title: Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin.
abstract: OBJECTIVE
  To understand the adaptation to lactation of obese rats, by studying the interplay among the gut hormone cholecystokinin (CCK), the adiposity hormone leptin and the affiliation hormone oxytocin in modulating body mass and fat storage.
  
  
  METHODS
  Strain differences were examined between Otsuka Long Evans Tokushima Fatty (OLETF) rats lacking expression of functional CCK-1 receptors and Long Evans Tokushima Otsuka (LETO) controls, tested as nulliparous dams, at the 7 and 15th lactation day, at weaning (lactation day 22) or 8 weeks postweaning.
  
  
  METHODS
  We measured body mass, fat pads (brown, retroperitoneal and inguinal) and inguinal adipocytes. Plasma levels of leptin and oxytocin were determined.
  
  
  RESULTS
  Fat depots of LETO female rats were larger during lactation compared to the levels found in postweaning and nulliparous female rats. LETO female rats gained weight and accumulated fat during pregnancy and lactation, returning to their normal fat levels postweaning. In contrast, OLETF female rats presented lower body weight and fat depots during the lactation period than nulliparous dams, and regained the weight and fat postweaning. Plasma leptin and oxytocin were highly correlated and followed the same pattern. OLETF leptin levels were highly correlated with fat depot and inguinal cell surface. No significant correlation was found for LETO parameters.
  
  
  CONCLUSIONS
  Pregnancy and lactation are energy-consuming events, which naturally induce female rats to increase food intake and accumulate fat. When challenged by the demands of rapidly growing preobese OLETF pups, OLETF dams' fat stores are reduced to lean, LETO levels. During lactation, sensitivity of the oxytocinergic neurons descending from the paraventricular nuclei to the nucleus of the solitary tract to CCK is reduced. We theorized that this pathway is not available to OLETF female rats that lack functional CCK-1 receptors to mediate the signal. The current study contributes to the understanding of the female body's adaptation to lactation.
authors.affiliation: Department of Psychology, The Leslie and Susan Gonda Goldschmied Multidisciplinary Brain Research Center, Bar Ilan University, Ramat Gan, Israel. Ornaza@gmail.com
authors.forename: O
authors.initials: O
authors.lastname: Zagoory-Sharon
authors.forename: M
authors.initials: M
authors.lastname: Schroeder
authors.forename: A
authors.initials: A
authors.lastname: Levine
authors.forename: T H
authors.initials: TH
authors.lastname: Moran
authors.forename: A
authors.initials: A
authors.lastname: Weller
mesh_terms: D000222:Adaptation, Physiological; D017667:Adipocytes / Q000473:pathology; D000273:Adipose Tissue / Q000473:pathology; D000818:Animals; D001835:Body Weight; D004195:Disease Models, Animal; D005260:Female; D006984:Hypertrophy / Q000473:pathology / Q000503:physiopathology; D007774:Lactation; D020738:Leptin / Q000097:blood; D009154:Mutation; D009765:Obesity / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D010121:Oxytocin / Q000097:blood; D051381:Rats; D020334:Rats, Inbred OLETF; D011949:Receptors, Cholecystokinin / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D014886:Weaning; D015430:Weight Gain
chemical_list: D020738:Leptin; D011949:Receptors, Cholecystokinin; D010121:Oxytocin