CKD⁺Gout⁻ group, and 23.06/1,000 PY in the CKD⁺Gout⁺ group. The presence of gout modified the ESRD risk in a status-dependent manner. Hazard ratios (HR) were 1.49 (95% confidence interval [CI], 1.32 to 1.69) and 2.24 (95% CI, 2.09 to 2.40) in patients without and with CKD, respectively, indicating a significant interaction (P<0.0001). The CKD⁺Gout⁺ group had a markedly higher risk of developing ESRD (HR, 18.9; 95% CI, 17.58 to 20.32) than the reference group (CKD⁻Gout⁻).
Conclusion
Gout substantially enhances the risk of ESRD, even in the absence of CKD. Concurrent CKD and gout synergistically increase the risk of ESRD. Therefore, physicians should carefully screen for hyperuricemia to prevent progression to ESRD.

Citations

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Undescribed phenylspirodrimane dimers with anti-gouty activity from the coral-derived fungus Stachybotrys chartarum
Shuang Lin, Yi-Fan Geng, Hanxiao Zeng, Zixue Chai, Baolei Fan, Jun-Cheng Su, Yonghui Zhang, Zhengxi Hu
Phytochemistry.2026; 248: 114891. CrossRef
Gout in the era of multimorbidity: pathogenesis, systemic comorbidities, and evolving therapeutic strategies
Phillip J Kim, Jihun Kang, Jesang Yu, Geun-Tae Kim, Yunkyung Kim
Kosin Medical Journal.2026; 41(1): 26. CrossRef
Acute gout attack in a peritoneal dialysis patient treated with Firsekibart: a case report
Wenqian Wei, Lijie Gu, Hanyu Meng, Nan Zhu, Shu Rong
Open Medicine.2026;[Epub] CrossRef
Polydatin alleviates adenine-induced nephropathy in mice
Tao Sheng, Tianhong Ma, Xin Jin, Debin Chen, Shipeng Che, Jie Wang, Jiadu Shen, Chaoqun Shi, Qiang Li, Yixin Sun, Deqing Chen, Guangtao Xu
Renal Failure.2026;[Epub] CrossRef
Association between TyHGB and hyperuricemia and gout in patients with type-2 diabetes mellitus
Qian Zhang, Jing Xu, Yanying Qian
BMC Endocrine Disorders.2026;[Epub] CrossRef
ปัจจัยที่สัมพันธ์กับระดับความเสี่ยงโรคไตเรื้อรังตามเกณฑ์ KDIGO ในผู้ป่วยโรคเบาหวานชนิดที่ 2 ในประเทศไทย: การวิเคราะห์ข้อมูลทุติยภูมิ ด้วยการถดถอยโลจิสติกเชิงอันดับ
สมฤทัย ไชยอักษร, ปราถนา สถิตย์วิภาวี, จุฑาธิป ศีลบุตร, ชูเกียรติ วิวัฒน์วงศ์เกษม, ราม รังสินธุ์
Thai Red Cross Nursing Journal.2026; 19(2): 18. CrossRef
Development and validation of a risk models for gout in patients with diabetic kidney disease
Ningyu Cai, Mengdie Chen, Yiyun Wang, Ping Feng, Xianping Zhu, Qidong Zheng
BMC Endocrine Disorders.2026;[Epub] CrossRef
СУЧАСНІ СТРАТЕГІЇ МЕНЕДЖМЕНТУ ГІПЕРУРИКЕМІЇ, ПОДАГРИ ТА КОМОРБІДНИХ СТАНІВ: АНАЛІЗ МІЖНАРОДНИХ ПРОТОКОЛІВ, НОВІТНІХ ТЕРАПЕВТИЧНИХ МІШЕНЕЙ ТА ПЕРСОНАЛІЗОВАНОЇ ТЕРАПІЇ
В.М. Ждан, В.Г. Лебідь, М.Ю. Бабаніна, О.А. Кир’ян, Г.В. Волченко, Є.М. Кітура, І.В. Іваницький, М.В. Ткаченко
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Heterogeneity in the development of diabetes-related complications: narrative review of the roles of ancestry and geographical determinants
Andrea O. Y. Luk, Yingnan Fan, Baoqi Fan, Edith W. K. Chow, Tony C. K. O
Diabetologia.2025; 68(11): 2386. CrossRef
Relationship between the Chinese visceral adiposity index and gout in individuals with type 2 diabetes mellitus: a cross-sectional population-based study
Ningyu Cai, Mengdie Chen, Ping Feng, Yiyun Wang, Xianping Zhu, Qidong Zheng
Frontiers in Nutrition.2025;[Epub] CrossRef

Thyroid
Adequate Dose of Levothyroxine for Thyroid-Stimulating Hormone Suppression after Total Thyroidectomy in Patients with Differentiated Thyroid Cancer: Hyun Jin Ryu, Min Sun Choi, Hyunju Park, Tae Hyuk Kim, Jae Hoon Chung, So Young Park, Sun Wook Kim; Endocrinol Metab. 2024;39(4):615-621. Published online August 7, 2024; DOI: https://doi.org/10.3803/EnM.2023.1896

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Background
The adequate dose of levothyroxine (LT4) for patients who have undergone total thyroidectomy (TT) for differentiated thyroid cancer (DTC) is uncertain. We evaluated the LT4 dose required to achieve mild thyroid-stimulating hormone (TSH) suppression in DTC patients after TT.
Methods
The electronic medical records of patients who underwent TT for DTC and received mild TSH suppression therapy were reviewed. Linear regression analysis was performed to evaluate the association between LT4 dose (μg/kg) and an ordinal group divided by body mass index (BMI). We also evaluated the trend in LT4 doses among groups divided by BMI and age.
Results
In total, 123 patients achieved mild TSH suppression (0.1 to 0.5 mIU/L). The BMI variable was divided into three categories: <23 kg/m² (n=46), ≥23 and <25 kg/m² (n=30), and ≥25 kg/m² (n=47). In the linear regression analysis, BMI was negatively associated with the LT4 dose after adjusting for age and sex (P<0.001). The LT4 doses required to achieve mild TSH suppression based on the BMI categories were 1.86, 1.71, and 1.71 μg/kg, respectively (P for trend <0.001). Further analysis with groups divided by age and BMI revealed that a higher BMI was related to a lower LT4 dose, especially in younger patients aged 20 to 39 (P for trend=0.011).
Conclusion
The study results suggest an appropriate LT4 dose for mild TSH suppression after TT based on body weight in patients with DTC. Considering body weight, BMI, and age in estimating LT4 doses might help to achieve the target TSH level promptly.

