Endocrinology and Metabolism

Original Articles

Diabetes, obesity and metabolism
Inhibition of Sodium-Glucose Cotransporter-2 during Serum Deprivation Increases Hepatic Gluconeogenesis via the AMPK/AKT/FOXO Signaling Pathway: Jinmi Lee, Seok-Woo Hong, Min-Jeong Kim, Yu-Mi Lim, Sun Joon Moon, Hyemi Kwon, Se Eun Park, Eun-Jung Rhee, Won-Young Lee; Endocrinol Metab. 2024;39(1):98-108. Published online January 3, 2024; DOI: https://doi.org/10.3803/EnM.2023.1786

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Abstract PDF Supplementary Material PubReader ePub: Background
Sodium-dependent glucose cotransporter 2 (SGLT2) mediates glucose reabsorption in the renal proximal tubules, and SGLT2 inhibitors are used as therapeutic agents for treating type 2 diabetes mellitus. This study aimed to elucidate the effects and mechanisms of SGLT2 inhibition on hepatic glucose metabolism in both serum deprivation and serum supplementation states.
Methods
Huh7 cells were treated with the SGLT2 inhibitors empagliflozin and dapagliflozin to examine the effect of SGLT2 on hepatic glucose uptake. To examine the modulation of glucose metabolism by SGLT2 inhibition under serum deprivation and serum supplementation conditions, HepG2 cells were transfected with SGLT2 small interfering RNA (siRNA), cultured in serum-free Dulbecco’s modified Eagle’s medium for 16 hours, and then cultured in media supplemented with or without 10% fetal bovine serum for 8 hours.
Results
SGLT2 inhibitors dose-dependently decreased hepatic glucose uptake. Serum deprivation increased the expression levels of the gluconeogenesis genes peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α), glucose 6-phosphatase (G6pase), and phosphoenolpyruvate carboxykinase (PEPCK), and their expression levels during serum deprivation were further increased in cells transfected with SGLT2 siRNA. SGLT2 inhibition by siRNA during serum deprivation induces nuclear localization of the transcription factor forkhead box class O 1 (FOXO1), decreases nuclear phosphorylated-AKT (p-AKT), and p-FOXO1 protein expression, and increases phosphorylated-adenosine monophosphate-activated protein kinase (p-AMPK) protein expression. However, treatment with the AMPK inhibitor, compound C, reversed the reduction in the protein expression levels of nuclear p- AKT and p-FOXO1 and decreased the protein expression levels of p-AMPK and PEPCK in cells transfected with SGLT2 siRNA during serum deprivation.
Conclusion
These data show that SGLT2 mediates glucose uptake in hepatocytes and that SGLT2 inhibition during serum deprivation increases gluconeogenesis via the AMPK/AKT/FOXO1 signaling pathway.

Calcium & bone metabolism
MicroRNA-181a-5p Curbs Osteogenic Differentiation and Bone Formation Partially Through Impairing Runx1-Dependent Inhibition of AIF-1 Transcription: Jingwei Liu, Xueying Chang, Daming Dong; Endocrinol Metab. 2023;38(1):156-173. Published online January 6, 2023; DOI: https://doi.org/10.3803/EnM.2022.1516

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Background
Evidence has revealed the involvement of microRNAs (miRNAs) in modulating osteogenic differentiation, implying the promise of miRNA-based therapies for treating osteoporosis. This study investigated whether miR-181a-5p influences osteogenic differentiation and bone formation and aimed to establish the mechanisms in depth.
Methods
Clinical serum samples were obtained from osteoporosis patients, and MC3T3-E1 cells were treated with osteogenic induction medium (OIM) to induce osteogenic differentiation. miR-181a-5p-, Runt-related transcription factor 1 (Runx1)-, and/or allograft inflammatory factor-1 (AIF-1)-associated oligonucleotides or vectors were transfected into MC3T3-E1 cells to explore their function in relation to the number of calcified nodules, alkaline phosphatase (ALP) staining and activity, expression levels of osteogenesis-related proteins, and apoptosis. Luciferase activity, RNA immunoprecipitation, and chromatin immunoprecipitation assays were employed to validate the binding relationship between miR-181a-5p and Runx1, and the transcriptional regulatory relationship between Runx1 and AIF-1. Ovariectomy (OVX)-induced mice were injected with a miR-181a-5p antagonist for in vivo verification.
Results
miR-181a-5p was highly expressed in the serum of osteoporosis patients. OIM treatment decreased miR-181a-5p and AIF-1 expression, but promoted Runx1 expression in MC3T-E1 cells. Meanwhile, upregulated miR-181a-5p suppressed OIM-induced increases in calcified nodules, ALP content, and osteogenesis-related protein expression. Mechanically, miR-181a-5p targeted Runx1, which acted as a transcription factor to negatively modulate AIF-1 expression. Downregulated Runx1 suppressed the miR-181a-5p inhibitor-mediated promotion of osteogenic differentiation, and downregulated AIF-1 reversed the miR-181a-5p mimic-induced inhibition of osteogenic differentiation. Tail vein injection of a miR-181a-5p antagonist induced bone formation in OVX-induced osteoporotic mice.
Conclusion
In conclusion, miR-181a-5p affects osteogenic differentiation and bone formation partially via the modulation of the Runx1/AIF-1 axis.

