Endocrinology and Metabolism

Original Article

Miscellaneous
DN200434 Inhibits Vascular Smooth Muscle Cell Proliferation and Prevents Neointima Formation in Mice after Carotid Artery Ligation: Sudeep Kumar, Jonghwa Jin, Hyeon Young Park, Mi-Jin Kim, Jungwook Chin, Sungwoo Lee, Jina Kim, Jung-Guk Kim, Yeon-Kyung Choi, Keun-Gyu Park; Endocrinol Metab. 2022;37(5):800-809. Published online September 28, 2022; DOI: https://doi.org/10.3803/EnM.2022.1462

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Background
Excessive proliferation and migration of vascular smooth muscle cells (VSMCs), which contributes to the development of occlusive vascular diseases, requires elevated mitochondrial oxidative phosphorylation to meet the increased requirements for energy and anabolic precursors. Therefore, therapeutic strategies based on blockade of mitochondrial oxidative phosphorylation are considered promising for treatment of occlusive vascular diseases. Here, we investigated whether DN200434, an orally available estrogen receptor-related gamma inverse agonist, inhibits proliferation and migration of VSMCs and neointima formation by suppressing mitochondrial oxidative phosphorylation.
Methods
VSMCs were isolated from the thoracic aortas of 4-week-old Sprague-Dawley rats. Oxidative phosphorylation and the cell cycle were analyzed in fetal bovine serum (FBS)- or platelet-derived growth factor (PDGF)-stimulated VSMCs using a Seahorse XF-24 analyzer and flow cytometry, respectively. A model of neointimal hyperplasia was generated by ligating the left common carotid artery in male C57BL/6J mice.
Results
DN200434 inhibited mitochondrial respiration and mammalian target of rapamycin complex 1 activity and consequently suppressed FBS- or PDGF-stimulated proliferation and migration of VSMCs and cell cycle progression. Furthermore, DN200434 reduced carotid artery ligation-induced neointima formation in mice.
Conclusion
Our data suggest that DN200434 is a therapeutic option to prevent the progression of atherosclerosis.

Citations

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Jatrorrhizine inhibits Piezo1 activation and reduces vascular inflammation in endothelial cells
Tianying Hong, Xianmei Pan, Han Xu, Zhijuan Zheng, Lizhen Wen, Jing Li, Mingfeng Xia
Biomedicine & Pharmacotherapy.2023; 163: 114755. CrossRef

Brief Report

Diabetes, Obesity and Metabolism
Year-Long Trend in Glycated Hemoglobin Levels in Patients with Type 2 Diabetes during the COVID-19 Pandemic: Jonghwa Jin, Seong Wook Lee, Won-Ki Lee, Jae-Han Jeon, Jung-Guk Kim, In-Kyu Lee, Yeon-Kyung Choi, Keun-Gyu Park; Endocrinol Metab. 2021;36(5):1142-1146. Published online October 21, 2021; DOI: https://doi.org/10.3803/EnM.2021.1154

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Abstract PDF Supplementary Material PubReader ePub

It has been suggested that the coronavirus disease 2019 (COVID-19) pandemic has had a negative impact on glycemic control in patients with type 2 diabetes mellitus (T2DM). However, no study has examined yearly trends in glycated hemoglobin (HbA1c) levels after the start of the COVID-19 outbreak. Here, we performed a retrospective analysis of HbA1c concentrations during the early period of the COVID-19 outbreak (COVID-19 cohort) and then compared the yearly trend in the mean HbA1c level, along with fluctuations in HbA1c levels, with those during previous years (non-COVID-19 cohorts). We observed that the mean HbA1c level in patients with T2DM increased during the first 6 months of the COVID-19 outbreak. After 6 months, HbA1c levels in the COVID-19 cohort returned to levels seen in the non-COVID-19 cohorts. The data suggest that vulnerable patients with T2DM should be monitored closely during the early period of a pandemic to ensure they receive appropriate care.

Citations

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Physical and Mental Health Characteristics of Hospitalized COVID-19 Patients with and without Type 2 Diabetes Mellitus in Turkey
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A Hybrid Model of In-Person and Telemedicine Diabetes Education and Care for Management of Patients with Uncontrolled Type 2 Diabetes Mellitus: Findings and Implications from a Multicenter Prospective Study
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The indirect impact of the COVID-19 pandemic on people with type 2 diabetes mellitus and without COVID-19 infection: Systematic review and meta-analysis
Zhuoran Hu, Hin Moi Youn, Jianchao Quan, Lily Luk Siu Lee, Ivy Lynn Mak, Esther Yee Tak Yu, David Vai-Kiong Chao, Welchie Wai Kit Ko, Ian Chi Kei Wong, Gary Kui Kai Lau, Chak Sing Lau, Cindy Lo Kuen Lam, Eric Yuk Fai Wan
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Evaluating Effects of Virtual Diabetes Group Visits in Community Health Centers During the COVID-19 Pandemic
Tracy Dinh, Erin M Staab, Daisy Nuñez, Mengqi Zhu, Wen Wan, Cynthia T Schaefer, Amanda Campbell, Michael Quinn, Arshiya A Baig
Journal of Patient Experience.2023;[Epub] CrossRef
Cardiovascular-related health behavior changes: lessons from the COVID-19 pandemic and post-pandemic challenges
Inha Jung, Won-Young Lee
Cardiovascular Prevention and Pharmacotherapy.2023; 5(4): 99. CrossRef