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A paper-based fluorescent aptasensor utilizing click chemistry strategy for portable detection of thyroid stimulating hormone
Changxin Huangfu, Yanting Duan, Chenyue Zhan, Ruimin Liang, Jiajie Xu, Minghua Ge
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The Starting Dosage of Levothyroxine for Hypothyroidism during Pregnancy
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International Journal of Thyroidology.2026; 19(1): 60. CrossRef
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Effects of 131I and TSH suppression therapy on METTL3, METTL14 levels and recurrence in thyroid cancer
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Developing a machine learning-based predictive model for levothyroxine dosage estimation in hypothyroid patients: a retrospective study
Tran Thi Ngan, Dang Huong Tra, Ngo Thi Quynh Mai, Hoang Van Dung, Nguyen Van Khai, Pham Van Linh, Nguyen Thi Thu Phuong
Frontiers in Endocrinology.2025;[Epub] CrossRef
Tailoring TSH suppression in differentiated thyroid carcinoma: evidence, controversies, and future directions
Xinxin Song, Xin Zhi, Linxue Qian
Endocrine.2025; 89(1): 1. CrossRef
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Eu Jeong Ku, Won Sang Yoo, Yu Been Hwang, Subin Jang, Jooyoung Lee, Shinje Moon, Eun Kyung Lee, Hwa Young Ahn
Endocrinology and Metabolism.2025; 40(2): 225. CrossRef
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Daham Kim, Min Jeong Kang, So Jeong Lee, Yoon Hee Cho, Gunuk Zi, Jeongsuk An, Jinjoo Park, Jaekyu Han, Susan Chi, Sang-hoon Cha, Eun Jig Lee
Endocrine-Related Cancer.2025;[Epub] CrossRef
Levothyroxine Dosing for Thyroid-Stimulating Hormone Suppression in Patients with Differentiated Thyroid Cancer after Total Thyroidectomy
Mijin Kim
Endocrinology and Metabolism.2024; 39(4): 576. CrossRef

Review Articles

Mineral, Bone & Muscle
Effects of Endocrine-Disrupting Chemicals on Bone Health: So Young Park, Sung Hye Kong, Kyoung Jin Kim, Seong Hee Ahn, Namki Hong, Jeonghoon Ha, Sihoon Lee, Han Seok Choi, Ki-Hyun Baek, Jung-Eun Kim, Sang Wan Kim, on Behalf of Metabolic Bone Disease Study Group of Korean Endocrine Society; Endocrinol Metab. 2024;39(4):539-551. Published online July 17, 2024; DOI: https://doi.org/10.3803/EnM.2024.1963

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This comprehensive review critically examines the detrimental impacts of endocrine-disrupting chemicals (EDCs) on bone health, with a specific focus on substances such as bisphenol A (BPA), per- and polyfluoroalkyl substances (PFASs), phthalates, and dioxins. These EDCs, by interfering with the endocrine system’s normal functioning, pose a significant risk to bone metabolism, potentially leading to a heightened susceptibility to bone-related disorders and diseases. Notably, BPA has been shown to inhibit the differentiation of osteoblasts and promote the apoptosis of osteoblasts, which results in altered bone turnover status. PFASs, known for their environmental persistence and ability to bioaccumulate in the human body, have been linked to an increased osteoporosis risk. Similarly, phthalates, which are widely used in the production of plastics, have been associated with adverse bone health outcomes, showing an inverse relationship between phthalate exposure and bone mineral density. Dioxins present a more complex picture, with research findings suggesting both potential benefits and adverse effects on bone structure and density, depending on factors such as the timing and level of exposure. This review underscores the urgent need for further research to better understand the specific pathways through which EDCs affect bone health and to develop targeted strategies for mitigating their potentially harmful impacts.

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Jialing Yu, Sihan Huang, Jianbin Zhang, Zijian Su, Yiming Chang, Keke Liu, Lu Yang, Huiying Guo, Jinshao Ye, Xujing Liang, Xiaojia Chen, An Hong, Yibo Zhang
Journal of Hazardous Materials.2026; 501: 140750. CrossRef
Unraveling the Mechanisms of Osteoporosis Triggered by Methylparaben and Monomethyl Phthalate through Integrated Mendelian Randomization, In Silico Simulations, and Experimental Validation
Hailong Liu, Xin Xu, Longzhuo Du, Wencan Zhang, Yongyuan Guo, Fujian Zhang, Houyi Sun, Haipeng Si, Peilai Liu
Environmental Science & Technology.2026; 60(1): 228. CrossRef
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Yun-Cheng Mei, Tesfaye Abebe Geleta, Ashkan Miri, Prashanth Venkatesan, Yu-Chiang Chao, Yutong Chen, Pei-Hsin Chou, Ren Qian Tee, Yang-hsin Shih
Journal of Environmental Chemical Engineering.2026; 14(1): 121018. CrossRef
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Deren KAYA, Rabia ŞEMSİ
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Methyl-4-hydroxybenzoate induces osteoporosis via the AKT1/LC3B/Beclin1 autophagy signaling pathway: Integrating network toxicology and experimental validation
Furui Fu, Wenhao Wang, Yunqi Li, Senjie Shi, Jin Huang, Tianpeng Liu, Yi Shen, Mengting Yuan, Chuanglong Xu, Hongyu Wang, Haitao Zhang, Xiang Gao, Dezhi Tang
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Mineral, Bone & Muscle
Bone Loss after Solid Organ Transplantation: A Review of Organ-Specific Considerations: Kyoung Jin Kim, Jeonghoon Ha, Sang Wan Kim, Jung-Eun Kim, Sihoon Lee, Han Seok Choi, Namki Hong, Sung Hye Kong, Seong Hee Ahn, So Young Park, Ki-Hyun Baek, on Behalf of Metabolic Bone Disease Study Group of Korean Endocrine Society; Endocrinol Metab. 2024;39(2):267-282. Published online April 25, 2024; DOI: https://doi.org/10.3803/EnM.2024.1939

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This review article investigates solid organ transplantation-induced osteoporosis, a critical yet often overlooked issue, emphasizing its significance in post-transplant care. The initial sections provide a comprehensive understanding of the prevalence and multifactorial pathogenesis of transplantation osteoporosis, including factors such as deteriorating post-transplantation health, hormonal changes, and the impact of immunosuppressive medications. Furthermore, the review is dedicated to organ-specific considerations in transplantation osteoporosis, with separate analyses for kidney, liver, heart, and lung transplantations. Each section elucidates the unique challenges and management strategies pertinent to transplantation osteoporosis in relation to each organ type, highlighting the necessity of an organ-specific approach to fully understand the diverse manifestations and implications of transplantation osteoporosis. This review underscores the importance of this topic in transplant medicine, aiming to enhance awareness and knowledge among clinicians and researchers. By comprehensively examining transplantation osteoporosis, this study contributes to the development of improved management and care strategies, ultimately leading to improved patient outcomes in this vulnerable group. This detailed review serves as an essential resource for those involved in the complex multidisciplinary care of transplant recipients.

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Original Articles

Diabetes, obesity and metabolism
Phloretin Ameliorates Succinate-Induced Liver Fibrosis by Regulating Hepatic Stellate Cells: Cong Thuc Le, Giang Nguyen, So Young Park, Hanh Nguyen Dong, Yun Kyung Cho, Jae-Ho Lee, Seung-Soon Im, Dae-Hee Choi, Eun-Hee Cho; Endocrinol Metab. 2023;38(4):395-405. Published online August 3, 2023; DOI: https://doi.org/10.3803/EnM.2023.1661

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Background
Hepatic stellate cells (HSCs) are the major cells which play a pivotal role in liver fibrosis. During injury, extracellular stimulators can induce HSCs transdifferentiated into active form. Phloretin showed its ability to protect the liver from injury, so in this research we would like to investigate the effect of phloretin on succinate-induced HSCs activation in vitro and liver fibrosis in vivo study.
Methods
In in vitro, succinate was used to induce HSCs activation, and then the effect of phloretin on activated HSCs was examined. In in vivo, succinate was used to generated liver fibrosis in mouse and phloretin co-treated to check its protection on the liver.
Results
Phloretin can reduce the increase of fibrogenic markers and inhibits the proliferation, migration, and contraction caused by succinate in in vitro experiments. Moreover, an upregulation of proteins associated with aerobic glycolysis occurred during the activation of HSCs, which was attenuated by phloretin treatment. In in vivo experiments, intraperitoneal injection of phloretin decreased expression of fibrotic and glycolytic markers in the livers of mice with sodium succinate diet-induced liver fibrosis. These results suggest that aerobic glycolysis plays critical role in activation of HSCs and succinate can induce liver fibrosis in mice, whereas phloretin has therapeutic potential for treating hepatic fibrosis.
Conclusion
Intraperitoneal injection of phloretin attenuated succinate-induced hepatic fibrosis and alleviates the succinate-induced HSCs activation.

