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Review Article
Calcium & bone metabolism
Nuclear Factor-Kappa B Regulation of Osteoclastogenesis and Osteoblastogenesis
Brendan F. Boyce, Jinbo Li, Zhenqiang Yao, Lianping Xing
Endocrinol Metab. 2023;38(5):504-521.   Published online September 26, 2023
DOI: https://doi.org/10.3803/EnM.2023.501
  • 1,870 View
  • 93 Download
  • 1 Web of Science
  • 3 Crossref
AbstractAbstract PDFPubReader   ePub   
Maintenance of skeletal integrity requires the coordinated activity of multinucleated bone-resorbing osteoclasts and bone-forming osteoblasts. Osteoclasts form resorption lacunae on bone surfaces in response to cytokines by fusion of precursor cells. Osteoblasts are derived from mesenchymal precursors and lay down new bone in resorption lacunae during bone remodeling. Nuclear factorkappa B (NF-κB) signaling regulates osteoclast and osteoblast formation and is activated in osteoclast precursors in response to the essential osteoclastogenic cytokine, receptor activator of NF-κB ligand (RANKL), which can also control osteoblast formation through RANK-RANKL reverse signaling in osteoblast precursors. RANKL and some pro-inflammatory cytokines, including tumor necrosis factor (TNF), activate NF-κB signaling to positively regulate osteoclast formation and functions. However, these cytokines also limit osteoclast and osteoblast formation through NF-κB signaling molecules, including TNF receptor-associated factors (TRAFs). TRAF6 mediates RANKL-induced osteoclast formation through canonical NF-κB signaling. In contrast, TRAF3 limits RANKL- and TNF-induced osteoclast formation, and it restricts transforming growth factor β (TGFβ)-induced inhibition of osteoblast formation in young and adult mice. During aging, neutrophils expressing TGFβ and C-C chemokine receptor type 5 (CCR5) increase in bone marrow of mice in response to increased NF-κB-induced CC motif chemokine ligand 5 (CCL5) expression by mesenchymal progenitor cells and injection of these neutrophils into young mice decreased bone mass. TGFβ causes degradation of TRAF3, resulting in decreased glycogen synthase kinase-3β/β-catenin-mediated osteoblast formation and age-related osteoporosis in mice. The CCR5 inhibitor, maraviroc, prevented accumulation of TGFβ+/CCR5+ neutrophils in bone marrow and increased bone mass by inhibiting bone resorption and increasing bone formation in aged mice. This paper updates current understanding of how NF-κB signaling is involved in the positive and negative regulation of cytokine-mediated osteoclast and osteoblast formation and activation with a focus on the role of TRAF3 signaling, which can be targeted therapeutically to enhance bone mass.

Citations

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  • The Role of Rosavin in the Pathophysiology of Bone Metabolism
    Piotr Wojdasiewicz, Paweł Turczyn, Anna Lach-Gruba, Łukasz A. Poniatowski, Daryush Purrahman, Mohammad-Reza Mahmoudian-Sani, Dariusz Szukiewicz
    International Journal of Molecular Sciences.2024; 25(4): 2117.     CrossRef
  • The role of monocyte/macrophage chemokines in pathogenesis of osteoarthritis: A review
    Hao Luo, Linfeng Li, Song Han, Tao Liu
    International Journal of Immunogenetics.2024;[Epub]     CrossRef
  • Genetic Deficiency of the Long Pentraxin 3 Affects Osteogenesis and Osteoclastogenesis in Homeostatic and Inflammatory Conditions
    Valentina Granata, Dario Strina, Maria Lucia Schiavone, Barbara Bottazzi, Alberto Mantovani, Antonio Inforzato, Cristina Sobacchi
    International Journal of Molecular Sciences.2023; 24(23): 16648.     CrossRef
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Original Articles
Thyroid
BRAFV600E Mutation Enhances Estrogen-Induced Metastatic Potential of Thyroid Cancer by Regulating the Expression of Estrogen Receptors
Minjun Kim, Su-jin Kim, Seong Yun Ha, Zhen Xu, Youngjin Han, Hyeon-Gun Jee, Sun Wook Cho, Young Joo Park, Kyu Eun Lee
Endocrinol Metab. 2022;37(6):879-890.   Published online December 26, 2022
DOI: https://doi.org/10.3803/EnM.2022.1563
  • 2,548 View
  • 213 Download
  • 2 Web of Science
  • 2 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Cross-talk between mitogen-activated protein kinase and estrogen has been reported; however, the role of BRAFV600E in the estrogen responsiveness of thyroid cancer is unknown. We elucidated the effect of BRAFV600E on the estrogen-induced increase in metastatic potential in thyroid cancer.
Methods
Using a pair of cell lines, human thyroid cell lines which harbor wild type BRAF gene (Nthy/WT) and Nthy/BRAFV600E (Nthy/V600E), the expression of estrogen receptors (ERs) and estrogen-induced metastatic phenotypes were evaluated. Susceptibility to ERα- and ERβ-selective agents was evaluated to confirm differential ER expression. ESR expression was analyzed according to BRAFV600E status and age (≤50 years vs. >50 years) using The Cancer Genome Atlas (TCGA) data.
Results
Estradiol increased the ERα/ERβ expression ratio in Nthy/V600E, whereas the decreased ERα/ERβ expression ratio was found in Nthy/WT. BRAFV600E-mutated cell lines showed a higher E2-induced increase in metastatic potential, including migration, invasion, and anchorage-independent growth compared with Nthy/WT. An ERα antagonist significantly inhibited migration in Nthy/V600E cells, whereas an ERβ agonist was more effective in Nthy/WT. In the BRAFV600E group, ESR1/ESR2 ratio was significantly higher in younger age group (≤50 years) compared with older age group (>50 years) by TCGA data analysis.
Conclusion
Our data show that BRAFV600E mutation plays a crucial role in the estrogen responsiveness of thyroid cancer by regulating ER expression. Therefore, BRAFV600E might be used as a biomarker when deciding future hormone therapies based on estrogen signaling in thyroid cancer patients.

