The role of Akt and Lpl in formation of nonalcoholic steatohepatitis in rat with a fat-rich diet
- VernacularTitle:Akt与Lpl在高脂饮食大鼠非酒精性脂肪肝形成中的作用
- Author:
Jiwu HAN
;
Xiaorog ZHAN
;
Huiqing YIN
;
Shumei LIU
- Publication Type:Journal Article
- Keywords:
serine/threonine kinase (Akt), lipoprotein lipase (Lpl), nonalcoholic steatohepatitis (NASH), insulin resistance index (IRI), hyperlipidemia
- From:
Chinese Journal of Rehabilitation Theory and Practice
2005;11(12):1002-1004
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the role of serine/threonine kinase (Akt) and lipoprotein lipase (Lpl) in formation of nonalcoholic steatohepatitis (NASH) in rat with a fat-rich diet.Methods40 male Wistar rats were randomly divided into the 8-week-rich-fat group (n=10), 8-week-common-diet control group (n=10), 12-week-rich-fat group (n=10) and 12-week-common-diet control group (n=10). The lipid, cholesterol, glucose and insulin were examined, insulin resistance index (IRI) and insulin sensitivity index (ISI) were calculated, the expression of Akt and Lpl were detected with immunohistochemical method and morphological changes of liver were observed by transmission electron microscope (TEM).ResultsNASH was formed in each rat of 8-week-rich-fat group with characteristics of individual obese, increased liver volume, full and clear contour, gray-yellowish luster, greasy section and crisp quality. And it was accompanied by high lipoidemia (HL), liver fat cell denaturation, inflammatory cell infiltration in liver lobuler and cell death in liver. The expression of Akt was obviously reduced and the expression of Lpl was obviously weakened in liver. Lipid, cholesterol, glucose and insulin and IRI were gradually advancing. ISI was reducing and the insulin resistance formed. The data of fat-rich diet groups was significantly different with that of common-diet control groups (P<0.0001).Conclusion Steatohepatitis and insulin resistance can form in rat by feeding with rich-fat diet for 8 weeks. It causes the insulin and Lpl activeness reducing, and steatolysis barrier.
