JOURNAL ARTICLE

The protective role of amla (Emblica officinalis Gaertn.) against fructose-induced metabolic syndrome in a rat model

Hyun Young Kim, Tsutomu Okubo, Lekh Raj Juneja, Takako Yokozawa
British Journal of Nutrition 2010, 103 (4): 502-12
19878614
We investigated the effects of amla (Emblica officinalis Gaertn.) on fructose-induced metabolic syndrome using a rat model. Male Wistar rats were fed a high-fructose (65 %) diet or standard chow for 1 week, and treated with an ethyl acetate (EtOAc) extract of amla, a polyphenol-rich fraction, at 10 or 20 mg/kg body weight per d, or vehicle, for 2 weeks. Serum glucose, TAG, total cholesterol and blood pressure levels of the high-fructose diet-fed rats were increased compared with those of the normal rats (P < 0.001). However, the EtOAc extract of amla ameliorated the high fructose-induced metabolic syndrome, including hypertriacylglycerolaemia and hypercholesterolaemia. Also, the elevated levels of hepatic TAG and total cholesterol in rats given the high-fructose diet were significantly reduced by 33.8 and 24.6 %, respectively (P < 0.001), on the administration of the EtOAc extract of amla at the dose of 20 mg/kg with the regulation of sterol regulatory element-binding protein (SREBP)-1 expression. The protein levels of PPARalpha and SREBP-2 were not affected by the feeding of the high-fructose diet or EtOAc extract of amla. In addition, oral administration of the amla extract at the dose of 20 mg/kg significantly inhibited the increased serum and hepatic mitochondrial thiobarbituric acid-reactive substance levels (21.1 and 43.1 %, respectively; P < 0.001). Furthermore, the amla extract inhibited the increase of cyclo-oxygenase-2 with the regulation of NF-kappaB and bcl-2 proteins in the liver, while the elevated expression level of bax was significantly decreased by 8.5 and 10.2 % at the doses of 10 and 20 mg/kg body weight per d, respectively. These findings suggest that fructose-induced metabolic syndrome is attenuated by the polyphenol-rich fraction of amla.

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