Citations

Citations to this article as recorded by  
  • Association of DNA Promoter Methylation and BRAF Mutation in Thyroid Cancer
    Farzana Jasmine, Briseis Aschebrook-Kilfoy, Mohammad M. Rahman, Garrett Zaagman, Raymon H. Grogan, Mohammed Kamal, Habibul Ahsan, Muhammad G. Kibriya
    Current Oncology.2023; 30(3): 2978.     CrossRef
  • Editorial: Recent advances in papillary thyroid carcinoma: Progression, treatment and survival predictors
    Erivelto Martinho Volpi, Margarita Carmen Ramirez-Ortega, Jose Federico Carrillo
    Frontiers in Endocrinology.2023;[Epub]     CrossRef
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Thyroid
Usefulness of Real-Time Quantitative Microvascular Ultrasonography for Differentiation of Graves’ Disease from Destructive Thyroiditis in Thyrotoxic Patients
Han-Sang Baek, Ji-Yeon Park, Chai-Ho Jeong, Jeonghoon Ha, Moo Il Kang, Dong-Jun Lim
Endocrinol Metab. 2022;37(2):323-332.   Published online April 13, 2022
DOI: https://doi.org/10.3803/EnM.2022.1413
  • 3,512 View
  • 140 Download
  • 4 Web of Science
  • 4 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Microvascular ultrasonography (MVUS) is a third-generation Doppler technique that was developed to increase sensitivity compared to conventional Doppler. The purpose of this study was to compare MVUS with conventional color Doppler (CD) and power Doppler (PD) imaging to distinguish Graves’ disease (GD) from destructive thyroiditis (DT).
Methods
This prospective study included 101 subjects (46 GDs, 47 DTs, and eight normal controls) from October 2020 to November 2021. All ultrasonography examinations were performed using microvascular flow technology (MV-Flow). The CD, PD, and MVUS images were semi-quantitatively graded according to blood flow patterns. On the MVUS images, vascularity indices (VIs), which were the ratio (%) of color pixels in the total grayscale pixels in a defined region of interest, were obtained automatically. Receiver operating characteristic curve analysis was performed to verify the diagnostic performance of MVUS. The interclass correlation coefficient and Cohen’s kappa analysis were used to analyze the reliability of MVUS (ClinicalTrials.gov:NCT04879173).
Results
The area under the curve (AUC) for CD, PD, MVUS, and MVUS-VI was 0.822, 0.844, 0.808, and 0.852 respectively. The optimal cutoff value of the MVUS-VI was 24.95% for distinguishing GD and DT with 87% sensitivity and 80.9% specificity. We found a significant positive correlation of MVUS-VI with thyrotropin receptor antibody (r=0.554) and with thyroid stimulating immunoglobulin bioassay (r=0.841). MVUS showed high intra- and inter-observer reliability from various statistical method.
Conclusion
In a real time and quantitative manner, MVUS-VI could be helpful to differentiate GD from thyroiditis in thyrotoxic patients, with less inter-observer variability.

