- 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
-
-
2,750
View
-
121
Download
-
2
Web of Science
-
2
Crossref
-
 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.
-
Citations
Citations to this article as recorded by  - The potential of flavonoids in hepatic fibrosis: A comprehensive review
Zhu Wenbo, Han Jianwei, Liu Hua, Tang Lei, Chen Guijuan, Tian Mengfei
Phytomedicine.2024; 133: 155932. CrossRef - Advancements in Plant-Based Therapeutics for Hepatic Fibrosis: Molecular Mechanisms and Nanoparticulate Drug Delivery Systems
Alina Ciceu, Ferenc Fenyvesi, Anca Hermenean, Simona Ardelean, Simona Dumitra, Monica Puticiu
International Journal of Molecular Sciences.2024; 25(17): 9346. 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
-
-
4,647
View
-
240
Download
-
7
Web of Science
-
7
Crossref
-
Abstract
PDFPubReader ePub
- 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
Citations to this article as recorded by - Insulin Resistance, Non-Alcoholic Fatty Liver Disease and Type 2 Diabetes Mellitus: Clinical and Experimental Perspective
Inha Jung, Dae-Jeong Koo, Won-Young Lee
Diabetes & Metabolism Journal.2024; 48(3): 327. CrossRef - 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 mitigates TGF-β-induced renal fibrosis through FGF21-mediated inhibition of the TGF-β/Smad3 signaling pathway
Jun-Kyu Byun, Gwon-Soo Jung
Biochemical and Biophysical Research Communications.2024; : 150425. CrossRef - Interference with mitochondrial function as part of the antifibrogenic effect of Rilpivirine: A step towards novel targets in hepatic stellate cell activation
Ana M. Benedicto, Federico Lucantoni, Isabel Fuster-Martínez, Pedro Diaz-Pozo, Dimitri Dorcaratto, Elena Muñoz-Forner, Victor M. Victor, Juan V. Esplugues, Ana Blas-García, Nadezda Apostolova
Biomedicine & Pharmacotherapy.2024; 178: 117206. CrossRef - DPP-IV as a potential candidate in anti-obesity and obesity-related diseases treatment
Xin Guo, Huolun Feng, Liyang Cai, Jiabin Zheng, Yong Li
Biomedicine & Pharmacotherapy.2024; 180: 117464. 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
-
-
6,223
View
-
219
Download
-
5
Web of Science
-
4
Crossref
-
Abstract
PDF
 Supplementary MaterialPubReader ePub
- 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
Citations to this article as recorded by - The potential of flavonoids in hepatic fibrosis: A comprehensive review
Zhu Wenbo, Han Jianwei, Liu Hua, Tang Lei, Chen Guijuan, Tian Mengfei
Phytomedicine.2024; 133: 155932. CrossRef - 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;[Epub] 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
-
-
7,419
View
-
190
Download
-
14
Web of Science
-
11
Crossref
-
Abstract
PDFPubReader ePub
- 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
Citations to this article as recorded by - Amplified response of drug-induced liver fibrosis via immune cell co-culture in a 3D in vitro hepatic fibrosis model
Hyewon Jung, Mi-lang Kyun, Ji-In Kwon, Jeongha Kim, Ju-Kang Kim, Daeui Park, Yu Bin Lee, Kyoung-Sik Moon
Biomaterials Science.2024;[Epub] CrossRef - Serum Irisin, Myostatin, and Myonectin Correlate with Metabolic Health Markers, Liver Disease Progression, and Blood Pressure in Patients with Metabolic Dysfunction-Associated Fatty Liver Disease and Hypertension
Anna F. Sheptulina, Elvira M. Mamutova, Anastasia Yu. Elkina, Yuriy S. Timofeev, Victoria A. Metelskaya, Anton R. Kiselev, Oxana M. Drapkina
Metabolites.2024; 14(11): 584. 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 - 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
- Bone Metabolism
- Association between Serum Fibroblast Growth Factor 21 Levels and Bone Mineral Density in Postmenopausal Women
-
Hoon Sung Choi, Hyang Ah Lee, Sang-Wook Kim, Eun-Hee Cho
-
Endocrinol Metab. 2018;33(2):273-277. Published online June 21, 2018
-
