Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 476, Issue 11, Pages 3879-3887Publisher
SPRINGER
DOI: 10.1007/s11010-021-04193-3
Keywords
Quercetin; Type 2 diabetes; mTOR; Bioactive compound; TBHP
Categories
Funding
- Kerala Biotechnology Commission
- Kerala State Council for Science, Technology and Environment, Government of Kerala
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Quercetin has a protective effect on pancreatic beta cells against oxidative stress-induced damage and promotes insulin secretion. It also enhances mitochondrial biogenesis, induces hypertrophy in pancreatic beta cells, and activates mTOR signaling.
Citrus flavonoids particularly quercetin which is abundant in grapefruit, onion, green tea, berries etc. are known to have a protective effect on oxidative stress. Pancreatic beta cells which synthesize and secrete insulin are prone to oxidative stress induced damage because of low cellular antioxidant enzymes. To delineate the effects of quercetin on pancreatic beta cells we evaluated the protective effect of quercetin on TC6 insulinoma cells subjected to oxidative stress induced by tert-butyl-hydrogen-peroxide (TBHP). Quercetin was found to reduce TBHP induced apoptosis and trigger insulin secretion in response to glucose, in a dose-dependent manner. Quercetin treatment increased mitochondrial biogenesis, caused hypertrophy in pancreatic beta cells and activated mTOR signaling with a transient change in mitochondrial membrane potential and AMP/ATP. Activation of mTOR signaling resulted in enhanced insulin secretion in TC6 cells.
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