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Succinate activates fibroblasts through GPR91-HIF-1α-TGF-β1-Smad signaling
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Zhu Wenbo, Han Jianwei, Liu Hua, Tang Lei, Chen Guijuan, Tian Mengfei
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Diabetes, Obesity and Metabolism
Sleep Duration and the Risk of Type 2 Diabetes: A Community-Based Cohort Study with a 16-Year Follow-up: Da Young Lee, Inha Jung, So Young Park, Ji Hee Yu, Ji A Seo, Kyeong Jin Kim, Nam Hoon Kim, Hye Jin Yoo, Sin Gon Kim, Kyung Mook Choi, Sei Hyun Baik, Seung Ku Lee, Chol Shin, Nan Hee Kim; Endocrinol Metab. 2023;38(1):146-155. Published online February 6, 2023; DOI: https://doi.org/10.3803/EnM.2022.1582

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Background
We aimed to investigate the moderating effects of obesity, age, and sex on the association between sleep duration and the development of diabetes in Asians.
Methods
We analyzed data from a cohort of the Korean Genome and Epidemiology Study conducted from 2001 to 2020. After excluding shift workers and those with diabetes at baseline, 7,407 participants were stratified into three groups according to sleep duration: ≤5 hours/night, >5 to 7 hours/night (reference), and >7 hours/night. The Cox proportional hazards analyses were used to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs) for incident type 2 diabetes mellitus (T2DM). Subgroup analyses were performed according to obesity, age, and sex.
Results
During 16 years of follow-up, 2,024 cases of T2DM were identified. Individuals who slept ≤5 h/night had a higher risk of incident diabetes than the reference group (HR, 1.17; 95% CI, 1.02 to 1.33). The subgroup analysis observed a valid interaction with sleep duration only for obesity. A higher risk of T2DM was observed in the ≤5 hours/night group in non-obese individuals, men, and those aged <60 years, and in the >7 hours/night group in obese individuals (HRs were 1.34 [95% CI, 1.11 to 1.61], 1.22 [95% CI, 1 to 1.49], and 1.18 [95% CI, 1.01 to 1.39], respectively).
Conclusion
This study confirmed the effect of sleep deprivation on the risk of T2DM throughout the 16-year follow-up period. This impact was confined to non-obese or young individuals and men. We observed a significant interaction between sleep duration and obesity.

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Diabetes, Obesity and Metabolism
Gemigliptin Alleviates Succinate-Induced Hepatic Stellate Cell Activation by Ameliorating Mitochondrial Dysfunction: Giang Nguyen, So Young Park, Dinh Vinh Do, Dae-Hee Choi, Eun-Hee Cho; Endocrinol Metab. 2022;37(6):918-928. Published online November 15, 2022; DOI: https://doi.org/10.3803/EnM.2022.1530

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Background
Dipeptidyl peptidase-4 inhibitors (DPP-4Is) are used clinically as oral antidiabetic agents. Although DPP-4Is are known to ameliorate liver fibrosis, the protective mechanism of DPP-4Is in liver fibrosis remains obscure. In this study, gemigliptin was used to investigate the potential of DPP-4Is to alleviate the progression of liver fibrosis.
Methods
To clarify the effects and mechanisms of gemigliptin, we conducted various experiments in LX-2 cells (immortalized human hepatic stellate cells [HSCs], the principal effectors of hepatic fibrogenesis), which were activated by succinate and exhibited elevated expression of α-smooth muscle actin, collagen type 1, and pro-inflammatory cytokines and increased cell proliferation. In vivo, we examined the effects and mechanisms of gemigliptin on a high-fat, high-cholesterol–induced mouse model of nonalcoholic steatohepatitis (NASH).
Results
Gemigliptin decreased the expression of fibrogenesis markers and reduced the abnormal proliferation of HSCs. In addition, gemigliptin reduced the succinate-induced production of mitochondrial reactive oxygen species (ROS), intracellular ROS, and mitochondrial fission in HSCs. Furthermore, in the mouse model of NASH-induced liver fibrosis, gemigliptin alleviated both liver fibrosis and mitochondrial dysfunction.
Conclusion
Gemigliptin protected against HSC activation and liver fibrosis by alleviating mitochondrial dysfunction and ROS production, indicating its potential as a strategy for preventing the development of liver disease.

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Diabetes, Obesity and Metabolism
The Effects of Irisin on the Interaction between Hepatic Stellate Cell and Macrophage in Liver Fibrosis: Dinh Vinh Do, So Young Park, Giang Thi Nguyen, Dae Hee Choi, Eun-Hee Cho; Endocrinol Metab. 2022;37(4):620-629. Published online July 22, 2022; DOI: https://doi.org/10.3803/EnM.2022.1412

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Background
Hepatic stellate cells (HSCs) are the central players interacting with multiple cell types in liver fibrosis. The crosstalk between HSCs and macrophages has recently become clearer. Irisin, an exercise-responsive myokine, was known to have a potentially protective role in liver and renal fibrosis, especially in connection with stellate cells. This study investigated the effects of irisin on the interaction between HSCs and macrophages.
Methods
Tamm-Horsfall protein-1 (THP-1) human monocytes were differentiated into macrophages, polarized into the inflammatory M1 phenotype with lipopolysaccharide. Lieming Xu-2 (LX-2) cells, human HSCs, were treated with conditioned media (CM) from M1 macrophages, with or without recombinant irisin. HSCs responses to CM from M1 macrophages were evaluated regarding activation, proliferation, wound healing, trans-well migration, contractility, and related signaling pathway.
Results
CM from M1 macrophages significantly promoted HSC proliferation, wound healing, transwell migration, and contractility, but not activation of HSCs. Irisin co-treatment attenuated these responses of HSCs to CM. However, CM and irisin treatment did not induce any changes in HSC activation. Further, irisin co-treatment alleviated CM-induced increase of phopho-protein kinase B (pAKT), matrix metalloproteinase-9 (MMP-9), and tissue inhibitor of metalloproteinases-1 (TIMP-1).
Conclusion
These findings suggested that irisin may play a protective role in the pathogenesis of liver fibrosis, especially when working in the crosstalk between HSCs and macrophages.

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Interactions between hepatic stellate cells and immune cells: Implications for liver fibrosis
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Exercise‐Induced Irisin Antagonizes TGFBR2 to Attenuate Islet Fibrosis and Improve Glucose Homeostasis in Type 2 Diabetes
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Irisin Attenuates Hepatic Stellate Cell Activation and Liver Fibrosis in Bile Duct Ligation Mice Model and Improves Mitochondrial Dysfunction
Thuy Linh Lai, So Young Park, Giang Nguyen, Phuc Thi Minh Pham, Seon Mee Kang, Jeana Hong, Jae-Ho Lee, Seung-Soon Im, Dae-Hee Choi, Eun-Hee Cho
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Matrix metalloproteinases induce extracellular matrix degradation through various pathways to alleviate hepatic fibrosis
Liang Shan, Fengling Wang, Dandan Zhai, Xiangyun Meng, Jianjun Liu, Xiongwen Lv
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Potential role of irisin in digestive system diseases
Yueming Zhang, Linxian Zhao, Huan Gao, Jinghui Zhai, Yanqing Song
Biomedicine & Pharmacotherapy.2023; 166: 115347. CrossRef
The effect of sarcopenia and serum myokines on prognosis and survival in cirrhotic patients: a multicenter cross-sectional study
Salih Boga, Abdullah Emre Yildirim, Enver Ucbilek, Ali Riza Koksal, Sevil Tokdemir Sisman, Ibrahim Durak, Ilker Sen, Beril Dogu, Erdinc Serin, Ayse Bolat Ucbilek, Makbule Ozge Yildirim, Sukru Mehmet Erturk, Huseyin Alkim, Canan Alkim
European Journal of Gastroenterology & Hepatology.2022; 34(12): 1261. CrossRef