Citations

Citations to this article as recorded by  
  • The Early Changes in Thyroid-Stimulating Immunoglobulin Bioassay over Anti-Thyroid Drug Treatment Could Predict Prognosis of Graves’ Disease
    Jin Yu, Han-Sang Baek, Chaiho Jeong, Kwanhoon Jo, Jeongmin Lee, Jeonghoon Ha, Min Hee Kim, Jungmin Lee, Dong-Jun Lim
    Endocrinology and Metabolism.2023; 38(3): 338.     CrossRef
  • Duplex Hemodynamic Parameters of Both Superior and Inferior Thyroid Arteries in Evaluation of Thyroid Hyperfunction Disorders
    Maha Assem Hussein, Alaa Abdel Hamid, Rasha M Abdel Samie, Elshaymaa Hussein, Shereen Sadik Elsawy
    International Journal of General Medicine.2022; Volume 15: 7131.     CrossRef
  • Case 5: A 41-Year-Old Woman With Palpitation
    Jiwon Yang, Kabsoo Shin, Jeongmin Lee, Jeonghoon Ha, Dong-Jun Lim, Han-Sang Baek
    Journal of Korean Medical Science.2022;[Epub]     CrossRef
  • Microvascular assessment of fascio-cutaneous flaps by ultrasound: A large animal study
    Guillaume Goudot, Yanis Berkane, Eloi de Clermont-Tonnerre, Claire Guinier, Irina Filz von Reiterdank, Antonia van Kampen, Korkut Uygun, Curtis L. Cetrulo, Basak E. Uygun, Anahita Dua, Alexandre G. Lellouch
    Frontiers in Physiology.2022;[Epub]     CrossRef
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Diabetes, Obesity and Metabolism
The Effects of PPAR Agonists on Atherosclerosis and Nonalcoholic Fatty Liver Disease in ApoE−/−FXR−/− Mice
Yenna Lee, Bo-Rahm Kim, Geun-Hyung Kang, Gwan Jae Lee, Young Joo Park, Haeryoung Kim, Hak Chul Jang, Sung Hee Choi
Endocrinol Metab. 2021;36(6):1243-1253.   Published online December 28, 2021
DOI: https://doi.org/10.3803/EnM.2021.1100
  • 5,437 View
  • 155 Download
  • 11 Web of Science
  • 11 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Farnesoid X receptor (FXR), a bile acid–activated nuclear receptor, is a potent regulator of glucose and lipid metabolism as well as of bile acid metabolism. Previous studies have demonstrated that FXR deficiency is associated with metabolic derangements, including atherosclerosis and nonalcoholic fatty liver disease (NAFLD), but its mechanism remains unclear. In this study, we investigated the role of FXR in atherosclerosis and NAFLD and the effect of peroxisome proliferator-activated receptor (PPAR) agonists in mouse models with FXR deficiency.
Methods
En face lipid accumulation analysis, liver histology, serum levels of glucose and lipids, and mRNA expression of genes related to lipid metabolism were compared between apolipoprotein E (ApoE)−/− and ApoE−/−FXR−/− mice. The effects of PPARα and PPARγ agonists were also compared in both groups of mice.
Results
Compared with ApoE−/− mice, ApoE−/−FXR−/− mice showed more severe atherosclerosis, hepatic steatosis, and higher levels of serum cholesterol, low-density lipoprotein cholesterol, and triglycerides, accompanied by increased mRNA expression of FAS, ApoC2, TNFα, IL-6 (liver), ATGL, TGH, HSL, and MGL (adipocytes), and decreased mRNA expressions of CPT2 (liver) and Tfam (skeletal muscle). Treatment with a PPARα agonist, but not with a PPARγ agonist, partly reversed atherosclerosis and hepatic steatosis, and decreased plasma triglyceride levels in the ApoE−/−FXR−/− mice, in association with increased mRNA expression of CD36 and FATP and decreased expression of ApoC2 and ApoC3 (liver).
Conclusion
Loss of FXR is associated with aggravation of atherosclerosis and hepatic steatosis in ApoE-deficient mice, which could be reversed by a PPARα agonist through induction of fatty acid uptake, β-oxidation, and triglyceride hydrolysis.

