title: Inherent capacity for lipogenesis or dietary fat retention is not increased in obesity-prone rats.
abstract: Obesity results from positive energy balance and, perhaps, abnormalities in lipid and glycogen metabolism. The purpose of this study was to determine whether differences in lipogenesis, retention of dietary fat, and/or glycogenesis influenced susceptibility to dietary obesity. After 1 wk of free access to a high-fat diet (HFD; 45% fat by energy) rats were separated on the basis of 1 wk body weight gain into obesity-prone (OP; > or =48 g) or obesity-resistant groups (OR; < or =40 g). Rats were either studied at this time (OR1, OP1) or continued on the HFD for an additional 4 wk (OR5, OP5). Weight gain and energy intake were greater (P < or = 0.05) in OP vs. OR at both 1 (53 +/- 2 vs. 34 +/- 1 g; 892 +/- 27 vs. 755 +/- 14 kcal) and 5 (208 +/- 7 vs. 170 +/- 7 g; 4,484 +/- 82 vs. 4,008 +/- 72 kcal) wk, respectively. Rats were injected with (3)H(2)O and were either provided free access to an HFD meal containing labeled fatty acids (fed; n = 10 or 11/group) or were fasted (n = 10/group) overnight. The amount of food or (14)C tracer eaten overnight was equivalent between OP and OR rats. In liver, the fraction of (3)H retained in glycogen or lipid was not significantly different between OR and OP groups. Retention of dietary fat in the liver was not increased in OP rats. In adipose tissue, retention of (3)H was approximately 49% greater (P < or = 0.05) in OP1 vs. OR1 and approximately 30% greater in OP5 vs. OR5, but retention of dietary fat was not elevated in OP vs. OR. At the same time, fat pad weight (sum of epididymal, retroperitoneal, mesenteric) was 49% greater in OP1 rats vs. OR1 rats and 65% greater in OP5 vs. OR5 rats (P < or = 0.05). Thus a greater capacity for lipogenesis or retention of dietary fat does not appear to be included in the OP phenotype. The characteristic increase in energy intake associated with OP rats appears to be necessary and critical to accelerated weight and fat gain.
authors.affiliation: Department of Pediatrics, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA. commerfordr@msx.dept-med.pitt.edu
authors.forename: S R
authors.initials: SR
authors.lastname: Commerford
authors.forename: M J
authors.initials: MJ
authors.lastname: Pagliassotti
authors.forename: C L
authors.initials: CL
authors.lastname: Melby
authors.forename: Y
authors.initials: Y
authors.lastname: Wei
authors.forename: J O
authors.initials: JO
authors.lastname: Hill
mesh_terms: D000273:Adipose Tissue / Q000033:anatomy & histology / Q000378:metabolism; D000818:Animals; D001835:Body Weight; D004041:Dietary Fats / Q000008:administration & dosage / Q000378:metabolism*; D004198:Disease Susceptibility; D002149:Energy Intake; D006003:Glycogen / Q000378:metabolism; D008055:Lipids / Q000096:biosynthesis*; D008099:Liver / Q000033:anatomy & histology / Q000378:metabolism; D008297:Male; D009765:Obesity / Q000209:etiology*; D009929:Organ Size; D009994:Osmolar Concentration; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000378:metabolism
chemical_list: D004041:Dietary Fats; D008055:Lipids; D014280:Triglycerides; D006003:Glycogen