Endocrinology and Metabolism

Review Article

Calcium & bone metabolism
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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Abstract PDF: 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.

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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Abstract PDF PubReader ePub: 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.

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.

Citations

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Attention to Innate Circadian Rhythm and the Impact of Its Disruption on Diabetes
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, Nan Hee Kim
Diabetes & Metabolism Journal.2024; 48(1): 37. CrossRef
Role of Sleep and Sleep Disorders in Cardiometabolic Risk: a Review and Update
Shaden O. Qasrawi, Ahmed S. BaHammam
Current Sleep Medicine Reports.2024; 10(1): 34. CrossRef
Evaluating reliability in wearable devices for sleep staging
Vera Birrer, Mohamed Elgendi, Olivier Lambercy, Carlo Menon
npj Digital Medicine.2024;[Epub] CrossRef
All That Glitters Is Not Gold: The Same Sleep Time, but Different Diabetogenic Outcomes
Bohye Kim, Obin Kwon
Endocrinology and Metabolism.2023; 38(1): 78. CrossRef
The Link Between Sleeping and Type 2 Diabetes: A Systematic Review
Ali Darraj
Cureus.2023;[Epub] CrossRef

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.

Citations

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Improvement effect of gemigliptin on salivary gland dysfunction in exogenous methylglyoxal-injected rats
Woo Kwon Jung, Su-Bin Park, Hwa Young Yu, Junghyun Kim
Heliyon.2024; 10(8): e29362. CrossRef
Gemigliptin, a DPP4 inhibitor, ameliorates nonalcoholic steatohepatitis through AMP-activated protein kinase-independent and ULK1-mediated autophagy
Youngmi Song, Hyekyung Yang, Juhee Kim, Yoonjin Lee, Sung-Ho Kim, In-Gu Do, Cheol-Young Park
Molecular Metabolism.2023; 78: 101806. CrossRef
DPP-4 Inhibitor in Type 2 Diabetes Mellitus Patient with Non-Alcoholic Fatty Liver Disease: Achieving Two Goals at Once?
Ji Cheol Bae
Endocrinology and Metabolism.2022; 37(6): 858. CrossRef

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.

Citations

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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
Biomedicine & Pharmacotherapy.2023; 161: 114472. CrossRef
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.

Citations

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Big Data Research in the Field of Endocrine Diseases Using the Korean National Health Information Database
Sun Wook Cho, Jung Hee Kim, Han Seok Choi, Hwa Young Ahn, Mee Kyoung Kim, Eun Jung Rhee
Endocrinology and Metabolism.2023; 38(1): 10. CrossRef
Cushing Syndrome
Martin Reincke, Maria Fleseriu
JAMA.2023; 330(2): 170. CrossRef
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
Endocrine Reviews.2022; 43(6): 1003. CrossRef

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.

Citations

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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
Potential role of irisin in lung diseases and advances in research
Hongna Dong, Xuejiao Lv, Peng Gao, Yuqiu Hao
Frontiers in Pharmacology.2023;[Epub] CrossRef
Stem bark of Fraxinus rhynchophylla ameliorates the severity of pancreatic fibrosis by regulating the TGF-β/Smad signaling pathway
Ji-Won Choi, Joon Yeon Shin, Ziqi Zhou, Dong-Uk Kim, Bitna Kweon, Hyuncheol Oh, Youn-Chul Kim, Ho-Joon Song, Gi-Sang Bae, Sung-Joo Park
Journal of Investigative Medicine.2022; 70(5): 1285. CrossRef
Circadian rhythms and cancers: the intrinsic links and therapeutic potentials
Li Zhou, Zhe Zhang, Edouard Nice, Canhua Huang, Wei Zhang, Yong Tang
Journal of Hematology & Oncology.2022;[Epub] CrossRef
Kinsenoside alleviates inflammation and fibrosis in experimental NASH mice by suppressing the NF-κB/NLRP3 signaling pathway
Yan-fang Deng, Qian-qian Xu, Tian-qi Chen, Jia-xiong Ming, Ya-fen Wang, Li-na Mao, Jia-jun Zhou, Wei-guang Sun, Qun Zhou, Hong Ren, Yong-hui Zhang
Phytomedicine.2022; 104: 154241. CrossRef
The potential role of FNDC5/irisin in various liver diseases: awakening the sleeping beauties
Xiaoyu Wang, Lihong Mao, Chaoqun Li, Yangyang Hui, Zihan Yu, Mingyu Sun, Yifan Li, Gaoyue Guo, Wanting Yang, Binxin Cui, Xiaofei Fan, Chao Sun
Expert Reviews in Molecular Medicine.2022;[Epub] CrossRef
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
Endocrinology and Metabolism.2022; 37(4): 620. CrossRef
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
Frontiers in Endocrinology.2021;[Epub] CrossRef
Physiopathology of Lifestyle Interventions in Non-Alcoholic Fatty Liver Disease (NAFLD)
David Carneros, Guillermo López-Lluch, Matilde Bustos
Nutrients.2020; 12(11): 3472. CrossRef

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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Abstract PDF PubReader ePub: 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.