Citations

Citations to this article as recorded by  
  • Evaluation of the hepatotoxicity of Psoralea corylifolia L. based on a zebrafish model
    Shu-Yan Gao, Jing-Cheng Zhao, Qing Xia, Chen Sun, Maimaiti Aili, Ainiwaer Talifu, Shi-Xia Huo, Yun Zhang, Zhi-Jian Li
    Frontiers in Pharmacology.2024;[Epub]     CrossRef
  • Mitochondrial carnitine palmitoyltransferase-II dysfunction: A possible novel mechanism for nonalcoholic fatty liver disease in hepatocarcinogenesis
    Min Yao, Ping Zhou, Yan-Yan Qin, Li Wang, Deng-Fu Yao
    World Journal of Gastroenterology.2023; 29(12): 1765.     CrossRef
  • Emerging Roles of Gut Microbial Modulation of Bile Acid Composition in the Etiology of Cardiovascular Diseases
    Tess Yntema, Debby P. Y. Koonen, Folkert Kuipers
    Nutrients.2023; 15(8): 1850.     CrossRef
  • The interplay between nonalcoholic fatty liver disease and atherosclerotic cardiovascular disease
    Alexandra C. Finney, Sandeep Das, Dhananjay Kumar, M. Peyton McKinney, Bishuang Cai, Arif Yurdagul, Oren Rom
    Frontiers in Cardiovascular Medicine.2023;[Epub]     CrossRef
  • Targeting PPARs for therapy of atherosclerosis: A review
    Miao Miao, Xue Wang, Tian Liu, Yan-Jie Li, Wen-Qian Yu, Tong-Mei Yang, Shou-Dong Guo
    International Journal of Biological Macromolecules.2023; 242: 125008.     CrossRef
  • Cabernet sauvignon dry red wine ameliorates atherosclerosis in mice by regulating inflammation and endothelial function, activating AMPK phosphorylation, and modulating gut microbiota
    Xinlong Cheng, Xue Han, Liangfu Zhou, Yasai Sun, Qian Zhou, Xuan Lin, Zhe Gao, Jie Wang, Wen Zhao
    Food Research International.2023; 169: 112942.     CrossRef
  • Impacts of dietary lipids derived from animal or vegetable sources on healthy rats
    Mostafa M Dalal, Gamal M Edrees, Hanaa A Hassan, Mamdouh Abdel-Mogib, Mai Alaa El-Dein
    Egyptian Journal of Basic and Applied Sciences.2023; 10(1): 618.     CrossRef
  • Whey protein hydrolysate alleviated atherosclerosis and hepatic steatosis by regulating lipid metabolism in apoE-/- mice fed a Western diet
    Kai Wang, Zixin Fu, Xiaoyi Li, Hui Hong, Xin Zhan, Xiaohong Guo, Yongkang Luo, Yuqing Tan
    Food Research International.2022; 157: 111419.     CrossRef
  • Melatonin alleviates PM2.5‐induced glucose metabolism disorder and lipidome alteration by regulating endoplasmic reticulum stress
    Zhou Du, Junjie Hu, Lisen Lin, Qingqing Liang, Mengqi Sun, Zhiwei Sun, Junchao Duan
    Journal of Pineal Research.2022;[Epub]     CrossRef
  • Lipoprotein Lipase: Is It a Magic Target for the Treatment of Hypertriglyceridemia
    Joon Ho Moon, Kyuho Kim, Sung Hee Choi
    Endocrinology and Metabolism.2022; 37(4): 575.     CrossRef
  • The role of the gut microbiota in health and cardiovascular diseases
    Lu Wang, Shiqi Wang, Qing Zhang, Chengqi He, Chenying Fu, Quan Wei
    Molecular Biomedicine.2022;[Epub]     CrossRef
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Miscellaneous
Clinical Value of Serum Mitochondria-Inhibiting Substances in Assessing Renal Hazards: A Community-Based Prospective Study in Korea
Hoon Sung Choi, Jin Taek Kim, Hong Kyu Lee, Wook Ha Park, Youngmi Kim Pak, Sung Woo Lee
Endocrinol Metab. 2021;36(6):1298-1306.   Published online November 26, 2021
DOI: https://doi.org/10.3803/EnM.2021.1226
  • 3,139 View
  • 94 Download
  • 1 Web of Science
  • 1 Crossref
AbstractAbstract PDFPubReader   ePub   
Background
Mitochondrial dysfunction is strongly associated with several kidney diseases. However, no studies have evaluated the potential renal hazards of serum mitochondria-inhibiting substance (MIS) and aryl hydrocarbon receptor ligand (AhRL) levels.
Methods
We used serum level of MIS and AhRL and clinical renal outcomes from 1,511 participants of a prospective community-based cohort in Ansung. MIS was evaluated based on intracellular adenosine triphosphate (MIS-ATP) or reactive oxygen species (MIS-ROS) generation measured using cell-based assays.
Results
During a mean 6.9-year follow-up, 84 participants (5.6%) developed a rapid decline in kidney function. In the lowest quartile group of MIS-ATP, patients were older and had metabolically deleterious parameters. In multivariate logistic regression analysis, higher MIS-ATP was associated with decreased odds for rapid decline: the odds ratio (OR) of 1% increase was 0.977 (95% confidence interval [CI], 0.957 to 0.998; P=0.031), while higher MIS-ROS was marginally associated with increased odds for rapid decline (OR, 1.014; 95% CI, 0.999 to 1.028; P=0.055). However, serum AhRL was not associated with the rapid decline in kidney function. In subgroup analysis, the renal hazard of MIS was particularly evident in people with hypertension and low baseline kidney function.
Conclusion
Serum MIS was independently associated with a rapid decline in kidney function, while serum AhRL was not. The clinical implication of renal hazard on serum MIS requires further evaluation in future studies.

