title: Role of liver fatty acid binding protein in hepatocellular injury: effect of CrPic treatment.
abstract: This study was designed to investigate the molecular mechanisms of chromium picolinate (CrPic, Fig. 1) hepatoprotective activity from alloxan-induced hepatic injury. Diabetes is induced by alloxan-treatment concurrently with the hepatic injury in mice. In this study, we investigate the protective effect of CrPic treatment in hepatic injury and the signal role of liver fatty acid binding protein in early hepatocellular injury diagnostics. In this study, alanine aminotransferase (ALT; EC 2.6.1.2) and aspartate aminotransferase (AST; EC 2.6.1.1) levels in the alloxan group were higher 71% and 50%, respectively, than those of the control group (ALT: 14.51±0.74; AST: 22.60±0.69). The AST and ALT levels in CrPic group were of minimal difference compared to the control groups. Here, CrPic exhibited amelioration alloxan induced oxidative stress in mouse livers. A significant increase in liver fatty acid-binding protein (L-FABP) was observed, which indicates increased fatty acid utilization in liver tissue [1]. In this study, the mRNA levels of L-FABP increased in both the control (1.1 fold) and CrPic (0.78 fold) groups compared the alloxan group. These findings suggest that hepatic injury may be prevented by CrPic, and is a potential target for use in the treatment of early hepatic injury.
authors.affiliation: Shandong Key Laboratory of Storage and Transportation Technology of Agricultural Products, National Engineering Research Center for Agricultural Products Logistics, Shandong Institute of Commerce and Technology, Jinan 250103, China.
authors.forename: Weijiang
authors.initials: W
authors.lastname: Fan
authors.forename: Kun
authors.initials: K
authors.lastname: Chen
authors.forename: Guoqiang
authors.initials: G
authors.lastname: Zheng
authors.forename: Wenhang
authors.initials: W
authors.lastname: Wang
authors.forename: Anguo
authors.initials: A
authors.lastname: Teng
authors.forename: Anjun
authors.initials: A
authors.lastname: Liu
authors.forename: Dongfeng
authors.initials: D
authors.lastname: Ming
authors.forename: Peng
authors.initials: P
authors.lastname: Yan
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000496:Alloxan / Q000633:toxicity; D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000188:drug therapy / Q000378:metabolism*; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D050556:Fatty Acid-Binding Proteins / Q000378:metabolism*; D005227:Fatty Acids / Q000378:metabolism*; D007502:Iron Chelating Agents / Q000494:pharmacology*; D008099:Liver / Q000378:metabolism*; D051379:Mice; D008813:Mice, Inbred ICR; D018384:Oxidative Stress / Q000187:drug effects; D010848:Picolinic Acids / Q000494:pharmacology*; D012333:RNA, Messenger / Q000096:biosynthesis
chemical_list: C493320:Fabp1 protein, mouse; D050556:Fatty Acid-Binding Proteins; D005227:Fatty Acids; D007502:Iron Chelating Agents; D010848:Picolinic Acids; D012333:RNA, Messenger; D000496:Alloxan; D000410:Alanine Transaminase; C030614:picolinic acid