DOI: https://doi.org/10.3803/EnM.2018.33.2.273
-
-
4,049
View
-
54
Download
-
9
Web of Science
-
7
Crossref
-
Abstract
PDFPubReader ePub
- Background
Despite the beneficial effect of fibroblast growth factor 21 (FGF21) on metabolic disease, there are concerns about adverse effects on bone metabolism, supported by animal studies. However, a recent human study showed the positive association between serum FGF21 level and bone mineral density (BMD) in healthy premenopausal women. We undertook this study to examine the association between FGF21 level and BMD in healthy postmenopausal Korean women who are susceptible to osteoporosis. MethodsWe used data of 115 participants from a cohort of healthy postmenopausal women (>50 years old) to examine the association between serum FGF21 level and BMD. The clinical characteristics were obtained from the participants, and blood testing and serum FGF21 testing were undertaken. BMD of the lumbar spine, femoral neck and total hip area, and bone markers were used in the analyses. ResultsThe mean age of the participants was 60.2±7.2 years. Serum FGF21 levels showed negative correlation with BMD and T-scores in all three areas, but there were no statistically significant differences. Multivariate analyses with adjustment for age and body mass index also did not show significant association between serum FGF21 level and BMD. In addition, serum FGF21 level also showed no correlation with osteocalcin and C-telopeptide levels. ConclusionIn our study, serum FGF21 level showed no significant correlation with BMD and T-scores.
-
Citations
Citations to this article as recorded by - Effect of Fibroblast Growth Factor (FGF) 19 and 21 on Hip Geometry and Strength in Post-menopausal Osteoporosis (PMO)
EunJi Kim, Amelia. E. Moore, Dwight Dulnoan, Geeta Hampson
Calcified Tissue International.2024; 115(5): 562. CrossRef - Fibroblast growth factor 21 and bone homeostasis
Yan Tang, Mei Zhang
Biomedical Journal.2023; 46(4): 100548. CrossRef - FGF21 negatively affects long-term female fertility in mice
Beat Moeckli, Thuy-Vy Pham, Florence Slits, Samuel Latrille, Andrea Peloso, Vaihere Delaune, Graziano Oldani, Stéphanie Lacotte, Christian Toso
Heliyon.2022; 8(11): e11490. CrossRef - Potential role of fibroblast growth factor 21 in the deterioration of bone quality in impaired glucose tolerance
D. T. W. Lui, C. H. Lee, V. W. K. Chau, C. H. Y. Fong, K. M. Y. Yeung, J. K. Y. Lam, A. C. H. Lee, W. S. Chow, K. C. B. Tan, Y. C. Woo, K. S. L. Lam
Journal of Endocrinological Investigation.2021; 44(3): 523. CrossRef - Skeletal Muscle and Bone – Emerging Targets of Fibroblast Growth Factor-21
Hui Sun, Matthew Sherrier, Hongshuai Li
Frontiers in Physiology.2021;[Epub] CrossRef - Age‐related bone loss is associated with FGF21 but not IGFBP1 in healthy adults
Shuen Yee Lee, Kai Deng Fam, Kar Ling Chia, Margaret M. C. Yap, Jorming Goh, Kwee Poo Yeo, Eric P. H. Yap, Sanjay H. Chotirmall, Chin Leong Lim
Experimental Physiology.2020; 105(4): 622. CrossRef - Chronic Kidney Disease Is Associated with Increased Plasma Levels of Fibroblast Growth Factors 19 and 21
Małgorzata Marchelek-Myśliwiec, Violetta Dziedziejko, Monika Nowosiad-Magda, Katarzyna Dołęgowska, Barbara Dołęgowska, Andrzej Pawlik, Krzysztof Safranow, Magda Wiśniewska, Joanna Stępniewska, Maciej Domański, Kazimierz Ciechanowski
Kidney and Blood Pressure Research.2019; 44(5): 1207. CrossRef
- Identification of Maturity-Onset Diabetes of the Young Caused by Glucokinase Mutations Detected Using Whole-Exome Sequencing
-
Eun-Hee Cho, Jae Woong Min, Sun Shim Choi, Hoon Sung Choi, Sang-Wook Kim
-
Endocrinol Metab. 2017;32(2):296-301. Published online May 29, 2017
-
DOI: https://doi.org/10.3803/EnM.2017.32.2.296
-
Correction in: Endocrinol Metab 2021;36(2):468
-
5,431
View
-
71
Download
-
13
Web of Science
-
11
Crossref
-
Abstract
PDFPubReader