Citations

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  • An Interactive Online App for Predicting Diabetes via Machine Learning from Environment-Polluting Chemical Exposure Data
    Rosy Oh, Hong Kyu Lee, Youngmi Kim Pak, Man-Suk Oh
    International Journal of Environmental Research and Public Health.2022; 19(10): 5800.     CrossRef
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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
  • 4,381 View
  • 167 Download
  • 7 Web of Science
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AbstractAbstract PDFPubReader   ePub   
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
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Original Article
Adrenal Gland
Aldosterone Inhibits In Vitro Myogenesis by Increasing Intracellular Oxidative Stress via Mineralocorticoid Receptor
Jin Young Lee, Da Ae Kim, Eunah Choi, Yun Sun Lee, So Jeong Park, Beom-Jun Kim
Endocrinol Metab. 2021;36(4):865-874.   Published online July 30, 2021
DOI: https://doi.org/10.3803/EnM.2021.1108
  • 4,075 View
  • 109 Download
  • 5 Web of Science
  • 8 Crossref
AbstractAbstract PDFPubReader   ePub   
Background
Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it.
Methods
Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reversetranscription polymerase chain reaction, Western blot, viability, and migration analyses were performed for experimental research.
Results
Recombinant aldosterone treatment suppressed muscle differentiation from mouse C2C12 myoblasts in a dose-dependent manner, and consistently reduced the expression of myogenic differentiation markers. Furthermore, aldosterone significantly increased intracellular reactive oxygen species (ROS) levels in myotubes, and treatment with N-acetyl cysteine, a potent biological thiol antioxidant, reversed the decrease of myotube area, myotube area per myotube, nucleus number per myotube, and fusion index due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular ROS generation during myogenesis and markedly attenuated the suppression of in vitro myogenesis by aldosterone.
Conclusion
These findings support the hypothesis that hypersecretion of aldosterone, like PA, directly contributes to muscular deterioration and suggest that antioxidants and/or MR antagonists could be effective therapeutic options to reduce the risk of sarcopenia in these patients.

Citations

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  • Molecular mechanisms underlying sarcopenia in heart failure
    Cody A. Rutledge
    The Journal of Cardiovascular Aging.2024;[Epub]     CrossRef
  • Role of glucocorticoid and mineralocorticoid receptors in rainbow trout (Oncorhynchus mykiss) skeletal muscle: A transcriptomic perspective of cortisol action
    Jorge E. Aedo, Rodrigo Zuloaga, Daniela Aravena-Canales, Alfredo Molina, Juan Antonio Valdés
    Frontiers in Physiology.2023;[Epub]     CrossRef
  • Effect of 11-Deoxycorticosterone in the Transcriptomic Response to Stress in Rainbow Trout Skeletal Muscle
    Rodrigo Zuloaga, Daniela Aravena-Canales, Jorge Eduardo Aedo, Cesar Osorio-Fuentealba, Alfredo Molina, Juan Antonio Valdés
    Genes.2023; 14(2): 512.     CrossRef
  • Heart Failure Medication and Muscle Wasting
    Yasuhiro Izumiya
    Circulation Journal.2023; 88(1): 20.     CrossRef
  • 2023 Korean Endocrine Society Consensus Guidelines for the Diagnosis and Management of Primary Aldosteronism
    Jeonghoon Ha, Jung Hwan Park, Kyoung Jin Kim, Jung Hee Kim, Kyong Yeun Jung, Jeongmin Lee, Jong Han Choi, Seung Hun Lee, Namki Hong, Jung Soo Lim, Byung Kwan Park, Jung-Han Kim, Kyeong Cheon Jung, Jooyoung Cho, Mi-kyung Kim, Choon Hee Chung
    Endocrinology and Metabolism.2023; 38(6): 597.     CrossRef
  • Higher Plasma Stromal Cell-Derived Factor 1 Is Associated with Lower Risk for Sarcopenia in Older Asian Adults
    Sunghwan Ji, Kyunggon Kim, So Jeong Park, Jin Young Lee, Hee-Won Jung, Hyun Ju Yoo, Il-Young Jang, Eunju Lee, Ji Yeon Baek, Beom-Jun Kim
    Endocrinology and Metabolism.2023; 38(6): 701.     CrossRef
  • The Role of Aldosterone in OSA and OSA-Related Hypertension
    Yi Wang, Chuan Xiang Li, Ying Ni Lin, Li Yue Zhang, Shi Qi Li, Liu Zhang, Ya Ru Yan, Fang Ying Lu, Ning Li, Qing Yun Li
    Frontiers in Endocrinology.2022;[Epub]     CrossRef
  • Mineralocorticoid Receptor Antagonists in Diabetic Kidney Disease
    Daiji Kawanami, Yuichi Takashi, Yoshimi Muta, Naoki Oda, Dai Nagata, Hiroyuki Takahashi, Makito Tanabe
    Frontiers in Pharmacology.2021;[Epub]     CrossRef
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Review Article
Diabetes, Obesity and Metabolism
Receptor-Mediated Muscle Homeostasis as a Target for Sarcopenia Therapeutics
Jong Hyeon Yoon, Ki-Sun Kwon
Endocrinol Metab. 2021;36(3):478-490.   Published online June 28, 2021
DOI: https://doi.org/10.3803/EnM.2021.1081
  • 8,595 View
  • 328 Download
  • 9 Web of Science
  • 8 Crossref
AbstractAbstract PDFPubReader   ePub   
Sarcopenia is a disease characterized by age-related decline of skeletal muscle mass and function. The molecular mechanisms of the pathophysiology of sarcopenia form a complex network due to the involvement of multiple interconnected signaling pathways. Therefore, signaling receptors are major targets in pharmacological strategies in general. To provide a rationale for pharmacological interventions for sarcopenia, we herein describe several druggable signaling receptors based on their role in skeletal muscle homeostasis and changes in their activity with aging. A brief overview is presented of the efficacy of corresponding drug candidates under clinical trials. Strategies targeting the androgen receptor, vitamin D receptor, Insulin-like growth factor-1 receptor, and ghrelin receptor primarily focus on promoting anabolic action using natural ligands or mimetics. Strategies involving activin receptors and angiotensin receptors focus on inhibiting catabolic action. This review may help to select specific targets or combinations of targets in the future.