Hypothalamus and Pituitary Gland Big Data Articles (National Health Insurance Service Database)
Descriptive Epidemiology and Survival Analysis of Prolactinomas and Cushing’s Disease in Korea: Jin Sun Park, Soo Jin Yun, Jung Kuk Lee, So Young Park, Sang Ouk Chin; Endocrinol Metab. 2021;36(3):688-696. Published online June 28, 2021; DOI: https://doi.org/10.3803/EnM.2021.1000

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Background
Only a few studies have established the epidemiology of prolactinoma and Cushing’s disease in Korea. Furthermore, the incidence of these disease are increasing than before associated with the development of technologies. This study was designed to evaluate the epidemiology of prolactinoma and Cushing’s disease and their survival analysis according to treatment.
Methods
The nationwide, population-based study evaluated incidence and prevalence of prolactinoma and Cushing’s disease using de-identified claims data in The Korean Health Insurance Review and Assessment Service database between 2013 and 2017. The survival analysis investigated regarding treatment over a period of 6 years. A log-rank test and Cox proportional hazard regression analysis were used.
Results
The 6,056 patients with newly diagnosed prolactinoma and 584 patients with Cushing’s disease were recorded between 2013 and 2017. The annual incidence of prolactinoma was 23.5 cases per million, and its prevalence was 82.5 cases per million, and 2.3 cases per million/year and 9.8 cases per million for Cushing’s disease. The survival benefit was insignificant in prolactinoma according to treatment, but treatment of Cushing’s disease ameliorated the survival rate significantly.
Conclusion
Overall, the incidence of prolactinoma and Cushing’s disease was similar with those found previously, but the prevalence of two diseases were inconsistent when compared with the early studies. The present study also proposed necessity of treatment in Cushing’s disease for improving the survival rate.

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Endocrine Journal.2026; 73(2): 355. CrossRef
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Elena V. Varlamov, Amit Akirov, Monica L. Gheorghiu, Maria Fleseriu
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Sun Wook Cho, Jung Hee Kim, Kyoung Jin Kim, Beom-Jun Kim, Mee Kyoung Kim, Eun Jung Rhee
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Association between Prolactinoma and Incident Type 2 Diabetes Mellitus: Evidence from a Korean Nationwide Cohort
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Minwoo Bang, Suyong Shin, Jungsang Kim, Minwhee Kang, Donghun Lee, Junho Kim, Chunghee Kim, Jiyoung Son, Seonghyeon Jeon, Byungsoo Kang
Journal of Korean Medicine for Obesity Research.2026; 26(1): 22. CrossRef
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Hernan Daniel Sacoto, Vivian A. Fonseca
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The 24-Hour Urinary Cortisol/Urinary Creatinine Ratio Helps Differentiate Cushing's Syndrome From Simple Obesity
Meng Wang, Xueting Sun, Shiwei Li, Xin Li, Jingqiu Cui
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Reframing the Paradigm: A Nuanced Approach to Prolactinoma Management
Jung Hee Kim
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Elucidating Clinical Queries for Tailored Therapy in Patients with Prolactinoma
Min-Ho Lee, Jae Won Hong, Kyungwon Kim, Cheol Ryong Ku, Eun Jig Lee
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Sun Wook Cho, Jung Hee Kim, Han Seok Choi, Hwa Young Ahn, Mee Kyoung Kim, Eun Jung Rhee
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Cushing Syndrome
Martin Reincke, Maria Fleseriu
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Clinical Biology of the Pituitary Adenoma
Shlomo Melmed, Ursula B Kaiser, M Beatriz Lopes, Jerome Bertherat, Luis V Syro, Gerald Raverot, Martin Reincke, Gudmundur Johannsson, Albert Beckers, Maria Fleseriu, Andrea Giustina, John A H Wass, Ken K Y Ho
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Endocrine Research
Irisin Regulates the Functions of Hepatic Stellate Cells: Hanh Nguyen Dong, So Young Park, Cong Thuc Le, Dae-Hee Choi, Eun-Hee Cho; Endocrinol Metab. 2020;35(3):647-655. Published online September 22, 2020; DOI: https://doi.org/10.3803/EnM.2020.658

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Background
Hepatic stellate cells (HSCs) are known to play a fundamental role in the progression of liver fibrosis. Once HSCs are activated, they are involved in proliferation, migration, and contractility which are characteristics of liver fibrogenesis. Recent studies have shown that irisin, a myokine secreted during physical exercise, has a protective effect in various metabolic diseases, especially in renal fibrosis. However, whether irisin is involved in HSC activation and other processes associated with liver fibrosis has not yet been investigated. In this study, we reveal the role of irisin in HSC activation as well as in proliferation, migration, and contractile properties of HSCs in vitro.
Methods
LX-2 cells, immortalized human HSCs, were treated with transforming growth factor beta 1 (TGF-β1), a core regulator of HSC fibrosis, with or without irisin, and markers of the aforementioned processes were analyzed. Further, an inflammatory response was stimulated with TGF-β1 and lipopolysaccharide (LPS) in combination with irisin and the expression of cytokines was measured.
Results
Recombinant irisin significantly suppressed the expression of TGF-β1-stimulated fibrosis markers including alpha-smooth muscle actin and collagen type 1 alpha 1 and prevented the TGF-β1-induced proliferation, migration, and contractility of LX-2 cells. Additionally, irisin ameliorated the production of interleukin-6 (IL-6) and IL-1β induced by TGF-β1 and LPS treatments.
Conclusion
These findings suggested that irisin potently improved the progression of hepatic fibrosis by regulating HSC activation, proliferation, migration, contractility, and HSC-mediated production of inflammatory cytokine.

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Interactions between hepatic stellate cells and immune cells: Implications for liver fibrosis
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Type 2 Diabetes Mellitus as a Multisystem Disease: From Insulin Resistance to Organ Crosstalk—A Narrative Review
Héctor Fuentes-Barría, Raúl Aguilera-Eguía, Cherie Flores-Fernández, Lissé Angarita-Davila, Miguel Alarcón-Rivera
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Irisin in airway remodeling in COPD: Regulatory mechanisms from epithelial barrier to smooth muscle
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Potential role of irisin-mediated oxidative stress defense in systemic diseases
Xue Xiao, Liying Wu, Xiaoming Zhu, Jie Zhou
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Exercise induced irisin mitigates hepatitis in anabolic-androgenic steroids treated rats via modulation of PGC-1-α/PPARγ/Nrf2 and NRF2/NF-κB/TLR4 signaling
Gamal A. Salem, Mohamed Aref, Nanees F. El-Malkey, Haifa A. Alqahtani, Noha ali abd-almotaleb, Mohamed A. Nassan, Hadeel Elsherbiny
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Maria Ciałowicz, Marek Woźniewski, Eugenia Murawska-Ciałowicz, Piotr Dzięgiel
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Anna F. Sheptulina, Elvira M. Mamutova, Anastasia Yu. Elkina, Yuriy S. Timofeev, Victoria A. Metelskaya, Anton R. Kiselev, Oxana M. Drapkina
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Irisin Attenuates Hepatic Stellate Cell Activation and Liver Fibrosis in Bile Duct Ligation Mice Model and Improves Mitochondrial Dysfunction
Thuy Linh Lai, So Young Park, Giang Nguyen, Phuc Thi Minh Pham, Seon Mee Kang, Jeana Hong, Jae-Ho Lee, Seung-Soon Im, Dae-Hee Choi, Eun-Hee Cho
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Yueming Zhang, Linxian Zhao, Huan Gao, Jinghui Zhai, Yanqing Song
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The Effects of Irisin on the Interaction between Hepatic Stellate Cell and Macrophage in Liver Fibrosis
Dinh Vinh Do, So Young Park, Giang Thi Nguyen, Dae Hee Choi, Eun-Hee Cho
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Hepatic Steatosis Contributes to the Development of Muscle Atrophy via Inter-Organ Crosstalk
Kenneth Pasmans, Michiel E. Adriaens, Peter Olinga, Ramon Langen, Sander S. Rensen, Frank G. Schaap, Steven W. M. Olde Damink, Florian Caiment, Luc J. C. van Loon, Ellen E. Blaak, Ruth C. R. Meex
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Review Article

