title: Components of metabolic syndrome and coronary artery disease in female Ossabaw swine fed excess atherogenic diet.
abstract: Ossabaw swine have a 'thrifty genotype' (propensity to obesity) that enables them to survive seasonal food shortages in their native environment. Consumption of excess kcal causes animals of the thrifty genotype to manifest components of the metabolic syndrome, including central (intra-abdominal) obesity, insulin resistance, impaired glucose tolerance, dyslipidemia, and hypertension. We determined whether female Ossabaw swine manifest multiple components of the metabolic syndrome by comparing lean pigs fed a normal maintenance diet (7% kcal from fat; lean, n = 9) or excess chow with 45% kcal from fat and 2% cholesterol (obese, n = 8). After 9 wk, body composition, glucose tolerance, plasma lipids, and intravascular ultrasonography and histopathology of coronary arteries were assessed. Computed tomography (CT) assessed subcutaneous and intra-abdominal fat deposition and was compared with traditional methods, including anatomical measurements, backfat ultrasonography, and proximate chemical composition analysis. Compared with lean animals, obese swine showed 2-fold greater product of the plasma insulin x glucose concentrations, 4.1-fold greater total cholesterol, 1.6-fold greater postprandial triglycerides, 4.6-fold greater low- to high-density lipoprotein cholesterol ratio, hypertension, and neointimal hyperplasia of coronary arteries. The 1.5-fold greater body weight in obese swine was largely accounted for by the 3-fold greater carcass fat mass. High correlation (0.79 to 0.95) of CT, anatomical measurements, and ultrasonography with direct chemical measures of subcutaneous, retroperitoneal, and visceral fat indicates high validity of all indirect methods. We conclude that relatively brief feeding of excess atherogenic diet produces striking features of metabolic syndrome and coronary artery disease in female Ossabaw swine.
authors.affiliation: Department of Medical Pharmacology & Physiology, University of Missouri, Columbia, Missouri, USA.
authors.forename: Melissa C
authors.initials: MC
authors.lastname: Dyson
authors.forename: Mouhamad
authors.initials: M
authors.lastname: Alloosh
authors.forename: James P
authors.initials: JP
authors.lastname: Vuchetich
authors.forename: Eric A
authors.initials: EA
authors.lastname: Mokelke
authors.forename: Michael
authors.initials: M
authors.lastname: Sturek
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D001823:Body Composition; D001837:Body Weights and Measures / Q000379:methods; D003324:Coronary Artery Disease / Q000097:blood / Q000150:complications / Q000473:pathology*; D003331:Coronary Vessels / Q000473:pathology*; D004036:Diet, Atherogenic; D004195:Disease Models, Animal; D005260:Female; D006965:Hyperplasia; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D024821:Metabolic Syndrome / Q000097:blood / Q000150:complications / Q000473:pathology*; D015203:Reproducibility of Results; D013552:Swine; D017539:Tunica Intima / Q000473:pathology*
chemical_list: D001786:Blood Glucose; D008055:Lipids