title: Traits of the metabolic syndrome alter corpulent obesity in LAN, SHR and DSS rats: behavioral and metabolic interactions with adrenalectomy.
abstract: Obesity results from a complex interaction of genes with environmental factors. Our experimental design compared obesity in three rat strains with the corpulent (cp) mutation. The three strains included Lister and Albany NIH (LAN) rats, Spontaneously Hypertensive Rats (SHR) and Dahl Salt Sensitive (DSS) rats that were congenically bred. The strains were selected because of different reported metabolic complications generally clustered with obesity, and defined as the metabolic syndrome. Body weight, food intake, carcass composition, plasma hormones and hypothalamic expression of Y5 receptors were assessed in obese (cp) and lean (wt) rats after adrenalectomy (ADX) or sham surgeries. Plasma corticosterone in sham-operated wtDSS and cpDSS were significantly higher (approx. 165ng/ml) than that in cpLAN and cpSHR (~77 and 68ng/ml respectively). All cp groups had a higher % carcass fat than wt groups. The % carcass fat was greater in cpDSS>cpLAN>cpSHR but plasma leptin was greatest in cpLAN>cpSHR>cpDSS. Hypothalamic expression of the Y5R after ADX resulted in a phenotype×surgery interaction since Y5R expression was slightly increased in cp rats and slightly decreased in wt rats. The strain with greatest number of metabolic syndrome traits, SHR, was not the fattest of the strains and had little response to ADX. The strains with fewer metabolic syndrome traits LAN and DSS had more extreme obesities which were attenuated after ADX. The results of the current experiment provide evidence that the corpulent mutation is not fully characterized in one strain.
authors.affiliation: Department of Nutrition, University of North Carolina of Greensboro, Greensboro, NC 27402, United States. lmbrown6@uncg.edu
authors.forename: Lynda M
authors.initials: LM
authors.lastname: Brown
authors.forename: Carl T
authors.initials: CT
authors.lastname: Hansen
authors.forename: Andrea F
authors.initials: AF
authors.lastname: Huberty
authors.forename: T W
authors.initials: TW
authors.lastname: Castonguay
mesh_terms: D000273:Adipose Tissue / Q000473:pathology; D000315:Adrenalectomy; D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal / Q000502:physiology*; D001823:Body Composition / Q000235:genetics; D001835:Body Weight / Q000235:genetics; D003345:Corticosterone / Q000097:blood; D004195:Disease Models, Animal; D004435:Eating / Q000235:genetics; D007031:Hypothalamus / Q000378:metabolism; D020738:Leptin / Q000097:blood; D008297:Male; D008659:Metabolic Diseases / Q000235:genetics*; D009765:Obesity / Q000097:blood / Q000235:genetics / Q000503:physiopathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D020303:Rats, Inbred Dahl; D011918:Rats, Inbred SHR; D017476:Receptors, Neuropeptide Y / Q000235:genetics / Q000378:metabolism; D013997:Time Factors
chemical_list: D020738:Leptin; D012333:RNA, Messenger; D017476:Receptors, Neuropeptide Y; C100568:neuropeptide Y5 receptor; D003345:Corticosterone