Miscellaneous
Search for Novel Mutational Targets in Human Endocrine Diseases: So Young Park, Myeong Han Seo, Sihoon Lee; Endocrinol Metab. 2019;34(1):23-28. Published online March 21, 2019; DOI: https://doi.org/10.3803/EnM.2019.34.1.23

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The identification of disease-causing genetic variations is an important goal in the field of genetics. Advancements in genetic technology have changed scientific knowledge and made it possible to determine the basic mechanism and pathogenesis of human disorders rapidly. Many endocrine disorders are caused by genetic variations of a single gene or by mixed genetic factors. Various genetic testing methods are currently available, enabling a more precise diagnosis of many endocrine disorders and facilitating the development of a concrete therapeutic plan. In this review article, we discuss genetic testing technologies for genetic endocrine disorders, with relevant examples. We additionally describe our research on implementing genetic analysis strategies to identify novel causal mutations in hypocalcemia-related disorders.

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A novel gain-of-function mutation (W818R) of calcium-sensing receptor in a family with autosomal dominant hypocalcemia type 1
Min Fu, Yanxiang Luo, Kexin Xu, Lixin Guo, Qi Pan
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EndoGene database: reported genetic variants for 5,926 Russian patients diagnosed with endocrine disorders
Anton A. Buzdin, Marianna A. Zolotovskaia, Sergey A. Roumiantsev, Aleksandra G. Emelyanova, Olga O. Golounina, Polina A. Pugacheva, Daniil V. Luppov, Anastasia V. Kuzminyh, Arseniya O. Alexeeva, Anna A. Emelianova, Alexey L. Novoselov, Alina Matrosova, An
Frontiers in Endocrinology.2025;[Epub] CrossRef

Original Articles

Miscellaneous
Novel Mutation in PTHLH Related to Brachydactyly Type E2 Initially Confused with Unclassical Pseudopseudohypoparathyroidism: Jihong Bae, Hong Seok Choi, So Young Park, Do-Eun Lee, Sihoon Lee; Endocrinol Metab. 2018;33(2):252-259. Published online June 21, 2018; DOI: https://doi.org/10.3803/EnM.2018.33.2.252

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Background

Autosomal-dominant brachydactyly type E is a congenital abnormality characterized by small hands and feet, which is a consequence of shortened metacarpals and metatarsals. We recently encountered a young gentleman exhibiting shortening of 4th and 5th fingers and toes. Initially, we suspected him having pseudopseudohypoparathyroidism (PPHP) because of normal biochemical parameters, including electrolyte, Ca, P, and parathyroid hormone (PTH) levels; however, his mother and maternal grandmother had the same conditions in their hands and feet. Furthermore, his mother showed normal biochemical parameters. To the best of our knowledge, PPHP is inherited via a mutated paternal allele, owing to the paternal imprinting of GNAS (guanine nucleotide binding protein, alpha stimulating) in the renal proximal tubule. Therefore, we decided to further analyze the genetic background in this family.

Methods

Whole exome sequencing was performed using genomic DNA from the affected mother, son, and the unaffected father as a negative control.

Results

We selected the intersection between 45,490 variants from the mother and 45,646 variants from the son and excluded 27,512 overlapping variants identified from the father. By excluding homogenous and compound heterozygous variants and removing all previously reported variants, 147 variants were identified to be shared by the mother and son. Variants that had least proximities among species were excluded and finally 23 variants remained.

Conclusion

Among them, we identified a defect in parathyroid hormone like hormone (PTHLH), encoding the PTH-related protein, to be disease-causative. Herein, we report a family affected with brachydactyly type E2 caused by a novel PTHLH mutation, which was confused with PPHP with unclassical genetic penetrance.

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PTHLH gene variant in an Indian boy with brachydactyly type E: A case report and literature review
Anjana Hulse, Priya Ranganath
Clinical Pediatric Endocrinology.2026; 35(3): 266. CrossRef
Case Report: A novel PTHLH nonsense variant in a mother–son pair with brachydactyly type E and short stature, with a genotype–stature review
Hui Huang, Binyang Zhu, Zaisheng Wang, Zhuqiang Wu, Jinqiu Rao, Yu Yang, Xiangyu Xiong
Frontiers in Endocrinology.2026;[Epub] CrossRef
Human diseases caused by homozygous PTH1R mutations
Ignacio Portales-Castillo, Jakob Höppner, Harald Jüppner, Thomas J. Gardella
Frontiers in Endocrinology.2025;[Epub] CrossRef
A novel heterozygous mutation in PTHLH causing autosomal dominant brachydactyly type E complicated with short stature
Jian Sun, Nian Yang, Zhengquan Xu, Hongbo Cheng, Xiangxin Zhang
Molecular Genetics & Genomic Medicine.2024;[Epub] CrossRef
A novel mutation in PTHLH in a family with a variable phenotype with brachydactyly, short stature, oligodontia and developmental delay
Mirjam E.A. Scheffer-Rath, Hermine E. Veenstra-Knol, Annemieke M. Boot
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Characterization and expression profiling of G protein-coupled receptors (GPCRs) in Spodoptera litura (Lepidoptera: Noctuidae)
Yanxiao Li, Han Gao, Hui Zhang, Runnan Yu, Fan Feng, Jing Tang, Bin Li
Comparative Biochemistry and Physiology Part D: Genomics and Proteomics.2022; 44: 101018. CrossRef
Genes with specificity for expression in the round cell layer of the growth plate are enriched in genomewide association study (GWAS) of human height
Nora E. Renthal, Priyanka Nakka, John M. Baronas, Henry M. Kronenberg, Joel N. Hirschhorn
Journal of Bone and Mineral Research.2020; 36(12): 2300. CrossRef
Search for Novel Mutational Targets in Human Endocrine Diseases
So Young Park, Myeong Han Seo, Sihoon Lee
Endocrinology and Metabolism.2019; 34(1): 23. CrossRef
A Heterozygous Splice-Site Mutation in PTHLH Causes Autosomal Dominant Shortening of Metacarpals and Metatarsals
Monica Reyes, Bert Bravenboer, Harald Jüppner
Journal of Bone and Mineral Research.2019; 34(3): 482. CrossRef
A 3.06-Mb interstitial deletion on 12p11.22-12.1 caused brachydactyly type E combined with pectus carinatum
Jia Huang, Hong-Yan Liu, Rong-Rong Wang, Hai Xiao, Dong Wu, Tao Li, Ying-Hai Jiang, Xue Zhang
Chinese Medical Journal.2019; 132(14): 1681. CrossRef
Parathyroid Hormone-Related Protein in the Hand or Out of Hand?
Sang Wan Kim
Endocrinology and Metabolism.2018; 33(2): 202. CrossRef

