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The Molecular and Cellular Aspects of Insulin Resistance

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

Deadline for manuscript submissions: 20 May 2025 | Viewed by 1519

Special Issue Editors


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Guest Editor
Laboratory of Signal Transduction, Department of Biochemistry, Center for Research and Advanced Studies of the National Polytechnic Institute, Cinvestav-IPN, Mexico City 07360, Mexico
Interests: cell signaling and hypertension; cell signaling and insulin resistance; metabolic syndrome and diabetes; cell signaling and stress

E-Mail Website
Guest Editor
Laboratory of Cardiovascular Biochemistry and Physiology, Department of Bio-Chemistry, Center for Research and Advanced Studies of the National Polytechnic Institute, Cinvestav-IPN, Mexico City 07360, Mexico
Interests: calcium handling proteins; metabolic syndrome and diabetes; metabolic alterations

Special Issue Information

Dear Colleagues,

Insulin resistance is a systemic disorder in which cells fail to respond to normal circulating insulin levels. Under this condition, the biological actions of insulin on hepatic, muscular, and adipose tissues, such as glucose uptake and the synthesis of glycogen, lipids, and proteins, are altered. Experimental and clinical trials have provided evidence that insulin resistance in metabolic tissues constitutes a hallmark of metabolic dysfunction, mainly induced by obesity. This peripheral insulin resistance causes pancreatic β-cells to secrete more insulin in a process known as compensatory hyperinsulinemia. However, together with insulin resistance, there is reduced β-cell function, resulting in sustained hyperglycemia and type 2 diabetes mellitus. At the molecular level, insulin resistance is the consequence of insulin signaling impairment resulting from mutations or post-translation modification of the insulin receptor itself or any of its downstream effectors, including the insulin receptor substrate, PI3K, and Akt.

Despite being a subject widely studied from a molecular and clinical perspective, insulin resistance continues to be an area of study that poses new challenges in basic and clinical research, such as its impact on metabolic syndrome, inflammation, neuronal, cognitive, and cardiovascular disorders, among others.

We invite scientists working on this topic to contribute to this Special Issue. Original research articles or reviews on all aspects of the molecular and cellular mechanisms of insulin resistance and its implications in the development of pathologies associated with inflammatory processes, metabolism, cardiovascular, neurological, cognitive disorders, and cancer, among others, will be welcome.

Prof. Dr. Jesús Alberto Olivares-Reyes
Prof. Dr. Angélica Rueda
Guest Editors

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Keywords

  • insulin resistance
  • insulin receptor
  • IRS
  • Akt
  • PI3K
  • protein phosphorylation
  • protein dephosphorylation
  • inflammation
  • metabolic syndrome
  • cardiometabolic syndrome
  • diabetic cardiomyopathy

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Published Papers (1 paper)

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Research

15 pages, 1764 KiB  
Article
Mitochondria-Targeted DNA Repair Glycosylase hOGG1 Protects Against HFD-Induced Liver Oxidative Mitochondrial DNA Damage and Insulin Resistance in OGG1-Deficient Mice
by Larysa V. Yuzefovych, Hye Lim Noh, Sujin Suk, Anne Michele Schuler, Madhuri S. Mulekar, Viktor M. Pastukh, Jason K. Kim and Lyudmila I. Rachek
Int. J. Mol. Sci. 2024, 25(22), 12168; https://doi.org/10.3390/ijms252212168 - 13 Nov 2024
Viewed by 910
Abstract
8-oxoguanine DNA glycosylase-1 (OGG1) is a DNA glycosylase mediating the first step in base excision repair which removes 7,8-dihydro-8-oxoguanine (8-oxoG) and repairs oxidized nuclear and mitochondrial DNA. Previous studies showed that OGG1 deficiency results in an increased susceptibility to high-fat diet (HFD)-induced obesity [...] Read more.
8-oxoguanine DNA glycosylase-1 (OGG1) is a DNA glycosylase mediating the first step in base excision repair which removes 7,8-dihydro-8-oxoguanine (8-oxoG) and repairs oxidized nuclear and mitochondrial DNA. Previous studies showed that OGG1 deficiency results in an increased susceptibility to high-fat diet (HFD)-induced obesity and metabolic dysfunction in mice, suggesting a crucial role of OGG1 in metabolism. However, the tissue-specific mechanisms of how OGG1 deficiency leads to insulin resistance is unknown. Thus, in the current study, we used a hyperinsulinemic-euglycemic clamp to evaluate in-depth glucose metabolism in male wild-type (WT) mice and Ogg1−/− (Ogg1-KO) mice fed an HFD. Ogg1-KO mice fed HFD were more obese, with significantly lower hepatic insulin action compared to WT/HFD mice. Targeting human OGG1 to mitochondria protected against HFD-induced obesity, insulin resistance, oxidative mitochondrial DNA damage in the liver and showed decreased expression of liver gluconeogenic genes in Ogg1-KO mice, suggesting a putative protective mechanism. Additionally, several subunits of oxidative phosphorylation protein levels were noticeably increased in Ogg1-KO/Tg compared to Ogg1-KO mice fed an HFD which was associated with improved insulin signaling. Our findings demonstrate the crucial role of mitochondrial hOGG1 in HFD-induced insulin resistance and propose several protective mechanisms which can further direct the development of therapeutic treatment. Full article
(This article belongs to the Special Issue The Molecular and Cellular Aspects of Insulin Resistance)
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