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Molecular Research on Macrophages and Atherosclerosis in Diabetes Mellitus

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 3796

Special Issue Editors


E-Mail Website
Guest Editor
Division of Diabetes, Metabolism and Endocrinology, Showa University School of Medicine, Tokyo, Japan
Interests: diabetic comorbidities
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Division of Diabetes, Metabolism, and Endocrinology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan
Interests: Oxidative stress; Glycation; Diabetes; Cardiovascular disease; Aging

Special Issue Information

Dear Colleagues,

Diabetes increases the risk of atherosclerotic cardiovascular disease, such as coronary artery disease, peripheral artery disease, and stroke in patients with diabetes. Various biochemical pathways activated under diabetic conditions could contribute to the acceleration of atherosclerosis. Among them, accumulation of cholesterol esters into macrophages is the early characteristic feature of atherosclerosis, which is considered to play a crucial role in the development and progression of atherosclerotic cardiovascular disease. Therefore, it is important to clarify the underlying molecular mechanism for accelerated foam cell formation of macrophages and atherosclerotic progress in diabetes mellitus. For this Special Issue, we invite original research and review articles on recent progress in molecular mechanisms of macrophages and atherosclerosis in animals or patients with diabetes mellitus

Dr. Michishige Terasaki
Prof. Sho-ichi Yamagishi
Guest Editors

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Keywords

  • atherosclerosis
  • macrophages
  • foam cell
  • inflammation
  • molecular mechanisms

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Published Papers (1 paper)

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Research

18 pages, 3038 KiB  
Article
Sirt3 Pharmacologically Promotes Insulin Sensitivity through PI3/AKT/mTOR and Their Downstream Pathway in Adipocytes
by Alexandra Yatine Lee, Sabrina Marie Christensen, Nhi Duong, Quoc-Anh Tran, Hou Mai Xiong, Jennifer Huang, Sarah James, Dimple Vallabh, George Talbott, Melanie Rose and Linh Ho
Int. J. Mol. Sci. 2022, 23(7), 3740; https://doi.org/10.3390/ijms23073740 - 29 Mar 2022
Cited by 15 | Viewed by 3178
Abstract
Sirtuin-3 (Sirt3) is a major mitochondrial deacetylase enzyme that regulates multiple metabolic pathways, and its expression is decreased in diabetes type 1 and type 2 diabetes. This study aimed to elucidate Sirt3′s molecular mechanism in regulating insulin sensitivity in adipocytes that can contribute [...] Read more.
Sirtuin-3 (Sirt3) is a major mitochondrial deacetylase enzyme that regulates multiple metabolic pathways, and its expression is decreased in diabetes type 1 and type 2 diabetes. This study aimed to elucidate Sirt3′s molecular mechanism in regulating insulin sensitivity in adipocytes that can contribute to the effort of targeting Sirt3 for the treatment of obesity and type 2 diabetes. We found that the Sirt3 activator honokiol (HNK) induced adipogenesis compared to the control, in contrast to Sirt3 inhibitor, 3-TYP. Accordingly, HNK increased expression of adipocyte gene markers, gene-involved lipolysis and glucose transport (GLUT4), while 3-TYP reduced expression of those genes. Interestingly, 3-TYP caused an increase in gene expression of adipocyte-specific cytokines including IL6, resistin, and TNF-α. However, changes in adipocyte-specific cytokines in HNK treated cells were not significant. In addition, HNK stimulated insulin pathway by promoting insulin receptor beta (IRβ) and PI3K/AKT/mTOR pathways, resulting in an increase in phosphorylation of the forkhead family FoxO1/FoxO3a/FoxO4 and glycogen synthase kinase-3 (GSK-3β), opposing 3-TYP. In line with these findings, HNK increased free fatty acid and glucose uptake, contrary to 3-TYP. In conclusion, Sirt3 activator-HNK induced adipogenesis and lipolysis reduced adipocytes specific cytokines. Intriguingly, HNK activated insulin signaling pathway and increased free fatty acid as well as glucose uptake and transport, in sharp contrast to 3-TYP. These results indicate that, via insulin signaling regulation, Sirt3 activation by HNK improves insulin resistance, while Sirt3 inhibition by 3-TYP might precipitate insulin resistance. Full article
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