Endocrine Research
The Role of Nuclear Factor-E2-Related Factor 1 in the Oxidative Stress Response in MC3T3-E1 Osteoblastic Cells: So Young Park, Sung Hoon Kim, Hyun Koo Yoon, Chang Hoon Yim, Sung-Kil Lim; Endocrinol Metab. 2016;31(2):336-342. Published online April 25, 2016; DOI: https://doi.org/10.3803/EnM.2016.31.2.336

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Background

Reactive oxygen species (ROS) and antioxidants are associated with maintenance of cellular function and metabolism. Nuclear factor-E2-related factor 1 (NFE2L1, Nrf1) is known to regulate the expression of a number of genes involved in oxidative stress and inflammation. The purpose of this study was to examine the effects of NFE2L1 on the response to oxidative stress in osteoblastic MC3T3-E1 cells.

Methods

The murine calvaria-derived MC3T3-E1 cell line was exposed to lipopolysaccharide (LPS) for oxidative stress induction. NFE2L1 effects were evaluated using small interfering RNA (siRNA) for NFE2L1 mRNA. ROS generation and the levels of known antioxidant enzyme genes were assayed.

Results

NFE2L1 expression was significantly increased 2.4-fold compared to the control group at 10 µg/mL LPS in MC3T3-E1 cells (P<0.05). LPS increased formation of intracellular ROS in MC3T3-E1 cells. NFE2L1 knockdown led to an additional increase of ROS (20%) in the group transfected with NFE2L1 siRNA compared with the control group under LPS stimulation (P<0.05). RNA interference of NFE2L1 suppressed the expression of antioxidant genes including metallothionein 2, glutamatecysteine ligase catalytic subunit, and glutathione peroxidase 1 in LPS-treated MC3T3-E1 cells.

Conclusion

Our results suggest that NFE2L1 may have a distinct role in the regulation of antioxidant enzymes under inflammation-induced oxidative stress in MC3T3-E1 osteoblastic cells.

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Case Reports

Thyroid
Thyroid Dysfunction Associated with Administration of the Long-Acting Gonadotropin-Releasing Hormone Agonist: Eun Jin Han, Ha Do Song, Ji Hoon Yang, So Young Park, Sung Hoon Kim, Hyun Koo Yoon, Chang Hoon Yim; Endocrinol Metab. 2013;28(3):221-225. Published online September 13, 2013; DOI: https://doi.org/10.3803/EnM.2013.28.3.221

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Abstract PDF PubReader

Gonadotropin-releasing hormone (GnRH) agonist has been used in the treatment of a wide variety of sex-hormone-related diseases, as the administration of GnRH agonist can alter the secretion of gonadotropin and sex hormones. Recently, we found that the long-acting GnRH agonist aggravated hyperthyroidism and induced painless thyroiditis. This is the first report to demonstrate the association of thyroid dysfunction with GnRH agonist injection in Korea. Here, we report three cases and emphasize the clinical importance of this aggravating factor in autoimmune thyroid disease.

Citations

Citations to this article as recorded by

American Thyroid Association 2026 Guidelines for Thyroid Disease in Preconception, Pregnancy, and Postpartum
Tim I.M. Korevaar, Angela M. Leung, Erik K. Alexander, Sofie Bliddal, Kristien Boelaert, Gabriela Brenta, Roger Chou, Rima Dhillon-Smith, Chrysoula Dosiou, Jennifer L. Eaton, Haixia Guan, Sarah J. Kilpatrick, Bente J. Lasserre, Sun Y. Lee, Spyridoula Mara
Thyroid®.2026; 36(5): 481. CrossRef
Long-term maternal health outcomes following autologous in vitro fertilization compared with medically unassisted conceptions and with nulliparas
Hila Shalev-Ram, Amir Wiser, Roni Rahav-Koren, Einat Haikin-Herzberger, Roei Shlezinger, Mattan Levi, Netanella Miller
Journal of Assisted Reproduction and Genetics.2026; 43(8): 2433. CrossRef
New onset of Graves' disease after controlled ovarian stimulation: A case report and brief literature review
Alberto Vassallo, Luigi Di Filippo, Stefano Frara, Massimo Bertoli, Mauro Pagani, Barbara Presciuttini
International Journal of Gynecology & Obstetrics.2025; 168(3): 913. CrossRef
De Novo Graves’ Disease in a 10-Year-Old Girl Receiving Gonadotropin-Releasing Hormone Agonist Therapy for Idiopathic Central Precocious Puberty: A Case Report
Yoshimi Fujita, Kenta Horimukai, Mika Kiyohara, Noriko Takahata
Cureus.2025;[Epub] CrossRef
Thyroid Dysfunction after Gonadotropin-Releasing Hormone Agonist Administration in Women with Thyroid Autoimmunity
Loris Marin, Guido Ambrosini, Marco Noventa, Flavia Filippi, Eugenio Ragazzi, Francesco Dessole, Giampiero Capobianco, Alessandra Andrisani, Alexander Schreiber
International Journal of Endocrinology.2022; 2022: 1. CrossRef
Effects of controlled ovarian stimulation on thyroid function during pregnancy
Lingfei Li, Ling Li, Ping Li
Biology of Reproduction.2022; 107(6): 1376. CrossRef
Is gonadotropin-releasing hormone agonist usage really leading to thyroid dysfunction?
Nafiye Yilmaz, Necati Hancerliogullari, Mustafa Kara, Yaprak Engin-Ustun
Interventional Medicine and Applied Science.2020; 11(3): 136. CrossRef
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Eunyoung Ha, Seungmee Lee, So Min Lee, Jeeyeon Jung, Hyewon Chung, Eunsom Choi, Sun Young Kwon, Min Ho Cha, So-Jin Shin
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Effects of controlled ovarian stimulation on thyroid stimulating hormone in infertile women
Yuan-Jie Du, Xin Xin, Na Cui, Lei Jiang, Ai-Min Yang, Gui-Min Hao, Bu-Lang Gao
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The impact of thyroid autoimmunity on IVF/ICSI outcome: a systematic review and meta-analysis
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The Potential Role of GnRH Agonists and Antagonists in Inducing Thyroid Physiopathological Changes During IVF
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A Case of Hypothyroidism in Remission during Pregnancy.: Ha Do Song, Eun Jin Han, Sung Ja Lee, Ji Hoon Yang, So Young Park, Sung Hoon Kim, Ki Ok Han, Hyun Koo Yoon, Chang Hoon Yim; Endocrinol Metab. 2012;27(4):295-298. Published online December 20, 2012; DOI: https://doi.org/10.3803/EnM.2012.27.4.295

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Abstract PDF: Hypothyroidism should be treated in pregnancy, because it has been associated with an increased risk of adverse pregnancy complications, as well as detrimental effects upon fetal neurocognitive development. The goal of L-thyroxine (LT4) treatment is to normalize maternal serum TSH values within the trimester-specific pregnancy reference range. 50% to 85% of hypothyroid women being treated with exogenous LT4 need to increase the dose during pregnancy. In this study, we report a case of a 29-year-old woman with hypothyroidism who had been in remission and discontinued LT4 treatment during her pregnancy. Three months after delivery she had a relapse of hypothyroidism and was retreated with LT4. Many factors can influence the gestational requirement for LT4, therefore maternal serum TSH should be monitored and the LT4 dose should be adjusted in pregnant patients with treated hypothyroidism.