Glucokinase maturity-onset diabetes of the young (GCK-MODY) represents a distinct subgroup of MODY that does not require hyperglycemia-lowering treatment and has very few diabetes-related complications. Three patients from two families who presented with clinical signs of GCK-MODY were evaluated. Whole-exome sequencing was performed and the effects of the identified mutations were assessed using bioinformatics tools, such as PolyPhen-2, SIFT, and in silico modeling. We identified two mutations: p.Leu30Pro and p.Ser383Leu. In silico analyses predicted that these mutations result in structural conformational changes, protein destabilization, and thermal instability. Our findings may inform future GCK-MODY diagnosis; furthermore, the two mutations detected in two Korean families with GCK-MODY improve our understanding of the genetic basis of the disease. -
Citations
Citations to this article as recorded by - Two novel GCK mutations in Chinese patients with maturity-onset diabetes of the young
Tao Wang, Mengmeng Zhu, Yun Wang, Cheng Hu, Chen Fang, Ji Hu
Endocrine.2023; 83(1): 92. CrossRef - Maturity-onset diabetes of the young in a large Portuguese cohort
Sílvia Santos Monteiro, Tiago da Silva Santos, Liliana Fonseca, Guilherme Assunção, Ana M. Lopes, Diana B. Duarte, Ana Rita Soares, Francisco Laranjeira, Isaura Ribeiro, Eugénia Pinto, Sónia Rocha, Sofia Barbosa Gouveia, María Eugenia Vazquez-Mosquera, Ma
Acta Diabetologica.2022; 60(1): 83. CrossRef - Maturity-Onset Diabetes of the Young: Mutations, Physiological Consequences, and Treatment Options
Hazar Younis, Se Eun Ha, Brian G. Jorgensen, Arushi Verma, Seungil Ro
Journal of Personalized Medicine.2022; 12(11): 1762. CrossRef - Monogenic diabetes: recent updates on diagnosis and precision treatment: A narrative review
Kyung Mi Jang
Precision and Future Medicine.2022; 6(4): 209. CrossRef - Monogenic diabetes characteristics in a transnational multicenter study from Mediterranean countries
Martine Vaxillaire, Amélie Bonnefond, Stavros Liatis, Leila Ben Salem Hachmi, Aleksandra Jotic, Mathilde Boissel, Stefan Gaget, Emmanuelle Durand, Emmanuel Vaillant, Mehdi Derhourhi, Mickaël Canouil, Nicolas Larcher, Frédéric Allegaert, Rita Medlej, Asma
Diabetes Research and Clinical Practice.2021; 171: 108553. CrossRef - Etiologic distribution and clinical characteristics of pediatric diabetes in 276 children and adolescents with diabetes at a single academic center
Ja Hye Kim, Yena Lee, Yunha Choi, Gu-Hwan Kim, Han-Wook Yoo, Jin-Ho Choi
BMC Pediatrics.2021;[Epub] CrossRef - Gençlerin Erişkin Başlangıçlı Diyabeti (MODY) Sorumlu HNF4A, GCK ve HNF1 Gen Varyasyonlarının Dünya Genelinde Coğrafik Dağılımı
Deniz KANCA DEMİRCİ, Nurdan GÜL, İlhan SATMAN, Oguz OZTURK, Hülya YILMAZ AYDOĞAN
Haliç Üniversitesi Fen Bilimleri Dergisi.2021; 4(1): 41. CrossRef - Undernutrition and suboptimal growth during the first year are associated with glycemia but not with insulin resistance in adulthood
Isabel Pereyra, Sandra López-Arana, Bernardo L. Horta
Cadernos de Saúde Pública.2021;[Epub] CrossRef - Update on Monogenic Diabetes in Korea
Ye Seul Yang, Soo Heon Kwak, Kyong Soo Park
Diabetes & Metabolism Journal.2020; 44(5): 627. CrossRef - The epidemiology, molecular pathogenesis, diagnosis, and treatment of maturity-onset diabetes of the young (MODY)
Ken Munene Nkonge, Dennis Karani Nkonge, Teresa Njeri Nkonge
Clinical Diabetes and Endocrinology.2020;[Epub] CrossRef - Novel deletion mutation in the glucokinase gene from a Korean man with GCK-MODY phenotype and situs inversus
Yun Kyung Cho, Eun-Hee Cho, Hoon Sung Choi, Sang-Wook Kim
Diabetes Research and Clinical Practice.2018; 143: 263. CrossRef
- Serum Preadipocyte Factor 1 Levels Are Not Associated with Bone Mineral Density among Healthy Postmenopausal Korean Women
-
Hoon Sung Choi, Sang-Wook Kim, Eun-Hee Cho
-