Citations

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Scopolamine regulates the osteogenic differentiation of human periodontal ligament stem cells through lactylation modification of RUNX2 protein
Ying Wu, Pan Gong
Pharmacology Research & Perspectives.2024;[Epub] CrossRef

Review Article

Thyroid
The Role of Thyroid Hormone in the Regulation of Cerebellar Development: Sumiyasu Ishii, Izuki Amano, Noriyuki Koibuchi; Endocrinol Metab. 2021;36(4):703-716. Published online August 9, 2021; DOI: https://doi.org/10.3803/EnM.2021.1150

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The proper organized expression of specific genes in time and space is responsible for the organogenesis of the central nervous system including the cerebellum. The epigenetic regulation of gene expression is tightly regulated by an intrinsic intracellular genetic program, local stimuli such as synaptic inputs and trophic factors, and peripheral stimuli from outside of the brain including hormones. Some hormone receptors are expressed in the cerebellum. Thyroid hormones (THs), among numerous circulating hormones, are well-known major regulators of cerebellar development. In both rodents and human, hypothyroidism during the postnatal developmental period results in abnormal morphogenesis or altered function. THs bind to the thyroid hormone receptors (TRs) in the nuclei and with the help of transcriptional cofactors regulate the transcription of target genes. Gene regulation by TR induces cell proliferation, migration, and differentiation, which are necessary for brain development and plasticity. Thus, the lack of TH action mediators may directly cause aberrant cerebellar development. Various kinds of animal models have been established in a bid to study the mechanism of TH action in the cerebellum. Interestingly, the phenotypes differ greatly depending on the models. Herein we summarize the actions of TH and TR particularly in the developing cerebellum.

Citations

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Neuropeptides and Their Roles in the Cerebellum
Zi-Hao Li, Bin Li, Xiao-Yang Zhang, Jing-Ning Zhu
International Journal of Molecular Sciences.2024; 25(4): 2332. CrossRef
Exploring the underlying molecular mechanism of tri(1,3-dichloropropyl) phosphate-induced neurodevelopmental toxicity via thyroid hormone disruption in zebrafish by multi-omics analysis
Ying Xu, Lei Yang, Yanguo Teng, Jian Li, Na Li
Aquatic Toxicology.2023; 258: 106510. CrossRef
Association of Maternal TSH, FT4 With Children's BMI Trajectories, and Obesity: A Birth Cohort Study
Mengting Yang, Shanshan Zhang, Yuzhu Teng, Xue Ru, Linlin Zhu, Yan Han, Xingyong Tao, Hui Cao, Shuangqin Yan, Fangbiao Tao, Kun Huang
The Journal of Clinical Endocrinology & Metabolism.2023; 109(1): e190. CrossRef
Thyroid hormone receptor beta: Relevance in human health and diseases
Ghausiya Rehman, Neha Kumari, Farhad Bano, Rakesh K. Tyagi
Endocrine and Metabolic Science.2023; 13: 100144. CrossRef
Targeting Thyroid Hormone/Thyroid Hormone Receptor Axis: An Attractive Therapy Strategy in Liver Diseases
Qianyu Tang, Min Zeng, Linxi Chen, Nian Fu
Frontiers in Pharmacology.2022;[Epub] CrossRef
Histone Deacetylase 3 Inhibitor Alleviates Cerebellar Defects in Perinatal Hypothyroid Mice by Stimulating Histone Acetylation and Transcription at Thyroid Hormone-Responsive Gene Loci
Alvin Susetyo, Sumiyasu Ishii, Yuki Fujiwara, Izuki Amano, Noriyuki Koibuchi
International Journal of Molecular Sciences.2022; 23(14): 7869. CrossRef
Selection-driven adaptation to the extreme Antarctic environment in the Emperor penguin
Federica Pirri, Lino Ometto, Silvia Fuselli, Flávia A. N. Fernandes, Lorena Ancona, Nunzio Perta, Daniele Di Marino, Céline Le Bohec, Lorenzo Zane, Emiliano Trucchi
Heredity.2022; 129(6): 317. CrossRef
Long-term depression–inductive stimulation causes long-term potentiation in mouse Purkinje cells with a mutant thyroid hormone receptor
Ayane Ninomiya, Izuki Amano, Michifumi Kokubo, Yusuke Takatsuru, Sumiyasu Ishii, Hirokazu Hirai, Nobutake Hosoi, Noriyuki Koibuchi
Proceedings of the National Academy of Sciences.2022;[Epub] CrossRef

Original Articles

Clinical Study
Molecular Correlates and Nuclear Features of Encapsulated Follicular-Patterned Thyroid Neoplasms: Chan Kwon Jung, Andrey Bychkov, Dong Eun Song, Jang-Hee Kim, Yun Zhu, Zhiyan Liu, Somboon Keelawat, Chiung-Ru Lai, Mitsuyoshi Hirokawa, Kaori Kameyama, Kennichi Kakudo; Endocrinol Metab. 2021;36(1):123-133. Published online February 24, 2021; DOI: https://doi.org/10.3803/EnM.2020.860

