Abstract
We sought to evaluate the effects of Momordica charantia (bitter melon, BM) extract on insulin sensitivity, NAFLD, hepatic FGF21 and AMPK signaling in mice fed a high-fat diet. Male C57/B6 mice were randomly divided into HFD and HFD supplementation with BM for 12 week. Body weight, plasma glucose, FGF21 and insulin levels, hepatic FGF21 and AMPK signaling proteins were measured. The results showed that plasma FGF21 and insulin concentrations were significantly decreased and hepatic FGF21 content was significantly down-regulated, while FGF receptors 1, 3 and 4 (FGFR1, FGFR3 and FGFR4) were greatly up-regulated in BM group compared to the HFD group (P < 0.05 and P < 0.01). BM also significantly increased hepatic AMPK p, AMPK α1 AMPK α2 and Sirt1 content compared to the HFD mice. We, for the first time, demonstrated that BM extract attenuated hepatic steatosis in mice by enhancing hepatic FGF21 and AMPK/Sirt1 signaling.
Highlights
Bitter melon extract attenuating hepatic steatosis may be mediated by Fibroblast growth factor 21 (FGF21) and AMPK/Sirt[1] signaling in mice
The results showed that plasma FGF21 and insulin concentrations were significantly decreased and hepatic FGF21 content was significantly down-regulated, while fibroblast growth factor (FGF) receptors 1, 3 and 4 (FGFR1, FGFR3 and FGFR4) were greatly up-regulated in Bitter melon (BM) group compared to the High-fat diet (HFD) group (P, 0.05 and P, 0.01)
We evaluated the effects of a BM extract on glucose and lipid metabolism, liver fat content, insulin sensitivity, and FGF21 signaling in mice fed a HFD
Summary
Bitter melon extract attenuating hepatic steatosis may be mediated by FGF21 and AMPK/Sirt[1] signaling in mice. We sought to evaluate the effects of Momordica charantia (bitter melon, BM) extract on insulin sensitivity, NAFLD, hepatic FGF21 and AMPK signaling in mice fed a high-fat diet. BM extracts have been reported to increase glucose uptake, promote insulin release, and potentiate the effect of insulin, as well as improve obesity-associated peripheral inflammation and neuroinflammation, lower www.nature.com/scientificreports plasma apoB-100 and apoB-48 in HFD-fed mice, and modulate the phosphorylation of IR, IRS-1, and its downstream signaling molecules[20,21,22]. Based on the above rationale, and given the role of FGF21 in lipid metabolism, we postulated that FGF21 may mediate the hypoglycemic action of BM To test this hypothesis, we evaluated the effects of a BM extract on glucose and lipid metabolism, liver fat content, insulin sensitivity, and FGF21 signaling in mice fed a HFD
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