Study On The Mechanism Of Chinese Herbal Extracts Improving The Metabolism Of Glucose Metabolism In Rats Induced By High Fructose

Objective To observe the effect of ginger ethanol extract on mitigating fructose-induced fatty liver and to explore the possible mechanism.Methods Male SD rats consumed liquid fructose in their drinking water over 5 weeks. The ethanolic extract of ginger was co-administered(once daily by oral gavage). The indexes of lipid and glucose homeostasis were determined enzymatically, by ELISA and/or histologically.Gene/protein expression was analyzed by Real-time PCR and/or Western blot.Results Ginger treatment attenuated fructose overconsumption induced excessive hepatic triglyceride accumulation and increases in vacuolization and Oil Red O staining area in the liver of rats. However,ginger treatment did not affect chow intake and body weight. The anti-steatotic effect of ginger treatment was accompanied by suppression of hepatic over expression of acyl-coenzyme A:diacylglycerol acyltransferase(DGAT)-2 at the m RNA and protein levels. But hepatic expression of liverX receptor, DGAT-1, monoacyglycerol acyltransferase(MGAT)-1,MGAT-2, hormone-sensitive lipase and adipose triglyceride lipase remained unchanged after ginger treatment.Conclusions Our results suggest that ginger may diminish fructose-induced fatty liver in rats alternatively by inhibiting hepatic overexpression of DGAT-2 that mediates triglyceride biosynthesis.Objective Rhodiola species have been used for asthenia, depression,fatigue, poor work performance and cardiovascular diseases, all of which may be associated with insulin resistance. To disclose the underlying mechanisms of action, the effect of Rhodiola crenulata root(RCR) on insulin resistance was investigated.Methods Male rats were treated with liquid fructose in their drinking water over 18 weeks. The extract of RCR was co-administered(once daily by oral gavage) during the last 5 weeks. The indexes of lipid and glucose homeostasis were determined enzymatically and/or by ELISA. Gene expression was analyzed by Real-time PCR, Western blot and/or confocal immunofluorescence.Result RCR extract(50 mg · kg-1) suppressed fructose-induced hyperinsulinemia and the increases in the homeostasis model assessment of insulin resistance index and the adipose tissue insulin resistance index inrats. Additionally, this treatment intended to restore the ratios of glucose to insulin and non-esterified fatty acids(NEFA) to insulin. Mechanistically,RCR suppressed fructose-induced acceleration of the clearance of plasma NEFA during oral glucose tolerance test(OGTT), and decreased triglyceride content and Oil Red O staining area in the gastrocnemius. Furthermore,RCR restored fructose-induced sarcolemmal overexpression and intracellular less distribution of fatty acid translocase/CD36 that contributes to etiology of insulin resistance by facilitating fatty acid uptake.Conclusion These results suggest that RCR improves insulin resistance in fructose-fed rats by modulating sarcolemmal and intracellular CD36 redistribution in the skeletal muscle. Our findings may provide a better understanding of the traditional use of Rhodila species.