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Background
Assessing nuclear features is diagnostically challenging in the aspect of thyroid pathology. The aim of this study was to determine whether pathologists could distinguish BRAF-like and RAS-like nuclear features morphologically and identify morphological features to differentiate thyroid tumors with RAS-like mutations from encapsulated papillary thyroid carcinoma (PTC) with predominant follicular growth and BRAFV^600E mutation.
Methods
Representative whole slide images of 16 encapsulated thyroid tumors with predominant follicular growth were reviewed by 12 thyroid pathologists using a web browser-based image viewer. Total nuclear score was calculated from semi-quantitatively scored eight nuclear features. The molecular profile of RAS and BRAF genes was determined by Sanger sequencing.
Results
Total nuclear score ranging 0 to 24 could differentiate BRAF-like tumors from RAS-like tumors with a cut-off value of score 14. The interobserver agreement was the highest for the assessment of nuclear pseudoinclusions (NPIs) but the lowest for nuclear elongation and sickle-shaped nuclei. NPIs were found in tumors with BRAFV^600E mutation, but not in tumors with RAS-like mutations. Total nuclear scores were significantly higher for tumors with BRAFV^600E than for those with RAS-like mutations (P<0.001).
Conclusion
Our results suggest that NPIs and high nuclear scores have diagnostic utility as rule-in markers for differentiating PTC with BRAFV^600E mutation from benign or borderline follicular tumors with RAS-like mutations. Relaxation of rigid criteria for nuclear features resulted in an overdiagnosis of PTC. Immunostaining or molecular testing for BRAFV^600E mutation is a useful adjunct for cases with high nuclear scores to identify true PTC.

Citations

Citations to this article as recorded by

Differentiating BRAF V600E- and RAS-like alterations in encapsulated follicular patterned tumors through histologic features: a validation study
Chankyung Kim, Shipra Agarwal, Andrey Bychkov, Jen-Fan Hang, Agnes Stephanie Harahap, Mitsuyoshi Hirokawa, Kennichi Kakudo, Somboon Keelawat, Chih-Yi Liu, Zhiyan Liu, Truong Phan-Xuan Nguyen, Chanchal Rana, Huy Gia Vuong, Yun Zhu, Chan Kwon Jung
Virchows Archiv.2024;[Epub] CrossRef
The Presence of Typical “BRAFV600E-Like” Atypia in Papillary Thyroid Carcinoma is Highly Specific for the Presence of the BRAFV600E Mutation
John Turchini, Loretta Sioson, Adele Clarkson, Amy Sheen, Leigh Delbridge, Anthony Glover, Mark Sywak, Stan Sidhu, Anthony J. Gill
Endocrine Pathology.2023; 34(1): 112. CrossRef
Could Oxidative Stress Play a Role in the Development and Clinical Management of Differentiated Thyroid Cancer?
Maria Kościuszko, Angelika Buczyńska, Adam Jacek Krętowski, Anna Popławska-Kita
Cancers.2023; 15(12): 3182. CrossRef
Pitfalls in thyroid pathology and the medicolegal aspects of error
David N Poller
Diagnostic Histopathology.2023; 29(11): 495. CrossRef
Developing Models to Predict BRAFV600E and RAS Mutational Status in Papillary Thyroid Carcinoma Using Clinicopathological Features and pERK1/2 Immunohistochemistry Expression
Agnes Stephanie Harahap, Imam Subekti, Sonar Soni Panigoro, Asmarinah, Lisnawati, Retno Asti Werdhani, Hasrayati Agustina, Dina Khoirunnisa, Mutiah Mutmainnah, Fajar Lamhot Gultom, Abdillah Hasbi Assadyk, Maria Francisca Ham
Biomedicines.2023; 11(10): 2803. CrossRef
The Asian Thyroid Working Group, from 2017 to 2023
Kennichi Kakudo, Chan Kwon Jung, Zhiyan Liu, Mitsuyoshi Hirokawa, Andrey Bychkov, Huy Gia Vuong, Somboon Keelawat, Radhika Srinivasan, Jen-Fan Hang, Chiung-Ru Lai
Journal of Pathology and Translational Medicine.2023; 57(6): 289. CrossRef
Noninvasive Follicular Thyroid Neoplasm with Papillary-like Nuclear Features (NIFTP): Tumour Entity with a Short History. A Review on Challenges in Our Microscopes, Molecular and Ultrasonographic Profile
Ivana Kholová, Elina Haaga, Jaroslav Ludvik, David Kalfert, Marie Ludvikova
Diagnostics.2022; 12(2): 250. CrossRef
Update from the 2022 World Health Organization Classification of Thyroid Tumors: A Standardized Diagnostic Approach
Chan Kwon Jung, Andrey Bychkov, Kennichi Kakudo
Endocrinology and Metabolism.2022; 37(5): 703. CrossRef
Different Threshold of Malignancy for RAS-like Thyroid Tumors Causes Significant Differences in Thyroid Nodule Practice
Kennichi Kakudo
Cancers.2022; 14(3): 812. CrossRef
The Incidence of Noninvasive Follicular Thyroid Neoplasm with Papillary-Like Nuclear Features: A Meta-Analysis Assessing Worldwide Impact of the Reclassification
Chanchal Rana, Huy Gia Vuong, Thu Quynh Nguyen, Hoang Cong Nguyen, Chan Kwon Jung, Kennichi Kakudo, Andrey Bychkov
Thyroid.2021;[Epub] CrossRef