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  • The Current Landscape of Pharmacotherapies for Sarcopenia
    Gulistan Bahat, Serdar Ozkok
    Drugs & Aging.2024; 41(2): 83.     CrossRef
  • Associations of micronutrient dietary patterns with sarcopenia among US adults: a population-based study
    Yining Liu, Xiangliang Liu, Linnan Duan, Yixin Zhao, Yuwei He, Wei Li, Jiuwei Cui
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  • Impact of Vitamin D Level on Sarcopenia in Elderly People: A Critical Review
    Saniya Khan, Sunil Kumar, Sourya Acharya, Anil Wanjari
    Journal of Health and Allied Sciences NU.2023; 13(04): 453.     CrossRef
  • Novel Potential Targets for Function-Promoting Therapies: Orphan Nuclear Receptors, Anti-inflammatory Drugs, Troponin Activators, Mas Receptor Agonists, and Urolithin A
    Waly Dioh, Vihang Narkar, Anurag Singh, Fady Malik, Luigi Ferrucci, Cendrine Tourette, Jean Mariani, Rob van Maanen, Roger A Fielding, Lewis A Lipsitz
    The Journals of Gerontology: Series A.2023; 78(Supplement): 44.     CrossRef
  • Alverine citrate promotes myogenic differentiation and ameliorates muscle atrophy
    Jong Hyeon Yoon, Seung-Min Lee, Younglang Lee, Min Ju Kim, Jae Won Yang, Jeong Yi Choi, Ju Yeon Kwak, Kwang-Pyo Lee, Yong Ryoul Yang, Ki-Sun Kwon
    Biochemical and Biophysical Research Communications.2022; 586: 157.     CrossRef
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    Takahiro Eguchi, Yuji Yamanashi
    Biochemical and Biophysical Research Communications.2022; 589: 192.     CrossRef
  • Gastric Mobility and Gastrointestinal Hormones in Older Patients with Sarcopenia
    Hsien-Hao Huang, Tse-Yao Wang, Shan-Fan Yao, Pei-Ying Lin, Julia Chia-Yu Chang, Li-Ning Peng, Liang-Kung Chen, David Hung-Tsang Yen
    Nutrients.2022; 14(9): 1897.     CrossRef
  • Molecular Mechanisms Underlying Intensive Care Unit-Acquired Weakness and Sarcopenia
    Marcela Kanova, Pavel Kohout
    International Journal of Molecular Sciences.2022; 23(15): 8396.     CrossRef
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Original Articles
Clinical Study
High Serum-Induced AhRL Is Associated with Prevalent Metabolic Syndrome and Future Impairment of Glucose Tolerance in the Elderly
Youngmi Kim Pak, Hoon Sung Choi, Wook Ha Park, Suyeol Im, P. Monica Lind, Lars Lind, Hong Kyu Lee
Endocrinol Metab. 2021;36(2):436-446.   Published online April 19, 2021
DOI: https://doi.org/10.3803/EnM.2020.883
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  • 108 Download
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AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
High circulating levels of dioxins and dioxin-like chemicals, acting via the aryl hydrocarbon receptor (AhR), have previously been linked to diabetes. We now investigated whether the serum AhR ligands (AhRL) were higher in subjects with metabolic syndrome (MetS) and in subjects who had developed a worsened glucose tolerance over time.
Methods
Serum AhRL at baseline was measured by a cell-based AhRL activity assay in 70-year-old subjects (n=911) in the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study. The main outcome measures were prevalent MetS and worsening of glucose tolerance over 5 years of follow-up.
Results
AhRL was significantly elevated in subjects with prevalent MetS as compared to those without MetS, following adjustment for sex, smoking, exercise habits, alcohol intake and educational level (P=0.009). AhRL at baseline was higher in subjects who developed impaired fasting glucose or diabetes at age 75 years than in those who remained normoglycemic (P=0.0081). The odds ratio (OR) of AhRL for worsening glucose tolerance over 5 years was 1.43 (95% confidence interval [CI], 1.13 to 1.81; P=0.003, continuous variables) and 2.81 (95% CI, 1.31 to 6.02; P=0.008, in the highest quartile) adjusted for sex, life style factors, body mass index, and glucose.
Conclusion
These findings support a large body of epidemiologic evidence that exposure to AhR transactivating substances, such as dioxins and dioxin-like chemicals, might be involved in the pathogenesis of MetS and diabetes development. Measurement of serum AhRL in humans can be a useful tool in predicting the onset of metabolic disorders.

