title: Dyslipidemia is not associated with cardiovascular disease risk in an animal model of mild chronic suboptimal nutrition.
abstract: Previous studies performed in an experimental model of nutritional growth retardation (NGR) have observed metabolic adaptation. We hypothesized that changes in lipid-lipoprotein profile, glucose, and insulin levels occur, whereas overall body growth is reduced.The aim of this study was to assess serum lipid-lipoprotein profile, hepatogram, insulinemia and glycemia, and CVD risk markers in rats fed a suboptimal diet. Weanling male rats were assigned either to control (C) or NGR group. In this 4-week study, C rats were fed ad libitum a standard diet, and NGR rats received 80% of the amount of food consumed by C. Zoometric parameters, body fat content, serum lipid-lipoprotein profile, hepatogram, insulinemia, and glycemia were determined, and the cardiovascular disease (CVD) risk markers homeostasis model assessment-insulin resistance and homeostasis model assessment and β-cell function were calculated. Suboptimal food intake induced a significant decrease in body weight and length, which were accompanied by a reduction of 50% in body fat mass. Serum lipoproteins were significantly higher in NGR rats, with the exception of high-density lipoprotein cholesterol, which remained unchanged. Nutritional growth retardation rats had decreased triglycerides compared with C rats. No significant differences were detected in liver function parameters. The CVD risk markers homeostasis model assessment (HOMA)-insulin resistance and homeostasis model assessment and β-cell function were significantly lower in NGR rats. Mild chronic suboptimal nutrition in weanling male rats led to growth retardation and changes in the lipid-lipoprotein profile, glucose, and insulin levels while preserving the integrity of liver function. These data suggest a metabolic adaptation during suboptimal food intake, which ensures substrates flux to tissues that require constant energy-in detriment to body growth. The CVD risk markers suggested that mild chronic food restriction of approximately 20% could provide protection against this degenerative disease.
authors.affiliation: Pediatric Sunshine Academics and Sansum Diabetes Research Institute, Santa Barbara, CA 93105, USA.
authors.forename: Fima
authors.initials: F
authors.lastname: Lifshitz
authors.forename: Patricia M
authors.initials: PM
authors.lastname: Pintos
authors.forename: Christian E
authors.initials: CE
authors.lastname: Lezón
authors.forename: Elisa V
authors.initials: EV
authors.lastname: Macri
authors.forename: Silvia M
authors.initials: SM
authors.lastname: Friedman
authors.forename: Patricia M
authors.initials: PM
authors.lastname: Boyer
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D002318:Cardiovascular Diseases / Q000150:complications / Q000503:physiopathology*; D008076:Cholesterol, HDL / Q000097:blood; D004032:Diet; D004195:Disease Models, Animal; D050171:Dyslipidemias / Q000150:complications / Q000503:physiopathology*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D009752:Nutritional Status; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D008076:Cholesterol, HDL; D007328:Insulin; D014280:Triglycerides