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

To explore the effect of leech on lipid metabolism and liver function in hyperlipidemia rats and the possible mechanism, biochemical analyzer was used to examine the regulation of leech on levels of serum triglycerides(TG), total cholesterol(TC), low-density lipoprotein cholesterol(LDL-C), and high-density lipoprotein cholesterol(HDL-C). The levels of ALT and AST in serum were detected by ELISA. The proteins expression of ACAT-2, Fas and HMGCR in liver tissue was detected by Western blot. The weight of body and liver were weighed, and liver index was calculated. Oil red O staining was used to observe the lipid accumulation in liver tissue of rats by light Microscope. The results showed that leech could decrease the levels of TC, LDL-C obviously, and increase HDL-C, decrease the levels of ALT, AST and the liver index, down-regulate the proteins expression of ACAT-2, Fas and HMGCR. And oil red O staining indicated that the lipid accumulation was less in the liver tissue of the rats intervented by leech. These data indicated that leech may affect the expression of ACAT-2, Fas and HMGCR in liver tissue to reduce the synthesis of cholesterol and fatty acid, and promote the cholesterol transforming, then regulate lipid metabolism to decrease the levels of serum lipid, and reduce lipid accumulation in liver tissue and ease liver injury of rats, then slowing down the process of nonalcoholic fatty liver disease(NAFLD) in hyperlipidemia rats.
 ...
PMID:[Effect of leech on lipid metabolism and liver in hyperlipidemia rats]. 2960 Jun 57

Depletion of the cholesterol esterifying enzyme acyl-Coenzyme A: cholesterol acyltransferase 2 (ACAT2, encoded by Soat2) protects mice from atherosclerosis, diet-induced hypercholesterolemia, and hepatic steatosis when fed high-cholesterol diet. The glucose transporter 2 (GLUT2) represents the main gate of glucose uptake by the liver. Lipid synthesis from glucose (de novo lipogenesis; DNL) plays a pivotal role in the development of hepatic steatosis. Inhibition of DNL is a successful approach to reverse hepatic steatosis, as shown by different studies in mice and humans. Here we aimed to investigate whether depletion of Soat2 per se can reduce hepatic steatosis, also in the presence of very low levels of cholesterol in the diet, and the underlying mechanisms. Female Soat2-/- and wild type mice were either fed high-fat or high-carbohydrate diet and both contained <0.05% (w/w) cholesterol. Analysis in serum, liver, muscles and adipose tissues were performed. We found Soat2-/- mice fed high-fat, low-cholesterol diet to have less hepatic steatosis, decreased expression of genes involved in DNL and lower hepatic GLUT2. Similar findings were found in Soat2-/- mice fed high-carbohydrate, low-cholesterol diet. CONCLUSION: Depletion of Soat2 reduces hepatic steatosis independently of the presence of high levels of cholesterol in the diet. Our study provides a link between hepatic cholesterol esterification, DNL, and GLUT2.
 ...
PMID:Genetic depletion of Soat2 diminishes hepatic steatosis via genes regulating de novo lipogenesis and by GLUT2 protein in female mice. 3063 Jul 36