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  • An Interactive Online App for Predicting Diabetes via Machine Learning from Environment-Polluting Chemical Exposure Data
    Rosy Oh, Hong Kyu Lee, Youngmi Kim Pak, Man-Suk Oh
    International Journal of Environmental Research and Public Health.2022; 19(10): 5800.     CrossRef
  • A Novel Aryl Hydrocarbon Receptor Antagonist HBU651 Ameliorates Peripheral and Hypothalamic Inflammation in High-Fat Diet-Induced Obese Mice
    Sora Kang, Aden Geonhee Lee, Suyeol Im, Seung Jun Oh, Hye Ji Yoon, Jeong Ho Park, Youngmi Kim Pak
    International Journal of Molecular Sciences.2022; 23(23): 14871.     CrossRef
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Endocrine Research
DEHP Down-Regulates Tshr Gene Expression in Rat Thyroid Tissues and FRTL-5 Rat Thyrocytes: A Potential Mechanism of Thyroid Disruption
Min Joo Kim, Hwan Hee Kim, Young Shin Song, Ok-Hee Kim, Kyungho Choi, Sujin Kim, Byung-Chul Oh, Young Joo Park
Endocrinol Metab. 2021;36(2):447-454.   Published online March 31, 2021
DOI: https://doi.org/10.3803/EnM.2020.920
  • 4,899 View
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  • 11 Web of Science
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AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Di-2-ethylhexyl phthalate (DEHP) is known to disrupt thyroid hormonal status. However, the underlying molecular mechanism of this disruption is unclear. Therefore, we investigated the direct effects of DEHP on the thyroid gland.
Methods
DEHP (vehicle, 50 mg/kg, and 500 mg/kg) was administered to Sprague-Dawley rats for 2 weeks. The expression of the thyroid hormone synthesis pathway in rat thyroid tissues was analyzed through RNA sequencing analysis, quantitative reverse transcription-polymerase chain reaction (RT-PCR), and immunohistochemical (IHC) staining. DEHP was treated to FRTL-5 rat thyroid cells, and an RT-PCR analysis was performed. A reporter gene assay containing the promoter of thyroid stimulating hormone receptor (TSHR) in Nthy-ori 3-1 human thyroid cells was constructed, and luciferase activity was determined.
Results
After DEHP treatment, the free thyroxine (T4) and total T4 levels in rats significantly decreased. RNA sequencing analysis of rat thyroid tissues showed little difference between vehicle and DEHP groups. In the RT-PCR analysis, Tshr expression was significantly lower in both DEHP groups (50 and 500 mg/kg) compared to that in the vehicle group, and IHC staining showed that TSHR expression in the 50 mg/kg DEHP group significantly decreased. DEHP treatment to FRTL-5 cells significantly down-regulated Tshr expression. DEHP treatment also reduced luciferase activity in a reporter gene assay for TSHR.
Conclusion
Although overall genetic changes in the thyroid hormone synthesis pathway are not clear, DEHP exposure could significantly down-regulate Tshr expression in thyroid glands. Down-regulation of Tshr gene appears to be one of potential mechanisms of thyroid disruption by DEHP exposure.

