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Melatonin attenuates (-)-epigallocatehin-3-gallate-triggered hepatotoxicity without compromising its downregulation of hepatic gluconeogenic and lipogenic genes in mice.
- Source :
-
Journal of Pineal Research . Nov2015, Vol. 59 Issue 4, p497-507. 11p. - Publication Year :
- 2015
-
Abstract
- (-)-Epigallocatehin-3-gallate ( EGCG), a major constituent of green tea, can ameliorate metabolic syndrome at least in part through reducing gluconeogenesis and lipogenesis. Green tea extracts, of which EGCG is a key constituent, have been used for weight loss in humans. A potential adverse effect of high-dose EGCG or green tea extracts is hepatotoxicity. Melatonin, an endogenous antioxidant with a high safety profile, is effective in preventing various types of tissue damage. The current study investigated the influence of melatonin on EGCG-triggered hepatotoxicity and EGCG-downregulated hepatic genes responsible for gluconeogenesis and lipogenesis in mice. We found that (i) melatonin extended survival time of mice intoxicated with lethal doses of EGCG; (ii) melatonin ameliorated acute liver damage and associated hepatic Nrf2 suppression caused by a nonlethal toxic dose of EGCG; (iii) melatonin reduced subacute liver injury and hepatic Nrf2 activation caused by lower toxic doses of EGCG; and (iv) melatonin did not compromise the action of pharmacological doses of EGCG in downregulating a battery of hepatic genes responsible for gluconeogenesis and lipogenesis, including G6Pc, PEPCK, FOXO1 α, SCD1, Fasn, leptin, ACC α, ACC β, GAPT, and Srebp-1. Taken together, these results suggest that the combination of EGCG and melatonin is an effective approach for preventing potential adverse effects of EGCG as a dietary supplement for metabolic syndrome alleviation and body weight reduction. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 07423098
- Volume :
- 59
- Issue :
- 4
- Database :
- Academic Search Index
- Journal :
- Journal of Pineal Research
- Publication Type :
- Academic Journal
- Accession number :
- 110567999
- Full Text :
- https://doi.org/10.1111/jpi.12281