A Case of Graves' Disease Presented as Generalized Seizure Attack.: So Young Park, Su Kyoung Park, Sung Hwan Suh, Duk Kyu Kim, Sang Ho Kim, Mi Kyoung Park, Song Yee Han, Seung Hee Ryu, Su Mi Woo, Sung Woo Lee, Neul Bom Yoon; Endocrinol Metab. 2012;27(2):142-146. Published online June 20, 2012; DOI: https://doi.org/10.3803/EnM.2012.27.2.142

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Abstract PDF: Hyperthyroidism is diagnosed when a patient is presented with typical symptoms, such as weight loss, palpitation, and hand tremor. However, early diagnosis is difficult in elders, because they have no typical symptoms, but only cardiovascular or muscular symptoms. In hyperthyroidism, there are often with neurologic changes, leading to various neurologic symptoms. Generalized or focal seizures are rarely reported in thyrotoxicosis and thyrotoxic crisis. Further, cases of hyperthyroidism presented as generalized seizure attack are extremely rare. We report a case of hyperthyroidism. A patient is presented at the hospital with mental change, as well as generalized seizure, who was finally diagnosed to have Graves' disease. A 56-year-old male was admitted to the hospital because of mental change with generalized seizure attack. Initial neurologic evaluations, including a brain magnetic resonance imaging and electroencephalogram proved to be normal. But, thyroid function test showed abnormal results. We diagnosed him as Graves' disease and prescribed anti-thyroid drug. Thereafter, there has been no recurrence of neurologic symptoms for 12 months.

A Case of Primary Hyperparathyroidism with Rapid Regression of a Brown Tumor after Parathyroidectomy.: Ji Young Mok, Ha Yeon Kim, Hsing Chien Ter, Sang Ock Kim, Dong Kyun Kim, Ji Sun Han, So Young Park, Sa Rah Lee, Mi Kyoung Park, Duk Kyu Kim; J Korean Endocr Soc. 2010;25(1):50-55. Published online March 1, 2010; DOI: https://doi.org/10.3803/jkes.2010.25.1.50

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Abstract PDF: Primary hyperparathyroidism is mainly caused by parathyroid adenoma (85%) and is characterized by hypercalcemia, osteoporosis, renal stones, and gastrointestinal and neurological disorders. Because of improvements in blood analysis over the last two decades, primary hyperparathyroidism is typically diagnosed early and asymptomatically. A rare clinical manifestations of primary hyperparathyroidism, brown tumors (osteitis fibrosa cystica), are osteolytic lesions resulting from long-term hyperparathyroidism. Radiologically, it is difficult to distinguish a brown tumor from plasmacytoma, multiple myeloma, or bone metastasis. We report a case of a 44-year-old man with primary hyperparathyroidism that caused a large brown tumor (11 x 5 x 8 cm) that mimicked plasmacytoma or cancer metastasis on pelvic magnetic resonance imaging. After a bone biopsy report that was highly suggestive of a brown tumor, serum calcium and intact parathyroid hormone levels were determined. The lesion was ultimately diagnosed as a brown tumor and a parathyroidectomy was performed. After 1 year, the lesion has nearly regressed by follow up of the anteroposterior view of the pelvis and bone mineral density has improved. The present case highlights the importance of considering brown tumors in the evaluation of patients presenting with hypercalcemia and osteolytic lesions without definite primary neoplasm.

Original Articles

The Effect of Leptin Level Fluctuations by a Repeated Fasting/Refeeding on the Leptin Sensitivity in OLETF Rats.: Sung Chul Park, Yong Hoon Park, So Young Park, Jong Yeon Kim, Yoon Ki Park, Tae Hyung Lee, Kyu Chang Won, Yong Woon Kim; J Korean Endocr Soc. 2008;23(5):310-318. Published online October 1, 2008; DOI: https://doi.org/10.3803/jkes.2008.23.5.310

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Abstract PDF

BACKGROUND
Leptin resistance is a common feature in obese subjects and animals, and this is commonly accompanied with hyperleptinemia. We speculated that one of the causes of leptin resistance is a persistently elevated leptin concentration and then we hypothesized that fluctuations of serum leptin would increase leptin sensitivity in the leptin-resistant state. METHODS: We used a repeated fasting and refeeding (RFR) protocol to produce fluctuation in leptin levels in 7 month-old Otsuka Long-Evans Tokushima Fatty (OLETF) rats and Long-Evans Tokushima Otsuka (LETO) rats, We then measured the leptin sensitivity following an intracerebroventricular (i.c.v.) infusion of leptin. RESULTS: The OLETF rats exhibited severe visceral fat deposition, hyperleptinemia and leptin resistance. However, in the OLETF-RFR rats, the anorexic effect following i.c.v. leptin infusion was restored. Moreover, the visceral fat mass and serum leptin levels decreased, while the serum adiponectin levels were elevated in the OLETF-RFR rats compared to the OLETF-Control rats. The leptin receptor content in the hypothalamus increased in the OLETF-RFR rats compared to the OLETF-Control rats, and the leptin receptor content in the OLETF-RFR rats decreased compared to that in the the LETO-Control rats. CONCLUSION: These results suggest that the intermittent suppression of the serum leptin level reversed the leptin resistance in OLEFT rats, and this may have occurred due to an increased number of leptin receptors in the hypothalamus.

Citations

Citations to this article as recorded by

Dietary-dependent sensitization of neuronal leptin signaling promotes neural repair after injury via cAMP and gene transcription
Jessica S. Chadwick, Charlotte Decourt, Franziska Müller, Ines Maldonado-Lasuncion, Elisabeth Serger, Guiping Kong, Luming Zhou, Yayue Song, Yuyang Yan, Zhulin Yuan, Alessandro Falconieri, Phoebe Liddell, Linshan Chu, Wei Qin Chan, Lucia Luengo-Gutierrez,
Neuron.2025; 113(17): 2839. CrossRef
Reduced Striatal Dopamine Transporter Availability and Heightened Response to Natural and Pharmacological Stimulation in CCK-1R-Deficient Obese Rats
Sevag Hamamah, Andras Hajnal, Mihai Covasa
International Journal of Molecular Sciences.2023; 24(11): 9773. CrossRef
Improvement of Leptin Resistance
Yong Woon Kim
Yeungnam University Journal of Medicine.2013; 30(1): 4. CrossRef
The Effect of Food Restriction on Appetite Regulating Hormones and Adiponectin Activity
Ki Hoon Kim, Hyun Kook Kim
Korean Journal of Nutrition.2012; 45(1): 5. CrossRef
The Effect of Leptin Level Fluctuations by a Repeated Fasting/Refeeding on the Leptin Sensitivity in OLETF Rats
Min Seon Kim
Journal of Korean Endocrine Society.2008; 23(5): 298. CrossRef

Naloxone Increases the Anorexic Effect of MTII in OLETF Rats.: Jang Ho Bae, Yong Hoon Park, Sung Ho Kim, So Young Park, Jong Yeon Kim, Jo Young Son, Jung Yoon Huh, Kyu Chang Won, Yong Woon Kim; J Korean Endocr Soc. 2008;23(1):18-26. Published online February 1, 2008; DOI: https://doi.org/10.3803/jkes.2008.23.1.18