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  • ARTS is essential for di-2-ethylhexyl phthalate (DEHP)-induced apoptosis of mouse Leydig cells
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    Marie-Azélie Moralia, Clarisse Quignon, Marine Simonneaux, Valérie Simonneaux
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    Amel Jebara, Asma Beltifa, Guissepa Di Bella, Lotfi Mabrouk, Hedi Ben Mansour
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Review Articles
Thyroid
Best Achievements in Translational and Basic Thyroidology in 2020
Sun Wook Cho, Young Joo Park
Endocrinol Metab. 2021;36(1):36-40.   Published online February 24, 2021
DOI: https://doi.org/10.3803/EnM.2021.104
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AbstractAbstract PDFPubReader   ePub   
This review discusses articles published in 2020 that presented noteworthy achievements in translational and basic thyroidology. Previously unresolved questions about thyroid hormone receptor actions and signaling mechanisms were answered using various novel in vitro and in vivo models. Using high resolution cryo-electron microscopy, the fine functional structure of thyroglobulin was demonstrated, and new insights into the pathogenesis of thyroid disease were achieved, with a focus on research into thyroid-disrupting chemicals and the gut microbiome. Novel therapeutic approaches were tried in the field of advanced thyroid cancer treatments.
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Diabetes
Peptidyl and Non-Peptidyl Oral Glucagon-Like Peptide-1 Receptor Agonists
Hun Jee Choe, Young Min Cho
Endocrinol Metab. 2021;36(1):22-29.   Published online February 24, 2021
DOI: https://doi.org/10.3803/EnM.2021.102
  • 27,536 View
  • 641 Download
  • 9 Web of Science
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AbstractAbstract PDFPubReader   ePub   
Glucagon-like peptide-1 (GLP-1) receptor agonists are efficacious glucose-lowering medications with salient benefits for body weight and cardiovascular events. This class of medications is now recommended as the top priority for patients with established cardiovascular disease or indicators of high risk. Until the advent of oral semaglutide, however, GLP-1 receptor agonists were available only in the form of subcutaneous injections. Aversion to needles, discomfort with self-injection, or skin problems at the injection site are commonly voiced problems in people with diabetes, and thus, attempts for non-invasive delivery strategies have continued. Herein, we review the evolution of GLP-1 therapy from its discovery and the development of currently approved drugs to the unprecedented endeavor to administer GLP-1 receptor agonists via the oral route. We focus on the pharmacokinetic and pharmacodynamic properties of the recently approved oral GLP-1 receptor agonist, oral semaglutide. Small molecule oral GLP-1 receptor agonists are currently in development, and we introduce how these chemicals have addressed the challenge posed by interactions with the large extracellular ligand binding domain of the GLP-1 receptor. We specifically discuss the structure and pharmacological properties of TT-OAD2, LY3502970, and PF-06882961, and envision an era where more patients could benefit from oral GLP-1 receptor agonist therapy.

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Original Article
Endocrine Research
Liver X Receptor β Related to Tumor Progression and Ribosome Gene Expression in Papillary Thyroid Cancer
Seonhyang Jeong, In-Kyu Kim, Hyunji Kim, Moon Jung Choi, Jandee Lee, Young Suk Jo
Endocrinol Metab. 2020;35(3):656-668.   Published online August 20, 2020
DOI: https://doi.org/10.3803/EnM.2020.667
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AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Intracellular lipid deposition has been reported in thyroid glands in obese animal and human. To understand the regulatory mechanism of lipid metabolism in thyroid cancer, we investigated the expression status of liver X receptor (LXR) and analyzed its clinicopathological characteristics and molecular biological features.
Methods
Expression status of LXR and its transcriptional targets in human cancers were analyzed using The Cancer Genome Atlas (TCGA). The gene-sets related to high LXRβ expression was investigated by gene set enrichment analysis (GSEA) using Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathways and gene ontology biologic process. Quantitative reverse transcription polymerase chain reaction was performed in thyroid cancer samples using our validation cohort.
Results
In contrast to low expression of LXRα, LXRβ was highly expressed in thyroid cancer compared to the other types of human cancers. High LXRβ expression was correlated with the expression of LXRβ transcriptional targets genes, such as apolipoprotein C1 (APOC1), APOC2, apolipoprotein E (APOE), ATP binding cassette subfamily G member 8 (ABCG8), sterol regulatory elementbinding protein 1c (SREBP1c), and SPOT14. Furthermore, High LXRβ expression group indicated poor clinicopathological characteristics and aggressive molecular biological features independently from the drive mutation status. Mechanistically, high LXRβ expression was coordinately related to ribosome-related gene sets.
Conclusion
The mechanistic link between LXRβ and ribosomal activity will be addressed to develop new diagnostic and therapeutic targets in thyroid cancers.

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Review Articles
Thyroid
Bisphenols and Thyroid Hormone
Min Joo Kim, Young Joo Park
Endocrinol Metab. 2019;34(4):340-348.   Published online December 23, 2019
DOI: https://doi.org/10.3803/EnM.2019.34.4.340
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  • 60 Web of Science
  • 64 Crossref
AbstractAbstract PDFPubReader   ePub   

In recent decades, attention has been directed toward the effects of bisphenol A (BPA) on human health. BPA has estrogenic activity and is regarded as a representative endocrine disruptor. In addition, mounting evidence indicates that BPA can disrupt thyroid hormone and its action. This review examined human epidemiological studies to investigate the association between BPA exposure and thyroid hormone levels, and analyzed in vivo and in vitro experiments to identify the causal relationship and its mechanism of action. BPA is involved in thyroid hormone action not only as a thyroid hormone receptor antagonist, but also through several other mechanisms. Since the use of bisphenols other than BPA has recently increased, we also reviewed the effects of other bisphenols on thyroid hormone action.

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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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AbstractAbstract PDFPubReader   ePub   

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.

Citations

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