Endocrine Research
Danshen Extracts Prevents Obesity and Activates Mitochondrial Function in Brown Adipose Tissue: Yoon Hee Cho, Cheol Ryong Ku, Young-Suk Choi, Hyeon Jeong Lee, Eun Jig Lee; Endocrinol Metab. 2021;36(1):185-195. Published online February 24, 2021; DOI: https://doi.org/10.3803/EnM.2020.835

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Background
Danshen has been widely used in oriental medicine to improve body function. The purpose of this study is to investigate the effect of water-soluble Danshen extract (DE) on weight loss and on activation proteins involved in mitochondrial biogenesis in brown adipose tissue (BAT) in obese mice.
Methods
BAT was isolated from 7-week-old male Sprague-Dawley rats, and expression of proteins related to mitochondrial biogenesis was confirmed in both brown preadipocytes and mature brown adipocytes treated with DE. For the in vivo study, low-density lipoprotein receptor knock out mice were divided into three groups and treated for 17 weeks with: standard diet; high fat diet (HFD); HFD+DE. Body weight was measured every week, and oral glucose tolerance test was performed after DE treatment in streptozotocin-induced diabetic mice. To observe the changes in markers related to thermogenesis and adipogenesis in the BAT, white adipose tissue (WAT) and liver of experimental animals, tissues were removed and immediately frozen in liquid nitrogen.
Results
DE increased the expression of uncoupling protein 1 and peroxisome proliferator-activated receptor gamma coactivator 1-alpha in brown preadipocytes, and also promoted the brown adipocyte differentiation and mitochondrial function in the mature brown adipocytes. Reactive oxygen species production in brown preadipocytes was increased depending on the concentration of DE. DE activates thermogenesis in BAT and normalizes increased body weight and adipogenesis in the liver due to HFD. Browning of WAT was increased in WAT of DE treatment group.
Conclusion
DE protects against obesity and activates mitochondrial function in BAT.

Citations

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Pharmacological Benefits and Underlying Mechanisms of Salvia miltiorrhiza against Molecular Pathology of Various Liver Diseases: A Review
Cho Hyun Hwang, Eungyeong Jang, Jang-Hoon Lee
The American Journal of Chinese Medicine.2023; 51(07): 1675. CrossRef

Clinical Study
Identification of Novel Genetic Variants Related to Trabecular Bone Score in Community-Dwelling Older Adults: Sung Hye Kong, Ji Won Yoon, Jung Hee Kim, JooYong Park, Jiyeob Choi, Ji Hyun Lee, A Ram Hong, Nam H. Cho, Chan Soo Shin; Endocrinol Metab. 2020;35(4):801-810. Published online November 24, 2020; DOI: https://doi.org/10.3803/EnM.2020.735

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Abstract PDF Supplementary Material PubReader ePub: Background
As the genetic variants of trabecular bone microarchitecture are not well-understood, we performed a genome-wide association study to identify genetic determinants of bone microarchitecture analyzed by trabecular bone score (TBS).
Methods
TBS-associated genes were discovered in the Ansung cohort (discovery cohort), a community-based rural cohort in Korea, and then validated in the Gene-Environment Interaction and Phenotype (GENIE) cohort (validation cohort), consisting of subjects who underwent health check-up programs. In the discovery cohort, 2,451 participants were investigated for 1.42 million genotyped and imputed markers.
Results
In the validation cohort, identified as significant variants were evaluated in 2,733 participants. An intronic variant in iroquois homeobox 3 (IRX3), rs1815994, was significantly associated with TBS in men (P=3.74E-05 in the discovery cohort, P=0.027 in the validation cohort). Another intronic variant in mitogen-activated protein kinase kinase 5 (MAP2K5), rs11630730, was significantly associated with TBS in women (P=3.05E-09 in the discovery cohort, P=0.041 in the validation cohort). Men with the rs1815994 variant and women with the rs11630730 variant had lower TBS and lumbar spine bone mineral density. The detrimental effects of the rs1815994 variant in men and rs11630730 variant in women were also identified in association analysis (β=–0.0281, β=–0.0465, respectively).
Conclusion
In this study, the rs1815994 near IRX3 in men and rs11630730 near MAP2K5 in women were associated with deterioration of the bone microarchitecture. It is the first study to determine the association of genetic variants with TBS. Further studies are needed to confirm our findings and identify additional variants contributing to the trabecular bone microarchitecture.

