title: Arginase inhibition ameliorates hepatic metabolic abnormalities in obese mice.
abstract: OBJECTIVE
  We examined whether arginase inhibition influences hepatic metabolic pathways and whole body adiposity in diet-induced obesity.
  
  
  RESULTS
  After obesity induction by a high fat diet (HFD), mice were fed either the HFD or the HFD with an arginase inhibitor, Nω-hydroxy-nor-L-arginine (nor-NOHA). Nor-NOHA significantly prevented HFD-induced increases in body, liver, and visceral fat tissue weight, and ameliorated abnormal lipid profiles. Furthermore, nor-NOHA treatment reduced lipid accumulation in oleic acid-induced hepatic steatosis in vitro. Arginase inhibition increased hepatic nitric oxide (NO) in HFD-fed mice and HepG2 cells, and reversed the elevated mRNA expression of hepatic genes in lipid metabolism. Expression of phosphorylated 5' AMPK-activated protein kinase α was increased by arginase inhibition in the mouse livers and HepG2 cells.
  
  
  CONCLUSIONS
  Arginase inhibition ameliorated obesity-induced hepatic lipid abnormalities and whole body adiposity, possibly as a result of increased hepatic NO production and subsequent activation of metabolic pathways involved in hepatic triglyceride metabolism and mitochondrial function.
authors: Department of Food and Nutrition, Korea University, Seoul, Republic of Korea; Department of Public Health Sciences, Graduate School, Korea University, Seoul, Republic of Korea.
authors: Jiyoung
authors: J
authors: Moon
authors: Department of Food and Nutrition, Korea University, Seoul, Republic of Korea.
authors: Hyun Ju
authors: HJ
authors: Do
authors: Department of Food and Nutrition, Korea University, Seoul, Republic of Korea; Department of Public Health Sciences, Graduate School, Korea University, Seoul, Republic of Korea.
authors: Yoonsu
authors: Y
authors: Cho
authors: Department of Food and Nutrition, Korea University, Seoul, Republic of Korea; Department of Public Health Sciences, Graduate School, Korea University, Seoul, Republic of Korea; Korea University Guro Hospital, Korea University, Seoul, Republic of Korea.
authors: Min-Jeong
authors: MJ
authors: Shin
mesh_terms: D000818:Animals; D001119:Arginase / Q000037:antagonists & inhibitors*; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D019610:Cytoprotection / Q000187:drug effects; D059305:Diet, High-Fat; D056945:Hep G2 Cells; D022781:Hepatocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008107:Liver Diseases / Q000209:etiology* / Q000378:metabolism / Q000517:prevention & control*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D009765:Obesity / Q000150:complications* / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology
chemical_list: C404735:N(omega)-hydroxynorarginine; D001120:Arginine; C544448:Arg1 protein, mouse; D001119:Arginase