title: Physiological difference between dietary obesity-susceptible and obesity-resistant Sprague Dawley rats in response to moderate high fat diet.
abstract: The primary aim of the present study was to define central and peripheral physiological differences between dietary obesity-susceptible (DOS) and obesity-resistant (DOR) outbred Sprague Dawley (SD) rats when given a moderate high fat diet containing 32.34% of energy as a fat. After a 9-week feeding period, the DOS-SD rats consumed significantly more feed (11.1%) and had higher abdominal (39.9%) and epididymal (27.5%) fat pads than the DOR-SD rats. In addition, serum leptin and insulin levels were significantly increased in the DOS-SD rats compared with those in the DOR-SD rats. However, we did not observe significant differences in serum triglyceride, cholesterol and glucose. No differences in hypothalamic OB-Ra and Rb mRNA expressions were found between the two groups. In contrast, arcuate NPY immunohistochemical expression was much higher in the DOS-SD rats than in the DOR-SD rats, though NPY expression in the supraoptic and paraventricular nuclei was not different between the two phenotypes. In peripheral tissues, the DOS-SD rats showed noticeably increased acetyl CoA carboxylase (ACC) mRNA expression in the liver, not epididymal fat. However, Western blot of peroxisomal proliferator activated factor gamma (PPAR gamma) in the liver and epididymal fat was not different between the two phenotypes of SD rats. It was concluded that different body weight phenotypes within outbred SD population responded differently to the development of dietary induced obesity via altered anabolic features in the hypothalamus and liver.
authors.affiliation: Department of Animal Science & Biotechnology, RAIRC, Jinju National University, 150 Chilam-Dong, Jinju, KyeongNam, 660-758, Korea.
authors.forename: InSurk
authors.initials: I
authors.lastname: Jang
authors.forename: DaeYeon
authors.initials: D
authors.lastname: Hwang
authors.forename: JuEun
authors.initials: J
authors.lastname: Lee
authors.forename: KabRyong
authors.initials: K
authors.lastname: Chae
authors.forename: YongKyu
authors.initials: Y
authors.lastname: Kim
authors.forename: TaeSeok
authors.initials: T
authors.lastname: Kang
authors.forename: ChulKyu
authors.initials: C
authors.lastname: Kim
authors.forename: DongHwan
authors.initials: D
authors.lastname: Shin
authors.forename: JinHee
authors.initials: J
authors.lastname: Hwang
authors.forename: YoungBuhm
authors.initials: Y
authors.lastname: Huh
authors.forename: JungSik
authors.initials: J
authors.lastname: Cho
mesh_terms: D000104:Acetyl-CoA Hydrolase / Q000235:genetics; D000818:Animals; D001483:Base Sequence; D002784:Cholesterol / Q000097:blood; D017931:DNA Primers; D004032:Diet; D020022:Genetic Predisposition to Disease; D007150:Immunohistochemistry; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D009765:Obesity / Q000209:etiology* / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D011956:Receptors, Cell Surface / Q000235:genetics; D054411:Receptors, Leptin; D014280:Triglycerides / Q000097:blood
chemical_list: D017931:DNA Primers; D007328:Insulin; D020738:Leptin; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D014280:Triglycerides; D002784:Cholesterol; D000104:Acetyl-CoA Hydrolase