Endocrine Research
Serotonin Regulates De Novo Lipogenesis in Adipose Tissues through Serotonin Receptor 2A: Ko Eun Shong, Chang-Myung Oh, Jun Namkung, Sangkyu Park, Hail Kim; Endocrinol Metab. 2020;35(2):470-479. Published online June 24, 2020; DOI: https://doi.org/10.3803/EnM.2020.35.2.470; Correction in: Endocrinol Metab 2020;35(3):672

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Background
Obesity is defined as excessive fat mass and is a major cause of many chronic diseases such as diabetes, cardiovascular disease, and cancer. Increasing energy expenditure and regulating adipose tissue metabolism are important targets for the treatment of obesity. Serotonin (5-hydroxytryptophan [5-HT]) is a monoamine metabolite of the essential amino acid tryptophan. Here, we demonstrated that 5-HT in mature adipocytes regulated energy expenditure and lipid metabolism.
Methods
Tryptophan hydroxylase 1 (TPH1) is the rate-limiting enzyme during 5-HT synthesis in non-neural peripheral tissues. We generated adipose tissue-specific Tph1 knockout (Tph1 FKO) mice and adipose tissue-specific serotonin receptor 2A KO (Htr2a FKO) mice and analyzed their phenotypes during high-fat diet (HFD) induced obesity.
Results
Tph1 FKO mice fed HFD exhibited reduced lipid accumulation, increased thermogenesis, and resistance to obesity. In addition, Htr2a FKO mice fed HFD showed reduced lipid accumulation in white adipose tissue and resistance to obesity.
Conclusion
These data suggest that the inhibition of serotonin signaling might be an effective strategy in obesity.

Citations

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Gut microbiota dysbiosis and decreased levels of acetic and propionic acid participate in glucocorticoid-induced glycolipid metabolism disorder
Qin Zhang, Gaopeng Guan, Jie Liu, Wenmu Hu, Ping Jin, Yung-Fu Chang
mBio.2024;[Epub] CrossRef
The Chain-Mediating Effect of Obesity, Depressive Symptoms on the Association between Dietary Quality and Cardiovascular Disease Risk
Shuai Zhang, Limei E, Zhonghai Lu, Yingying Yu, Xuebin Yang, Yao Chen, Xiubo Jiang
Nutrients.2023; 15(3): 629. CrossRef
Metabolic and Molecular Response to High-Fat Diet Differs between Rats with Constitutionally High and Low Serotonin Tone
Petra Baković, Maja Kesić, Darko Kolarić, Jasminka Štefulj, Lipa Čičin-Šain
International Journal of Molecular Sciences.2023; 24(3): 2169. CrossRef
Linking serotonin homeostasis to gut function: Nutrition, gut microbiota and beyond
Lili Jiang, Dandan Han, Youling Hao, Zhuan Song, Zhiyuan Sun, Zhaolai Dai
Critical Reviews in Food Science and Nutrition.2023; : 1. CrossRef
Serotonin transporter-deficient mice display enhanced adipose tissue inflammation after chronic high-fat diet feeding
Johannes Hoch, Niklas Burkhard, Shanshan Zhang, Marina Rieder, Timoteo Marchini, Vincent Geest, Krystin Krauel, Timm Zahn, Nicolas Schommer, Muataz Ali Hamad, Carolina Bauer, Nadine Gauchel, Daniela Stallmann, Claus Normann, Dennis Wolf, Rüdiger Eberhard
Frontiers in Immunology.2023;[Epub] CrossRef
The role of serotonin in prenatal ontogenesis
Inna I. Evsyukova
Journal of obstetrics and women's diseases.2023; 72(4): 81. CrossRef
Genome-wide survey and functional analysis reveal TCF21 promotes chicken preadipocyte differentiation by directly upregulating HTR2A
Xinyang Zhang, Bohan Cheng, Yanyan Ma, Yumeng Liu, Ning Wang, Hui Zhang, Yumao Li, Yuxiang Wang, Peng Luan, Zhiping Cao, Hui Li
Biochemical and Biophysical Research Communications.2022; 587: 131. CrossRef
Maternal Metabolic State and Fetal Sex and Genotype Modulate Methylation of the Serotonin Receptor Type 2A Gene (HTR2A) in the Human Placenta
Marina Horvatiček, Maja Perić, Ivona Bečeheli, Marija Klasić, Maja Žutić, Maja Kesić, Gernot Desoye, Sandra Nakić Radoš, Marina Ivanišević, Dubravka Hranilovic, Jasminka Štefulj
Biomedicines.2022; 10(2): 467. CrossRef
Synthesis and biological evaluation of tyrosine derivatives as peripheral 5HT2A receptor antagonists for nonalcoholic fatty liver disease
Minhee Kim, Wonil Choi, Jihyeon Yoon, Byung-kwan Jeong, Suvarna H. Pagire, Haushabhau S. Pagire, Jungsun Park, Jung Eun Nam, Chang Joo Oh, Jae-Han Jeon, Seong Soon Kim, Byung Hoi Lee, Jin Sook Song, Myung Ae Bae, In-Kyu Lee, Hail Kim, Jin Hee Ahn
European Journal of Medicinal Chemistry.2022; 239: 114517. CrossRef
Serotonin in the regulation of systemic energy metabolism
Joon Ho Moon, Chang‐Myung Oh, Hail Kim
Journal of Diabetes Investigation.2022; 13(10): 1639. CrossRef
Traumatic brain injury alters the gut-derived serotonergic system and associated peripheral organs
Natosha M. Mercado, Guanglin Zhang, Zhe Ying, Fernando Gómez-Pinilla
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Modulation of adipose tissue metabolism by microbial-derived metabolites
Wenyun Liu, Ge Yang, Pinyi Liu, Xin Jiang, Ying Xin
Frontiers in Microbiology.2022;[Epub] CrossRef
Risperidone Exacerbates Glucose Intolerance, Nonalcoholic Fatty Liver Disease, and Renal Impairment in Obese Mice
Hsiao-Pei Tsai, Po-Hsun Hou, Frank-Chiahung Mao, Chia-Chia Chang, Wei-Cheng Yang, Ching-Feng Wu, Huei-Jyuan Liao, Tzu-Chun Lin, Lan-Szu Chou, Li-Wei Hsiao, Geng-Ruei Chang
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Pancreatic Sirtuin 3 Deficiency Promotes Hepatic Steatosis by Enhancing 5-Hydroxytryptamine Synthesis in Mice With Diet-Induced Obesity
Xing Ming, Arthur C.K. Chung, Dandan Mao, Huanyi Cao, Baoqi Fan, Willy K.K. Wong, Chin Chung Ho, Heung Man Lee, Kristina Schoonjans, Johan Auwerx, Guy A. Rutter, Juliana C.N. Chan, Xiao Yu Tian, Alice P.S. Kong
Diabetes.2021; 70(1): 119. CrossRef
Peripheral Selective Oxadiazolylphenyl Alanine Derivatives as Tryptophan Hydroxylase 1 Inhibitors for Obesity and Fatty Liver Disease
Eun Jung Bae, Won Gun Choi, Haushabhau S. Pagire, Suvarna H. Pagire, Saravanan Parameswaran, Jun-Ho Choi, Jihyeon Yoon, Won-il Choi, Ji Hun Lee, Jin Sook Song, Myung Ae Bae, Mijin Kim, Jae-Han Jeon, In-Kyu Lee, Hail Kim, Jin Hee Ahn
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A Systems Biology Approach to Investigating the Interaction between Serotonin Synthesis by Tryptophan Hydroxylase and the Metabolic Homeostasis
Suhyeon Park, Yumin Kim, Jibeom Lee, Jeong Yun Lee, Hail Kim, Sunjae Lee, Chang-Myung Oh
International Journal of Molecular Sciences.2021; 22(5): 2452. CrossRef
Metabolic Disturbances in Rat Sublines with Constitutionally Altered Serotonin Homeostasis
Maja Kesić, Petra Baković, Ranko Stojković, Jasminka Štefulj, Lipa Čičin-Šain
International Journal of Molecular Sciences.2021; 22(10): 5400. CrossRef
The Mechanism of Secretion and Metabolism of Gut-Derived 5-Hydroxytryptamine
Ning Liu, Shiqiang Sun, Pengjie Wang, Yanan Sun, Qingjuan Hu, Xiaoyu Wang
International Journal of Molecular Sciences.2021; 22(15): 7931. CrossRef
Inhibiting serotonin signaling through HTR2B in visceral adipose tissue improves obesity-related insulin resistance
Won Gun Choi, Wonsuk Choi, Tae Jung Oh, Hye-Na Cha, Inseon Hwang, Yun Kyung Lee, Seung Yeon Lee, Hyemi Shin, Ajin Lim, Dongryeol Ryu, Jae Myoung Suh, So-Young Park, Sung Hee Choi, Hail Kim
Journal of Clinical Investigation.2021;[Epub] CrossRef
Serotonergic Regulation of Hepatic Energy Metabolism
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Endocrine Research
Transformation of Mature Osteoblasts into Bone Lining Cells and RNA Sequencing-Based Transcriptome Profiling of Mouse Bone during Mechanical Unloading: A Ram Hong, Kwangsoo Kim, Ji Yeon Lee, Jae-Yeon Yang, Jung Hee Kim, Chan Soo Shin, Sang Wan Kim; Endocrinol Metab. 2020;35(2):456-469. Published online June 24, 2020; DOI: https://doi.org/10.3803/EnM.2020.35.2.456; Correction in: Endocrinol Metab 2021;36(6):1314

