Gallic acid improves glucose tolerance and triglyceride concentration in diet-induced obesity mice
Abstract Gallic acid, a phenolic phytochemical, has been shown to exert a variety of effects, including anti-oxidative, anti- carcinogenic, anti-allergic, and anti-inflammatory effects. In this study, we attempted to determine whether gallic acid affects metabolic syndrome such as obesity and diabet...
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Published in | Scandinavian journal of clinical and laboratory investigation Vol. 73; no. 8; pp. 607 - 614 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Informa Healthcare
01.12.2013
Taylor & Francis |
Subjects | |
Online Access | Get full text |
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Summary: | Abstract
Gallic acid, a phenolic phytochemical, has been shown to exert a variety of effects, including anti-oxidative, anti- carcinogenic, anti-allergic, and anti-inflammatory effects. In this study, we attempted to determine whether gallic acid affects metabolic syndrome such as obesity and diabetes. Diet-induced obesity mice were treated intraperitoneally once per day with gallic acid (10 mg/kg/day). After 2 weeks of treatment, the mice were sacrificed to collect the blood for metabolic parameter assessments, and the adipose tissues and liver to weigh and analyze. The triglyceride concentrations were significantly improved in the gallic acid group relative to those measured in the control group. And most importantly, the blood glucose concentrations in the gallic acid group were significantly improved. In the epididymal white adipose tissue of the gallic acid group, adipocyte size was reduced, PPARγ expression was induced, and the Akt signaling pathway was activated. Our results demonstrate that gallic acid improves glucose tolerance and lipid metabolism in the obesity mice, thereby showing evidence of anti-hyperglycemic activity. The findings of an upregulation of PPARγ expression and Akt activation also contribute to our current understanding of the mechanisms underlying the effects of gallic acid on glucose metabolism. |
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ISSN: | 0036-5513 1502-7686 |
DOI: | 10.3109/00365513.2013.831470 |