title: Chronic administration of palmitoleic acid reduces insulin resistance and hepatic lipid accumulation in KK-Ay Mice with genetic type 2 diabetes.
abstract: BACKGROUND
  Studies have demonstrated the beneficial effect of palmitoleic acid (C16:1 n-7) on reducing muscle insulin resistance and preventing beta-cell apoptosis. However, the effect of palmitoleic acid on diabetes remains to be elucidated. The aim of this study was to examine the antidiabetic effect of palmitoleic acid in KK-Ay mice, a spontaneous model for studies of obese type 2 diabetes with low insulin sensitivity.
  
  
  METHODS
  KK-Ay mice were orally administered vehicle, 300 mg/kg of palmitoleic acid, or 300 mg/kg of palmitic acid (C16:0) on a daily basis for 4 weeks.
  
  
  RESULTS
  Palmitoleic acid reduced body weight increase, ameliorated the development of hyperglycemia and hypertriglyceridemia, and improved insulin sensitivity. In addition, hepatic characteristics were significantly affected, as weight of the liver and hepatic triglyceride levels were lower in the palmitoleic acid group when compared to the control (vehicle and palmitic acid groups). Oil red O staining clearly indicated reduced hepatic lipid accumulation in response to palmitoleic acid. Furthermore, palmitoleic acid down-regulated mRNA expressions of proinflammatory adipocytokine genes (TNFα and resistin) in white adipose tissue and lipogenic genes (SREBP-1, FAS, and SCD-1) in liver.
  
  
  CONCLUSIONS
  These results suggest that palmitoleic acid improves hyperglycemia and hypertriglyceridemia by increasing insulin sensitivity, in part owing to suppressing proinflammatory gene expressions and improving hepatic lipid metabolism in diabetic mice.
authors.affiliation: Central Research Laboratory, Tokyo Innovation Center, Nippon Suisan Kaisha, Ltd,, 32-3 Nanakuni 1 Chome Hachioji, Tokyo 192-0991, Japan. yangzh@nissui.co.jp
authors.forename: Zhi-Hong
authors.initials: ZH
authors.lastname: Yang
authors.forename: Hiroko
authors.initials: H
authors.lastname: Miyahara
authors.forename: Akimasa
authors.initials: A
authors.lastname: Hatanaka
mesh_terms: D054392:Adipokines / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000188:drug therapy / Q000235:genetics*; D004353:Drug Evaluation, Preclinical; D064429:Fatty Acid Synthases / Q000235:genetics / Q000378:metabolism; D005229:Fatty Acids, Monounsaturated / Q000008:administration & dosage* / Q000627:therapeutic use; D005234:Fatty Liver / Q000188:drug therapy; D015870:Gene Expression; D007333:Insulin Resistance; D050356:Lipid Metabolism / Q000187:drug effects*; D008055:Lipids / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D008297:Male; D051379:Mice; D009929:Organ Size; D013230:Stearoyl-CoA Desaturase / Q000235:genetics / Q000378:metabolism; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics / Q000378:metabolism
chemical_list: D054392:Adipokines; D001786:Blood Glucose; D005229:Fatty Acids, Monounsaturated; D008055:Lipids; C497388:Srebf1 protein, mouse; D051780:Sterol Regulatory Element Binding Protein 1; C008757:palmitoleic acid; C490333:Scd1 protein, mouse; D013230:Stearoyl-CoA Desaturase; D064429:Fatty Acid Synthases