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Background
We investigated RNA sequencing-based transcriptome profiling and the transformation of mature osteoblasts into bone lining cells (BLCs) through a lineage tracing study to better understand the effect of mechanical unloading on bone loss.
Methods
Dmp1-CreERt2(+):Rosa26R mice were injected with 1 mg of 4-hydroxy-tamoxifen three times a week starting at postnatal week 7, and subjected to a combination of botulinum toxin injection with left hindlimb tenotomy starting at postnatal week 8 to 10. The animals were euthanized at postnatal weeks 8, 9, 10, and 12. We quantified the number and thickness of X-gal(+) cells on the periosteum of the right and left femoral bones at each time point.
Results
Two weeks after unloading, a significant decrease in the number and a subtle change in the thickness of X-gal(+) cells were observed in the left hindlimbs compared with the right hindlimbs. At 4 weeks after unloading, the decrease in the thickness was accelerated in the left hindlimbs, although the number of labeled cells was comparable. RNA sequencing analysis showed downregulation of 315 genes in the left hindlimbs at 2 and 4 weeks after unloading. Of these, Xirp2, AMPD1, Mettl11b, NEXN, CYP2E1, Bche, Ppp1r3c, Tceal7, and Gadl1 were upregulated during osteoblastogenic/osteocytic and myogenic differentiation in vitro.
Conclusion
These findings demonstrate that mechanical unloading can accelerate the transformation of mature osteoblasts into BLCs in the early stages of bone loss in vivo. Furthermore, some of the genes involved in this process may have a pleiotropic effect on both bone and muscle.