Endocrinol Metab. 2017;32(1):124-128. Published online February 28, 2017
-
DOI: https://doi.org/10.3803/EnM.2017.32.1.124
-
-
3,743
View
-
36
Download
-
1
Web of Science
-
Abstract
PDFSupplementary MaterialPubReader
- Background
Multipotent mesenchymal stem cells can differentiate into adipocytes or osteoblasts through closely regulated lineage-control processes. However, adipocyte precursor cells release preadipocyte factor 1 (Pref-1), which inhibits the differentiation of mesenchymal stem cells into mature adipocytes and osteoblasts. Previous studies have also reported an inverse association between Pref-1 levels and bone mineral density (BMD) among patients with anorexia nervosa. MethodsIn this retrospective study, we examined the correlations between Pref-1 levels and BMD among 124 healthy postmenopausal women (>50 years old). The patients had provided information regarding their clinical characteristics, and underwent blood testing and serum Pref-1 testing. ResultsThe subjects' mean age was 59.9±7.1 years and the median time since menopause onset was 9.1 years. A history of osteoporotic fracture was identified in 23 subjects (19%). Serum Pref-1 levels were not significantly correlated with BMD values at the lumbar spine (R2=0.038, P=0.109), femur neck (R2=0.017, P=0.869), and total hip (R2=0.041, P=0.09), and multivariate analyses with adjustment for age and body mass index also did not detect any significant correlations. Subgroup analyses according to a history of fracture also did not detect significant associations between Pref-1 levels and BMD values. ConclusionIn our study population, it does not appear that serum Pref-1 levels are significantly associated with BMD values and osteoporosis.
- Clinical Study
- Comparison of Age of Onset and Frequency of Diabetic Complications in the Very Elderly Patients with Type 2 Diabetes
-
Bong-Ki Lee, Sang-Wook Kim, Daehee Choi, Eun-Hee Cho
-
Endocrinol Metab. 2016;31(3):416-423. Published online August 26, 2016
-
DOI: https://doi.org/10.3803/EnM.2016.31.3.416
-
-
3,901
View
-
48
Download
-
9
Web of Science
-
9
Crossref
-
Abstract
PDFPubReader
- Background
The prevalence of type 2 diabetes in elderly people has increased dramatically in the last few decades. This study was designed to clarify the clinical characteristics of type 2 diabetes in patients aged ≥80 years according to age of onset. MethodsWe reviewed the medical records of 289 patients aged ≥80 years with type 2 diabetes at the outpatient diabetes clinics of Kangwon National University Hospital from September 2010 to June 2014. We divided the patients into middle-age-onset diabetes (onset before 65 years of age) and elderly-onset diabetes (onset at 65+ years of age). ResultsThere were 141 male and 148 female patients. The patients had a mean age of 83.2±2.9 years and the mean duration of diabetes was 14.3±10.4 years. One hundred and ninety-nine patients had elderly-onset diabetes. The patients with elderly-onset diabetes had a significantly lower frequency of diabetic retinopathy and nephropathy, lower serum creatinine levels, lower glycated hemoglobin (HbA1c) levels, and similar coronary revascularization and cerebral infarction rates compared to those with middle-age-onset diabetes. There was no frequency difference in coronary revascularization and cerebral infarction and HbA1c levels between three subgroups (<5, 5 to 15, and ≥15 years) of diabetes duration in elderly onset diabetes. However, both in the elderly onset diabetes and middle-age-onset diabetes, the cumulative incidence of retinopathy was increasing rapidly according to the duration of diabetes. ConclusionWe report that individuals with elderly-onset diabetes have a lower frequency of diabetic retinopathy and nephropathy and similar cardiovascular complications compared to those with middle-age-onset diabetes.
