ArticleJournal of diabetes investigation2019
p62-mediated autophagy affects nutrition-dependent insulin receptor substrate 1 dynamics in 3T3-L1 preadipocytes.
Article in Journal of diabetes investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Autophagic Regulation of Adipogenesis Through TP53INP2: Insights from In Silico and In Vitro Analysis.Molecular biotechnology · 2024Article
- Evaluation of histopathological changes and exosomal biogenesis in pulmonary tissue of diabetic rats.Veterinary research forum : an international quarterly journal · 2022Article
- The P-type ATPase transporter ATP7A promotes angiogenesis by limiting autophagic degradation of VEGFR2.Nature communications · 2021Article
- p62-mediated autophagy affects nutrition-dependent insulin receptor substrate 1 dynamics in 3T3-L1 preadipocytes.Journal of diabetes investigation · 2019Article
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6 authors at 1 institution in 1 country.
Funding
Abstract
AIMS/
introductionPrevious studies have shown that an organism's nutritional status changes the protein levels of insulin receptor substrate 1 (IRS-1) in a tissue-specific manner. Although the mechanisms underlying the regulation of IRS-1 in the nutrient-rich conditions associated with diabetes and insulin resistance have been well studied, those under nutrient-poor conditions remain unknown. The aim of the present study was to investigate how IRS-1 protein levels change depending on the nutritional status of 3T3-L1 preadipocytes. MATERIALS AND
methods3T3-L1 preadipocytes were treated with glucose-, amino acid- and serum-free medium for starvation. IRS-1 protein levels were detected by western blot. Autophagy activity was observed by western blot and fluorescence microscopy. The effect of autophagy and p62, an adaptor for selective autophagy, on IRS-1 protein levels under starvation conditions was examined by western blot and immunocytochemistry.
resultsWe showed that the levels of IRS-1, but not those of insulin receptor and protein kinase B, decreased when starvation activated autophagy. The inhibition of autophagy by chloroquine or autophagy-related 7 (Atg7) ribonucleic acid interference counteracted the starvation-induced decrease of IRS-1. Additionally, Atg7 knockdown increased insulin-stimulated phosphorylation of protein kinase B under starvation conditions. Furthermore, p62 colocalized with IRS-1 under starvation conditions, and p62 knockdown counteracted the starvation-induced degradation of IRS-1.
conclusionsAutophagy through p62 plays an important role in regulating IRS-1 protein levels in response to nutritional deficiency. The present findings suggest that autophagy might function as energy depletion-sensing machinery that finely tunes insulin signal transduction.
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