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Review Article

Miscellaneous
Rare PTH Gene Mutations Causing Parathyroid Disorders: A Review: Joon-Hyop Lee, Munkhtugs Davaatseren, Sihoon Lee; Endocrinol Metab. 2020;35(1):64-70. Published online March 19, 2020; DOI: https://doi.org/10.3803/EnM.2020.35.1.64

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Since parathyroid hormone (PTH) was first isolated and its gene (PTH) was sequenced, only eight PTH mutations have been discovered. The C18R mutation in PTH, discovered in 1990, was the first to be reported. This autosomal dominant mutation induces endoplasmic reticulum stress and subsequent apoptosis in parathyroid cells. The next mutation, which was reported in 1992, is associated with exon skipping. The substitution of G with C in the first nucleotide of the second intron results in the exclusion of the second exon; since this exon includes the initiation codon, translation initiation is prevented. An S23P mutation and an S23X mutation at the same residue were reported in 1999 and 2012, respectively. Both mutations resulted in hypoparathyroidism. In 2008, a somatic R83X mutation was detected in a parathyroid adenoma tissue sample collected from a patient with hyperparathyroidism. In 2013, a heterozygous p.Met1_Asp6del mutation was incidentally discovered in a case-control study. Two years later, the R56C mutation was reported; this is the only reported hypoparathyroidism-causing mutation in the mature bioactive part of PTH. In 2017, another heterozygous mutation, M14K, was detected. The discovery of these eight mutations in the PTH gene has provided insights into its function and broadened our understanding of the molecular mechanisms underlying mutation progression. Further attempts to detect other such mutations will help elucidate the functions of PTH in a more sophisticated manner.

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The Intricacies of Renal Phosphate Reabsorption—An Overview
Valerie Walker
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Smita Jha, William F Simonds
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Rare cause of persistent hypocalcaemia in infancy due to PTH gene mutation
Savita Khadse, Vrushali Satish Takalikar, Radha Ghildiyal, Nikhil Shah
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Homozygous Ser-1 to Pro-1 mutation in parathyroid hormone identified in hypocalcemic patients results in secretion of a biologically inactive pro-hormone
Patrick Hanna, Ashok Khatri, Shawn Choi, Severine Brabant, Matti L. Gild, Marie L. Piketty, Bruno Francou, Dominique Prié, John T. Potts, Roderick J. Clifton-Bligh, Agnès Linglart, Thomas J. Gardella, Harald Jüppner
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Homozygous missense variant of PTH (c.166C>T, p.(Arg56Cys)) as the cause of familial isolated hypoparathyroidism in a three-year-old child
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Case Report

A Case of Thyroid Hemiagenesis with Papillary Adenocarcinoma.: Je Ho Han, Bong Yun Cha, Ho Young Son, Yoo Bae Ahn, Kwang Woo Lee, Sung Koo Kang, Se Jeong Oh, Jong Soon Na, Sang Ah Jang, Moo Il Kang; J Korean Endocr Soc. 1994;9(4):385-389. Published online November 6, 2019

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Abstract PDF: Variation in the gross anatomy of the thyroid is relatively common. Although thyroid hemiagenesis is considered to be a rare congenital anomaly, its incidence is probably underestimated because the diagnosis is usually incidental.We present the case of a 26-year-old woman with right thyroid hemiagenesis associated with papillary adenocarcinoma. The diagnosis of hemiagenesis was established by isotope imaging, which showed hot nodule, thyroid ultrasonography and surgical exploration for proper management of a nodule in the left lobe of thyroid gland. As she was diagnosed to have papillary adenocarcinoma, total thyroidectomy was performed and at present she remains disease-free.

Original Article

Endocrine Research
Expression of NF2 Modulates the Progression of BRAF^V600E Mutated Thyroid Cancer Cells: Mi-Hyeon You, Min Ji Jeon, Tae Yong Kim, Won Bae Kim, Young Kee Shong, Won Gu Kim; Endocrinol Metab. 2019;34(2):203-212. Published online June 24, 2019; DOI: https://doi.org/10.3803/EnM.2019.34.2.203

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Background

We previously reported the frequent neurofibromatosis 2 (NF2) gene mutations in anaplastic thyroid cancers in association with the BRAF^V600E mutation. We aimed to investigate the role of NF2 in thyroid cancer with BRAF mutation.

Methods

To identify the function of NF2 in thyroid cancers, we investigated the changes in cell proliferation, colon formation, migration and invasion of thyroid cancer cells (8505C, BHT101, and KTC-1) with BRAF^V600E mutation after overexpression and knock-down of NF2. We also examined how cell proliferation changed when NF2 was mutagenized. Human NF2 expression in papillary thyroid carcinoma (PTC) was analyzed using the The Cancer Genome Atlas (TCGA) data.