-
Citations
Citations to this article as recorded by - Rescue of High Glucose Impairment of Cultured Human Osteoblasts Using Cinacalcet and Parathyroid Hormone
V. A. Shahen, A. Schindeler, M. S. Rybchyn, C. M. Girgis, B. Mulholland, R. S. Mason, I. Levinger, T. C. Brennan-Speranza
Calcified Tissue International.2023; 112(4): 452. CrossRef - Factors Related to the Occurrence and Number of Chronic Diabetic Complications in Patients with Type 2 Diabetes Mellitus: Utilizing The National Health Insurance Service-National Health Screening Cohort in Korea, 2002~2015
Haejung Lee, Misoon Lee, Gaeun Park, Ah Reum Khang
Journal of Korean Gerontological Nursing.2022; 24(1): 22. CrossRef - Prevalence of and Risk Factors for Diabetic Retinopathy and Diabetic Macular Edema in Patients with Early- and Late-Onset Diabetes Mellitus
Yu Wang, Zhong Lin, Gang Zhai, Xiao Xia Ding, Liang Wen, Dong Li, Bo Zou, Ke Mi Feng, Yuan Bo Liang, Cong Xie
Ophthalmic Research.2022; 65(3): 293. CrossRef - Associations of Age at Diagnosis and Duration of Diabetes With Morbidity and Mortality Among Older Adults
Christine T. Cigolle, Caroline S. Blaum, Chen Lyu, Jinkyung Ha, Mohammed Kabeto, Judy Zhong
JAMA Network Open.2022; 5(9): e2232766. CrossRef - Chart Review of Diagnostic Methods, Baseline Characteristics and Symptoms for European Patients with Pancreatic Cancer
Alfredo Carrato, Davide Melisi, Gerald Prager, Christoph B Westphalen, Anabel Ferreras, Nathalie D’Esquermes, Julien Taieb, Teresa M Mercadé
Future Oncology.2021; 17(15): 1843. CrossRef - Distinction of cardiometabolic profiles among people ≥75 years with type 2 diabetes: a latent profile analysis
Antoine CHRISTIAENS, Michel P. HERMANS, Benoit BOLAND, Séverine HENRARD
BMC Endocrine Disorders.2019;[Epub] CrossRef - Validity of diagnostic codes and estimation of prevalence of diabetic foot ulcers using a large electronic medical record database
Avivit Cahn, Talya Altaras, Tal Agami, Ori Liran, Colette E. Touaty, Michel Drahy, Rena Pollack, Itamar Raz, Gabriel Chodick, Inbar Zucker
Diabetes/Metabolism Research and Reviews.2019;[Epub] CrossRef - Response: Comparison of Age of Onset and Frequency of Diabetic Complications in the Very Elderly Patients with Type 2 Diabetes (Endocrinol Metab2016;31:416-23, Bong-Ki Lee et al.)
Eun-Hee Cho
Endocrinology and Metabolism.2017; 32(1): 142. CrossRef - Letter: Comparison of Age of Onset and Frequency of Diabetic Complications in the Very Elderly Patients with Type 2 Diabetes (Endocrinol Metab2016;31:416-23, Bong-Ki Lee et al.)