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Abstract PDF

BACKGROUND
Leptin, an adipocyte-derived hormone, inhibits obesity in lean subjects, but is not widely used because of leptin resistance. Thus, circumventing the arcuate nucleus of the hypothalamus, the site responsible for leptin resistance, has been evaluated for treatment of obesity. However, chronic treatment of melanotan II (MTII), a synthetic agonist of the melanocortin 3/4 receptor, induces tachyphylaxis. Here, we evaluated whether naloxone, a non-specific agouti-related peptide (AgRP) antagonist, increases the anorexic effect of MTII in Otsuka Long-Evans Tokushima Fatty (OLETF) rats. METHODS: We measured food intake following intracerebroventricular (i.c.v.) infusion of MTII and/or naloxone in OLETF rats. Sprague-Dawley rats were used as a normal control group. RESULTS: The anorexic effect of i.c.v. MTII infusion decreased with time in OLETF rats, indicating the development of tachyphylaxis. In normal control rats, naloxone alone decreased AgRP expression in the hypothalamus but failed to induce anorexia. Moreover, there was no additional anorexic effect with co-treatment of naloxone and MTII. In OLETF rats, naloxone alone did not show an anorexic effect despite increased POMC expression in the hypothalamus. However, naloxone sensitized the anorexic effect of MTII when treated together. CONCLUSION: These results suggest that naloxone augmented the anorexic effect of MTII when treated together in OLETF rats, but had no effect alone. These results suggest that a combination therapy of naloxone and a melanocortin receptor activator would be an effective modality for treatment of obesity.

Citations

Citations to this article as recorded by

Naloxone Increases the Anorexic Effect of Melanocortin II
Seungjoon Park
Journal of Korean Endocrine Society.2008; 23(1): 15. CrossRef

Osteoporosis and Atherosclerosis: Current and New Potential Medicines Targeting Both Diseases.: Sung Kil Lim, So Young Park; J Korean Endocr Soc. 2005;20(6):608-615. Published online December 1, 2005; DOI: https://doi.org/10.3803/jkes.2005.20.6.608

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Abstract PDF: No Abstract available.

Adiponectin Gene Polymorphism and Carotid Artery Intima-Media thickness in Type 2 Diabetes.: Eun Seok Kang, So Young Park, So Hun Kim, Hyun Joo Lee, Kyu Yeon Hur, Seung Jin Han, Se Eun Park, Hyeong Jin Kim, Chul Woo Ahn, Bong Soo Cha, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee; J Korean Endocr Soc. 2005;20(1):29-39. Published online February 1, 2005; DOI: https://doi.org/10.3803/jkes.2005.20.1.29

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Abstract PDF: BACKGROUND
The aim of this study was to examine the association between the common polymorphisms of the adiponectin gene(ACDC) and the intima-media thickness(IMT) of the common carotid arteries in type 2 diabetic patients. METHODS: The B mode ultrasound examination of carotid artery was performed on 133 type 2 diabetic patients. The carotid IMT was calculated using the Intimascope computer program. The SNP45 and SNP276 of the ACDC were examined. RESULTS: There was no significant difference in the carotid IMT among the SNP45 genotypes(0.66+/-0.18mm for TT, 0.71+/-0.12mm for TG and 0.64+/-0.15mm for GG, P=NS). Subjects carrying the SNP276 GG genotype had a markedly lower serum adiponectin concentration than those carrying the TT genotype(3.35+/-2.00microgram/mL vs. 4.98+/-2.24microgram/mL, P=0.029) The carotid IMT was significantly higher in patients with the SNP276 GG genotype than those with the TT genotype (0.70+/-0.17mm vs. 0.59+/-0.13mm, P=0.032). Patients with the +45GG/+276GG genotype combination showed significantly higher mean carotid IMT than the other genotype combinations(0.78+/-0.09mm vs. 0.71+/-0.15mm, P=0.013) CONCLUSIONS: These results suggest that the adiponectin gene, SNP276 is associated with the carotid IMT in type 2 diabetic patients. Further studies are will be needed to confirm these genotypephenotype associations.

Case Reports

A Case of Silent Corticotroph-cell Adenoma with Elevated Serum ACTH.: Jeong Geun Moon, So Young Park, Byoung Chul Cho, Jung Min Lee, Si Hoon Lee, Yoo Mee Kim, Yu Mie Rhee, Bong Soo Cha, Hyun Chul Lee, Sung Kil Lim; J Korean Endocr Soc. 2004;19(5):535-541. Published online October 1, 2004

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Abstract PDF: A 48 year-old man was referred to our Department with a headache, and also presented with an elevated serum ACTH level, but without an elevated serum cortisol. Although there was no clinical evidence of Cushing's syndrome, a brain CT and MRI showed a 4x4.5 cm sized pituitary mass, which was successfully removed by a transsphenoidal approach (TSA). A histopathological examination revealed the mass to have an ACTH positive reaction. Therefore, through hormonal and pathological evaluation, a silent corticotroph-cell adenoma (SCCA), with an elevated serum ACTH level, was diagnosed. Although reports on SCCA have been recently increased, this case is reported because these kinds of tumor are still rare, and those SCCA with an elevated serum ACTH even more so

A Case of Follicular Thyroid Carcinoma Developed in Pendred Syndrome.: So Hun Kim, Ji Young Jung, Sung Jae Shin, So Young Park, Si Hoon Lee, Yoo Mee Kim, Yu Mie Rhee, Soon Won Hong, Bong Soo Cha, Chul Woo Ahn, Kyung Rae Kim, Sung Kil Lim, Hyun Chul Lee; J Korean Endocr Soc. 2004;19(4):411-418. Published online August 1, 2004

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Abstract PDF: Pendred syndrome is an autosomal recessive genetic disorder, which is characterized by sensorineural hearing loss, goiter and a positive perchlorate discharge test. It is caused by mutations of the PDS gene, and its clinical characteristics vary widely. The thyroid function in most cases is normal, or shows only mild hypothyroidism. In Pendred syndrome, there is an organification defect that leads to defective thyroid hormone synthesis, followed by chronic TSH stimulation. Herein is reported a case of a follicular thyroid carcinoma associated with Pendred syndrome. To our knowledge, this is the first case reported in Korea. The patient presented with a huge anterior neck mass, sensorineural hearing loss and a positive perchlorate discharge test. Fine needle aspiration cytology suggested malignancy of the thyroid, and a total thyroidectomy, with central compartment node dissection, was performed. The pathology from the thyroid mass showed a poorly differentiated follicular thyroid carcinoma

A Case of Hypercalcemia Associated with Hepatic Tuberculosis.: So Young Park, Eun Seok Kang, So Hun Kim, Mi Young Do, Kyu Yeon Hur, Bong Soo Cha, Sung Kil Lim, Hyun Chul Lee, Sang Hoon Ahn, Young Myoung Moon, Young Nyun Park; J Korean Endocr Soc. 2004;19(1):64-68. Published online February 1, 2004

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Abstract PDF: In this report, a 70-year-old female patient was detected with laboratory findings of hypercalcemia. The most common causes of hypercalcemia are primary hyperparathyroidism and malignant disease. Her laboratory tests did not show any evidence for neither primary hyperparathyroidism nor malignant diseases. Thus, granulomatous disease was suspected as the cause of the hypercalcemia. Liver MRI (magnetic resonance image) was performed on the subject, which suggested the presence of hepatic tuberculosis and sarcoidosis. Because the chest x-ray did not show a definite tuberculous lesion, we performed a laparoscopic liver biopsy for a final diagnosis. Findings from the biopsy specimen showed typical tuberculosis. After treatment with tuberculosis medication, hypercalcemia of the subject was resolved. Hypercalcemia is a well recognized as a possible complication of active pulmonary tuberculosis. But one should consider hepatic tuberculosis without pulmonary tuberculosis as a cause of hypercalcemia.

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