Results

First, NF2 was overexpressed in 8505C and KTC-1 cells. Compared to control, NF2 overexpressed group of both thyroid cancer cells showed significant inhibition in cell proliferation and colony formation. These results were also confirmed by cell migration and invasion assay. After knock-down of NF2 in 8505C cells, there were no significant changes in cell proliferation and colony formation, compared with the control group. However, after mutagenized S288^* and Q470^* sites of NF2 gene, the cell proliferation increased compared to NF2 overexpression group. In the analysis of TCGA data, the mRNA expression of NF2 was significantly decreased in PTCs with lateral cervical lymph node (LN) metastasis compared with PTCs without LN metastasis.

Conclusion

Our study suggests that NF2 might play a role as a tumor suppressor in thyroid cancer with BRAF mutation. More studies are needed to elucidate the mechanism how NF2 acts in thyroid cancer with BRAF mutation.

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Review Articles

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.

Bone Metabolism
Recent Topics in Fibrodysplasia Ossificans Progressiva: Takenobu Katagiri, Sho Tsukamoto, Yutaka Nakachi, Mai Kuratani; Endocrinol Metab. 2018;33(3):331-338. Published online September 18, 2018; DOI: https://doi.org/10.3803/EnM.2018.33.3.331

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Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disease that is characterized by the formation of heterotopic bone tissues in soft tissues, such as skeletal muscle, ligament, and tendon. It is difficult to remove such heterotopic bones via internal medicine or invasive procedures. The identification of activin A receptor, type I (ACVR1)/ALK2 gene mutations associated with FOP has allowed the genetic diagnosis of FOP. The ACVR1/ALK2 gene encodes the ALK2 protein, which is a transmembrane kinase receptor in the transforming growth factor-β family. The relevant mutations activate intracellular signaling in vitro and induce heterotopic bone formation in vivo. Activin A is a potential ligand that activates mutant ALK2 but not wild-type ALK2. Various types of small chemical and biological inhibitors of ALK2 signaling have been developed to establish treatments for FOP. Some of these are in clinical trials in patients with FOP.

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Original Article

Thyroid
Combined Effects of Baicalein and Docetaxel on Apoptosis in 8505c Anaplastic Thyroid Cancer Cells via Downregulation of the ERK and Akt/mTOR Pathways: Chan Ho Park, Se Eun Han, Il Seong Nam-Goong, Young Il Kim, Eun Sook Kim; Endocrinol Metab. 2018;33(1):121-132. Published online March 21, 2018; DOI: https://doi.org/10.3803/EnM.2018.33.1.121

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Background

Anaplastic thyroid cancer (ATC) is one of the most lethal human malignancies. Docetaxel, a microtubule stabilizer, is a common chemotherapeutic agent used to treat various metastatic cancers. However, prolonged use results in various side effects and drug resistance. Flavonoids, such as baicalein, are accepted chemotherapeutic and dietary chemopreventive agents with many advantages, such as greater accessibility, affordability, and lower toxicity, compared with traditional chemotherapy agents. In this study, we evaluated whether baicalein enhances the effects of docetaxel on apoptosis and metastasis in 8505c ATC cells.

Methods

The 8505c cells were treated with baicalein or docetaxel individually and in combination. Cell viability was measured by MTT (thiazolyl blue tetrazolium bromide) assay, and apoptosis was detected by fluorescence microscopy of Hoechst-stained cells. The expression of apoptotic (Bax and caspase-3), anti-apoptotic (Bcl-2), angiogenic (vascular endothelial growth factor [VEGF], transforming growth factor β [TGF-β], E-cadherin, and N-cadherin), and signaling (extracellular signal-regulated kinase [ERK] mitogen activated protein kinase [MAPK], Akt, and mammalian target of rapamycin [mTOR]) proteins was determined by Western blot analysis.

Results

The combination of baicalein (50 or 100 µM) and docetaxel (10 nM) significantly inhibited proliferation and induced apoptosis compared with monotherapies. The combination treatment significantly inhibited the expression of Bax, caspase-3, VEGF, TGF-β1, E-cadherin, N-cadherin, and mTOR, but decreased the expression of Bcl-2 and significantly decreased the phosphorylation of ERK and Akt.

Conclusion

The combination of baicalein and docetaxel effectively induced apoptosis and inhibited metastasis in 8505c cells through downregulation of apoptotic and angiogenic protein expression and blocking of the ERK and Akt/mTOR pathways in 8505c cells. These results suggest that baicalein enhances the anticancer effects of docetaxel in ATC.

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Review Article

The SCAP/SREBP Pathway: A Mediator of Hepatic Steatosis: Young-Ah Moon; Endocrinol Metab. 2017;32(1):6-10. Published online January 19, 2017; DOI: https://doi.org/10.3803/EnM.2017.32.1.6

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Abstract PDF PubReader

Nonalcoholic fatty liver disease (NAFLD) is strongly associated with insulin resistance, obesity, and dyslipidemia. NAFLD encompasses a wide range of states from the simple accumulation of triglycerides in the hepatocytes to serious states accompanied by inflammation and fibrosis in the liver. De novo lipogenesis has been shown to be a significant factor in the development of hepatic steatosis in insulin-resistant states. Sterol regulatory element binding protein-1c (SREBP-1c) is the main transcription factor that mediates the activation of lipogenesis, and SREBP cleavage activating protein (SCAP) is required for the activation of SREBPs. Here, recent animal studies that suggest SCAP as a therapeutic target for hepatic steatosis and hypertriglyceridemia are discussed.

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