Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent experimental and clinical studies have indicated that bile acid-binding agents are effective not only for treating hypercholesterolemia, but also for type 2 diabetes. To investigate the molecular mechanism underlying the effect of cholestyramine, a bile acid-binding agent, on type 2 diabetes, we examined gene expression of the livers of cholestyramine-treated type 2 diabetic model mice. Type 2 diabetic NSY/Hos mice were fed a high fat diet supplemented with 1% (w/w) cholestyramine for 8 weeks. Cholestyramine treatment prevented the increase in body weight, plasma cholesterol, triglycerides, glucose, insulin levels, and hepatic steatosis. DNA microarray analysis was performed on the liver, which revealed that the genes related to synthesis of cholesterol and its derivatives were increased and the genes regulated by liver X receptors, such as the sterol regulatory element-binding protein 1 gene, were decreased in the group treated with cholestyramine. Expression of the genes related to carbohydrate metabolism was little changed in the cholestyramine group. Furthermore, we performed real-time RT-PCR analysis, which highly correlated with DNA microarray data (r=0.957, P<0.001). This study provides a valuable basis for further research on the biological functions of bile acid-binding agents in models of type 2 diabetes.
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PMID:Gene expression analysis on the liver of cholestyramine-treated type 2 diabetic model mice. 2034 70

Kaki-tannin, a highly polymerized-tannin from the young fruits of persimmon (Diospyros kaki 'Hachiya'), has been shown to have bile acid-binding activity. To verify the effect of kaki-tannin on the metabolism of lipid and glucose in type 2 diabetes, type 2 diabetic NSY/Hos mice were fed an AIN76-modified high fat diet supplemented with 1% (w/w) kaki-tannin for 8weeks. Kaki-tannin induced a 2-fold increase in fecal bile acid excretion and was significantly effective in the prevention of a rise in plasma cholesterol, triglyceride, and insulin levels. Kaki-tannin treatment also prevented fatty liver. To identify the molecular mechanism underlying these effects, gene expression analysis was performed on liver, brown adipose tissue (BAT), and skeletal muscle. The genes related to cholesterol metabolism, including 3-hydroxy-3-methylglutaryl-coenzyme A reductase and sterol regulatory element-binding protein 2, were increased in the liver of the kaki-tannin group. Interestingly, the uncoupling protein-1 (UCP1) gene and the UCP3 gene were significantly increased in the BAT of the kaki-tannin group, which was also confirmed at the protein level. These findings indicated that induction of UCP1 and UCP3 in the BAT by kaki-tannin treatment might influence the energy metabolism, thus contributing beneficial effects to type 2 diabetic NSY/Hos mice.
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PMID:Induction of uncoupling protein-1 and -3 in brown adipose tissue by kaki-tannin in type 2 diabetic NSY/Hos mice. 2207 82