Mee Kyoung Kim
Endocrinology and Metabolism.2017; 32(1): 140. CrossRef
- Clinical Study
- High Levels of Serum DPP-4 Activity Are Associated with Low Bone Mineral Density in Obese Postmenopausal Women
-
Sang-Wook Kim, Eun-Hee Cho
-
Endocrinol Metab. 2016;31(1):93-99. Published online March 16, 2016
-
DOI: https://doi.org/10.3803/EnM.2016.31.1.93
-
-
4,113
View
-
39
Download
-
12
Web of Science
-
14
Crossref
-
Abstract
PDFPubReader
- Background
Dipeptidyl peptidase 4/CD26 (DPP-4) is a widely expressed cell surface serine protease. DPP-4 inhibitors, one of common anti-diabetic agents play a protective role in bone metabolism in recent studies. A soluble form of DPP-4 is found in serum, and exhibits DPP-4 enzymatic activity. However, the physiological role of serum or soluble DPP-4 and its relationship with DPP-4 enzymatic function remain poorly understood. The aims of current study were to determine the association between serum DPP-4 activity and bone mineral density (BMD) in postmenopausal women. MethodsWe recruited data and serum samples from 124 consecutive healthy postmenopausal women aged >50 years. We divided study subjects into obese (body mass index [BMI] ≥25 kg/m2) and non-obese (BMI <25 kg/m2) postmenopausal women and examined the correlation between serum DPP-4 activity and clinical variables in each groups. ResultsA total of 124 postmenopausal women was enrolled, with a mean age of 59.9±7.1 years. The mean BMI of the study patients was 24.4±2.8 kg/m2. Regarding bone turnover markers, serum DPP-4 activity was positively correlated with serum calcium concentrations, intact parathyroid hormone, and serum C-telopeptide levels in all of the study subjects. However, there was no association between serum DPP-4 activity and BMD in the spine or femoral neck in all of the study subjects. Serum DPP-4 activity was negatively correlated (R=−0.288, P=0.038) with BMD of the spine in obese postmenopausal women. ConclusionThis study demonstrated for the first time that serum soluble DPP-4 activity was negatively correlated with BMD in obese postmenopausal women.
-
Citations
Citations to this article as recorded by - A novel mechanism of Vildagliptin in regulating bone metabolism and mitigating osteoporosis
Jinwen He, Dacheng Zhao, Bo Peng, Xingwen Wang, Shenghong Wang, Xiaobing Zhao, Peng Xu, Bin Geng, Yayi Xia
International Immunopharmacology.2024; 130: 111671. CrossRef - The multiple actions of dipeptidyl peptidase 4 (DPP-4) and its pharmacological inhibition on bone metabolism: a review
L. M. Pechmann, F. I. Pinheiro, V. F. C. Andrade, C. A. Moreira
Diabetology & Metabolic Syndrome.2024;[Epub] CrossRef - Comparative evaluation of Sodium-glucose co-transporter-2 inhibitors and dipeptidyl peptidase-4 inhibitors influence on bone turnover markers in rats with experimental type 2 diabetes mellitus
N. V. Timkina, A. V. Simanenkova, T. L. Karonova, T. D. Vlasov, N. Yu. Semenova, А. A. Bairamov, V. A. Timofeeva, A. A. Shimshilashvili, E. V. Shlyakhto
Osteoporosis and Bone Diseases.2022; 24(4): 27. CrossRef - The relationship between bone marrow adipose tissue and bone metabolism in postmenopausal osteoporosis
Jiao Li, Xiang Chen, Lingyun Lu, Xijie Yu
Cytokine & Growth Factor Reviews.2020; 52: 88. CrossRef - Update on: effects of anti-diabetic drugs on bone metabolism
Guillaume Mabilleau, Béatrice Bouvard
Expert Review of Endocrinology & Metabolism.2020; 15(6): 415. CrossRef - Soluble Dipeptidyl Peptidase-4 Levels Are Associated with Decreased Renal Function in Patients with Type 2 Diabetes Mellitus
Eun-Hee Cho, Sang-Wook Kim
Diabetes & Metabolism Journal.2019; 43(1): 97. CrossRef - Marrow Adipose Tissue: Its Origin, Function, and Regulation in Bone Remodeling and Regeneration
Qiwen Li, Yunshu Wu, Ning Kang
