F-DIO obesity-prone rat is insulin resistant before obesity onset

Am J Physiol Regul Integr Comp Physiol. 2005 Sep;289(3):R704-11. doi: 10.1152/ajpregu.00216.2005. Epub 2005 May 5.

Abstract

We previously created a novel F-DIO rat strain derived by crossing rats selectively bred for the diet-induced obesity (DIO) phenotype with obesity-resistant Fischer F344 rats. The offspring retained the DIO phenotype through 3 backcrosses with F344 rats but also had exaggerated insulin responses to oral glucose before they became obese on a 31% fat high-energy (HE) diet. Here, we demonstrate that chow-fed rats from the subsequent randomly bred progeny required 57% lower glucose infusions to maintain euglycemia during a hyperinsulinemic clamp in association with 45% less insulin-induced hepatic glucose output inhibition and 80% lower insulin-induced glucose uptake than F344 rats. The DIO phenotype and exaggerated insulin response to oral glucose in the nonobese, chow-fed state persisted in the F6 generation. Also, compared with F344 rats, chow-fed F-DIO rats had 68% higher arcuate nucleus proopiomelanocortin mRNA expression which, unlike the increase in F344 rats, was decreased by 26% on HE diet. Further, F-DIO lateral hypothalamic orexin expression was 18% lower than in F344 rats and was increased rather than decreased by HE diet intake. Finally, both maternal obesity and 30% caloric restriction during the third week of gestation produced F-DIO offspring which were heavier and had higher leptin and insulin levels than lean F-DIO dam offspring. Third-gestational week dexamethasone also produced offspring with higher leptin and insulin levels but with lower body weight. Thus F-DIO rats represent a novel and potentially useful model for the study of DIO, insulin resistance, and perinatal factors that influence the development and persistence of obesity.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Arcuate Nucleus of Hypothalamus / metabolism
  • Blood Glucose / metabolism
  • Diet / adverse effects*
  • Disease Models, Animal
  • Genetic Predisposition to Disease*
  • Glucose / antagonists & inhibitors
  • Glucose / pharmacology
  • Hypoglycemic Agents / blood
  • Hypoglycemic Agents / pharmacology
  • Hypothalamic Area, Lateral / metabolism
  • Insulin / blood
  • Insulin / pharmacology
  • Insulin Resistance / genetics*
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Liver / metabolism
  • Neuropeptides / metabolism
  • Obesity / etiology*
  • Obesity / genetics
  • Obesity / physiopathology*
  • Orexins
  • Phenotype
  • Pro-Opiomelanocortin / metabolism
  • Rats
  • Rats, Inbred F344
  • Rats, Inbred Strains

Substances

  • Blood Glucose
  • Hypoglycemic Agents
  • Insulin
  • Intracellular Signaling Peptides and Proteins
  • Neuropeptides
  • Orexins
  • Pro-Opiomelanocortin
  • Glucose