The protective role of amla (Emblica officinalis Gaertn.) against fructose-induced metabolic syndrome in a rat model.
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.
Kim
Hyun Young
HY
Department of Food Science, Jinju National University, 150 Chilamdong, Jinju 660-758, Korea.
Okubo
Tsutomu
T
Juneja
Lekh Raj
LR
Yokozawa
Takako
T
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D002784:Cholesterol / Q000097:blood*; D051546:Cyclooxygenase 2 / Q000097:blood; D019422:Dietary Sucrose / Q000494:pharmacology; D004195:Disease Models, Animal; D005632:Fructose; D005638:Fruit; D006937:Hypercholesterolemia / Q000188:drug therapy; D006949:Hyperlipidemias / Q000188:drug therapy; D008099:Liver / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome / Q000139:chemically induced / Q000517:prevention & control*; D008928:Mitochondria / Q000378:metabolism; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D047493:PPAR alpha / Q000378:metabolism; D029842:Phyllanthus emblica; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D051779:Sterol Regulatory Element Binding Proteins / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014280:Triglycerides / Q000097:blood* / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
D001786:Blood Glucose; D019422:Dietary Sucrose; D016328:NF-kappa B; D047493:PPAR alpha; D010936:Plant Extracts; D051779:Sterol Regulatory Element Binding Proteins; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; D051028:bcl-2-Associated X Protein; D005632:Fructose; D002784:Cholesterol; D051546:Cyclooxygenase 2