Stem Cells International.2018; 2018: 1. CrossRef - Association between Serum Dipeptidyl Peptidase-4 Concentration and Obesity-related Factors in Health Screen Examinees
Ji Yeon Lee, Byoung Kuk Jang, Min Kyung Song, Hye Soon Kim, Mi-Kyung Kim
Journal of Obesity & Metabolic Syndrome.2017; 26(3): 188. CrossRef - Association of DPP-4 activity with BMD, body composition, and incident hip fracture: the Cardiovascular Health Study
L. D. Carbone, P. Bůžková, H. A. Fink, J. A. Robbins, M. Bethel, C. M. Isales, W. D. Hill
Osteoporosis International.2017; 28(5): 1631. CrossRef - Adipocyte Accumulation in the Bone Marrow during Obesity and Aging Impairs Stem Cell-Based Hematopoietic and Bone Regeneration
Thomas H. Ambrosi, Antonio Scialdone, Antonia Graja, Sabrina Gohlke, Anne-Marie Jank, Carla Bocian, Lena Woelk, Hua Fan, Darren W. Logan, Annette Schürmann, Luis R. Saraiva, Tim J. Schulz
Cell Stem Cell.2017; 20(6): 771. CrossRef - The emerging role of bone marrow adipose tissue in bone health and dysfunction
Thomas H. Ambrosi, Tim J. Schulz
Journal of Molecular Medicine.2017; 95(12): 1291. CrossRef - Articles inEndocrinology and Metabolismin 2016
Won-Young Lee
Endocrinology and Metabolism.2017; 32(1): 62. CrossRef - Dipeptidyl Peptidase-4 and Adolescent Idiopathic Scoliosis: Expression in Osteoblasts
Emilie Normand, Anita Franco, Alain Moreau, Valérie Marcil
Scientific Reports.2017;[Epub] CrossRef - Effect of Dipeptidyl Peptidase-4 Inhibitors on Bone Metabolism and the Possible Underlying Mechanisms
Yinqiu Yang, Chenhe Zhao, Jing Liang, Mingxiang Yu, Xinhua Qu
Frontiers in Pharmacology.2017;[Epub] CrossRef
- Irisin Attenuates Hepatic Stellate Cell Activation and Liver Fibrosis in Bile Duct Ligation Mice Model and Improves Mitochondrial Dysfunction
-
Thuy Linh Lai, So Young Park, Giang Nguyen, Phuc Thi Minh Pham, Seon Mee Kang, Jeana Hong, Jae-Ho Lee, Seung-Soon Im, Dae-Hee Choi, Eun-Hee Cho
-
Received March 13, 2024 Accepted June 27, 2024 Published online November 5, 2024
-
DOI: https://doi.org/10.3803/EnM.2024.1984
[Epub ahead of print]
-
-
Abstract
PDFPubReader ePub
- Background
Liver fibrosis is a common outcome of chronic liver disease and is primarily driven by hepatic stellate cell (HSC) activation. Irisin, a myokine released during physical exercise, is beneficial for metabolic disorders and mitochondrial dysfunction. This study aimed to explore the effects of irisin on liver fibrosis in HSCs, a bile duct ligation (BDL) mouse model, and the associated mitochondrial dysfunction.
Methods
In vitro experiments utilized LX-2 cells, a human HSC line, stimulated with transforming growth factor-β1 (TGF-β1), a major regulator of HSC fibrosis, with or without irisin. Mitochondrial function was assessed using mitochondrial fission markers, transmission electron microscopy, mitochondrial membrane potential, and adenosine triphosphate (ATP) production. In vivo, liver fibrosis was induced in mice via BDL, followed by daily intraperitoneal injections of irisin (100 μg/kg/day) for 10 days.
Results
In vitro, irisin mitigated HSC activation and reduced reactive oxygen species associated with the TGF-β1/Smad signaling pathway. Irisin restored TGF-β1-induced increases in fission markers (Fis1, p-DRP1) and reversed the decreased expression of TFAM and SIRT3. Additionally, irisin restored mitochondrial membrane potential and ATP production lowered by TGF-β1 treatment. In vivo, irisin ameliorated the elevated liver-to-body weight ratio induced by BDL and alleviated liver fibrosis, as evidenced by Masson’s trichrome staining. Irisin also improved mitochondrial dysfunction induced by BDL surgery.
Conclusion
Irisin effectively attenuated HSC activation, ameliorated liver fibrosis in BDL mice, and improved associated mitochondrial dysfunction. These findings highlight the therapeutic potential of irisin for the treatment of liver fibrosis.
|
KES
