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Quamoclit angulata extract supplementation attenuates hepatic damage via regulation of AMPK/SIRT associated hepatic lipid metabolism in streptozotocin and high fat diet-induced T2DM mice

Authors
Lee, HeajiKim, YounmiKim, Sun YeouLim, Yunsook
Issue Date
Aug-2022
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Keywords
Quamoclit angulata; Type 2 diabetes mellitus; Fatty liver; Lipid metabolism; Energy metabolism
Citation
NUTRITION RESEARCH, v.104, pp.10 - 19
Journal Title
NUTRITION RESEARCH
Volume
104
Start Page
10
End Page
19
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/84991
DOI
10.1016/j.nutres.2022.03.012
ISSN
0271-5317
Abstract
Quamoclit angulata (QA) is a species of the Convolvulaceae family and has a regulatory effect on glucose homeostasis. However, the effects of QA on hyperglycemia-induced hepatic damage has not been elucidated. We hypothesized that QA extract (QAE) would alleviate hepatic damage through regulation of hepatic lipid accumulation in type 2 diabetes mellitus (T2DM). T2DM was induced by streptozotocin-high-fat diet in C57BL6 male mice for 8 weeks. The diabetic mice were supplemented with QAE at low dose (5 mg/kg) or high dose (HQ, 10 mg/kg) by oral gavage every day for 12 weeks. Histopathological changes in hepatic tissue were examined using hematoxylin and eosin staining, and the protein levels of biomarkers related to AMP-activation kinase (AMPK)/sirtuin-1 (SIRT1)-associated lipid metabolism were measured using Western blotting. QAE supplementation ameliorated plasma insulin and glycated hemoglobin in diabetic mice. Furthermore, QAE decreased hepatic lipid accumulation demonstrated by hepatic triglyceride and cholesterol levels. QAE supplementation induced hepatic AMPK, which activates SIRT1 accompanied by reduced lipogenesis in the HQ group. These changes were partially explained by the amelioration of advanced glycation end product, hepatic oxidative stress, inflammation, and fibrosis in diabetic mice.
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