Original Article

Lobeglitazone, a Novel Peroxisome Proliferator-Activated Receptor γ Agonist, Attenuates Renal Fibrosis Caused by Unilateral Ureteral Obstruction in Mice: Kwi-Hyun Bae, Jung Beom Seo, Yun-A Jung, Hye-Young Seo, Sun Hee Kang, Hui-Jeon Jeon, Jae Man Lee, Sungwoo Lee, Jung-Guk Kim, In-Kyu Lee, Gwon-Soo Jung, Keun-Gyu Park; Endocrinol Metab. 2017;32(1):115-123. Published online February 28, 2017; DOI: https://doi.org/10.3803/EnM.2017.32.1.115

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Abstract PDF PubReader

Background

Renal tubulointerstitial fibrosis is a common feature of the final stage of nearly all cause types of chronic kidney disease. Although classic peroxisome proliferator-activated receptor γ (PPARγ) agonists have a protective effect on diabetic nephropathy, much less is known about their direct effects in renal fibrosis. This study aimed to investigate possible beneficial effects of lobeglitazone, a novel PPARγ agonist, on renal fibrosis in mice.

Methods

We examined the effects of lobeglitazone on renal tubulointerstitial fibrosis in unilateral ureteral obstruction (UUO) induced renal fibrosis mice. We further defined the role of lobeglitazone on transforming growth factor (TGF)-signaling pathways in renal tubulointerstitial fibrosis through in vivo and in vitro study.

Results

Through hematoxylin/eosin and sirius red staining, we observed that lobeglitazone effectively attenuates UUO-induced renal atrophy and fibrosis. Immunohistochemical analysis in conjunction with quantitative reverse transcription polymerase chain reaction and Western blot analysis revealed that lobeglitazone treatment inhibited UUO-induced upregulation of renal Smad-3 phosphorylation, α-smooth muscle actin, plasminogen activator inhibitor 1, and type 1 collagen. In vitro experiments with rat mesangial cells and NRK-49F renal fibroblast cells suggested that the effects of lobeglitazone on UUO-induced renal fibrosis are mediated by inhibition of the TGF-β/Smad signaling pathway.

Conclusion

The present study demonstrates that lobeglitazone has a protective effect on UUO-induced renal fibrosis, suggesting that its clinical applications could extend to the treatment of non-diabetic origin renal disease.

Citations

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Comparative Efficacy of Lobeglitazone Versus Pioglitazone on Albuminuria in Patients with Type 2 Diabetes Mellitus
Kyung-Soo Kim, Sangmo Hong, Hong-Yup Ahn, Cheol-Young Park
Diabetes Therapy.2021; 12(1): 171. CrossRef
Lobeglitazone: A Novel Thiazolidinedione for the Management of Type 2 Diabetes Mellitus
Jaehyun Bae, Taegyun Park, Hyeyoung Kim, Minyoung Lee, Bong-Soo Cha
Diabetes & Metabolism Journal.2021; 45(3): 326. CrossRef
Lobeglitazone, A Peroxisome Proliferator-Activated Receptor-Gamma Agonist, Inhibits Papillary Thyroid Cancer Cell Migration and Invasion by Suppressing p38 MAPK Signaling Pathway
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Kyoung Min Kim, Hyun-Jin Jin, Seo Yeon Lee, Hyo Jin Maeng, Gha Young Lee, Tae Jung Oh, Sung Hee Choi, Hak Chul Jang, Soo Lim
Endocrinology and Metabolism.2017; 32(3): 389. CrossRef
Effects of Lobeglitazone, a Novel Thiazolidinedione, on Bone Mineral Density in Patients with Type 2 Diabetes Mellitus over 52 Weeks
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Review Article

Obesity and Metabolism
Transcriptional Regulation of Fibroblast Growth Factor 21 Expression: Kwi-Hyun Bae, Jung-Guk Kim, Keun-Gyu Park; Endocrinol Metab. 2014;29(2):105-111. Published online June 26, 2014; DOI: https://doi.org/10.3803/EnM.2014.29.2.105

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Abstract PDF PubReader

Fibroblast growth factor 21 (FGF21) is an attractive target for treating metabolic disease due to its wide-ranging beneficial effects on glucose and lipid metabolism. Circulating FGF21 levels are increased in insulin-resistant states; however, endogenous FGF21 fails to improve glucose and lipid metabolism in obesity, suggesting that metabolic syndrome is an FGF21-resistant state. Therefore, transcription factors for FGF21 are potential drug targets that could increase FGF21 expression in obesity and reduce FGF21 resistance. Despite many studies on the metabolic effects of FGF21, the transcriptional regulation of FGF21 gene expression remains controversial and is not fully understood. As the FGF21 transcription factor pathway is one of the most promising targets for the treatment of metabolic syndrome, further investigation of FGF21 transcriptional regulation is required.

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