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.

Citations

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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
Bone Reports.2023; 19: 101699. CrossRef
Bioactive phytoconstituents as potent inhibitors of casein kinase-2: dual implications in cancer and COVID-19 therapeutics
Farah Anjum, Md Nayab Sulaimani, Alaa Shafie, Taj Mohammad, Ghulam Md. Ashraf, Anwar L. Bilgrami, Fahad A. Alhumaydhi, Suliman A. Alsagaby, Dharmendra Kumar Yadav, Md. Imtaiyaz Hassan
RSC Advances.2022; 12(13): 7872. CrossRef
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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Xingzhu Liu, Chang Xu, Wanglong Xiao, Nianlong Yan
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Food and Chemical Toxicology.2021; 158: 112633. CrossRef
Long isoforms of NRF1 negatively regulate adipogenesis via suppression of PPARγ expression
Peng Xue, Yongyong Hou, Zhuo Zuo, Zhendi Wang, Suping Ren, Jian Dong, Jingqi Fu, Huihui Wang, Melvin E. Andersen, Qiang Zhang, Yuanyuan Xu, Jingbo Pi
Redox Biology.2020; 30: 101414. CrossRef
Protracted rosiglitazone treatment exacerbates inflammation in white adipose tissues of adipocyte-specific Nfe2l1 knockout mice
Suping Ren, Yongyong Hou, Zhuo Zuo, Zhiyuan Liu, Huihui Wang, Yuanyuan Xu, Masayuki Yamamoto, Qiang Zhang, Jingqi Fu, Jingbo Pi
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Nrf1 is paved as a new strategic avenue to prevent and treat cancer, neurodegenerative and other diseases
Jianxin Yuan, Shuwei Zhang, Yiguo Zhang
Toxicology and Applied Pharmacology.2018; 360: 273. CrossRef
Silencing of long isoforms of nuclear factor erythroid 2 like 1 primes macrophages towards M1 polarization
Huihui Wang, Jiayu Zhu, Zhiyuan Liu, Hang Lv, Peng Lv, Feng Chen, Jingqi Fu, Yongyong Hou, Rui Zhao, Yuanyuan Xu, Qiang Zhang, Jingbo Pi
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Costunolide increases osteoblast differentiation via ATF4-dependent HO-1 expression in C3H10T1/2 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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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

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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
FANCA Polymorphism Is Associated with the Rate of Proliferation in Uterine Leiomyoma in Korea
Eunyoung Ha, Seungmee Lee, So Min Lee, Jeeyeon Jung, Hyewon Chung, Eunsom Choi, Sun Young Kwon, Min Ho Cha, So-Jin Shin
Journal of Personalized Medicine.2020; 10(4): 228. CrossRef
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
European Journal of Obstetrics & Gynecology and Reproductive Biology.2019; 234: 207. CrossRef
Myxedema Coma Following the Administration of Gonadotropin-releasing Hormone Agonist Complicated by Acute Pancreatitis
Naoki Gocho, Ema Aoki, Chiho Okada, Takeshi Hirashima
Internal Medicine.2018; 57(21): 3117. CrossRef
The impact of thyroid autoimmunity on IVF/ICSI outcome: a systematic review and meta-analysis
Andrea Busnelli, Alessio Paffoni, Luigi Fedele, Edgardo Somigliana
Human Reproduction Update.2016; 22(6): 775. CrossRef
The Potential Role of GnRH Agonists and Antagonists in Inducing Thyroid Physiopathological Changes During IVF
Salvatore Gizzo, Marco Noventa, Michela Quaranta, Amerigo Vitagliano, Federica Esposito, Alessandra Andrisani, Roberta Venturella, Carlo Alviggi, Mario Plebani, Michele Gangemi, Giovanni Battista Nardelli, Donato D’Antona
Reproductive Sciences.2016; 23(4): 515. CrossRef
Brief Review of Articles in 'Endocrinology and Metabolism' in 2013
Won-Young Lee
Endocrinology and Metabolism.2014; 29(3): 251. CrossRef

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 Article

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

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
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Yong Woon Kim
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The Effect of Food Restriction on Appetite Regulating Hormones and Adiponectin Activity
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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

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