C-Y Oliver Chen1, Jimmy Crott, Zhenhua Liu, Donald E Smith. 1. Antioxidants Research Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, 711 Washington Street, Boston, MA, 02111, USA, oliver.chen@tufts.edu.
Abstract
BACKGROUND: Early exposure to suboptimal nutrition during perinatal period imposes risk to metabolic disorders later in life. Fructose intake has been associated with increases in de novo lipogenesis, dyslipidemia, insulin resistance, and obesity. Excess consumption of saturated fat is associated with metabolic disorders. AIM OF THE STUDY: Objective of this animal study was to investigate morphological, metabolic, and endocrine phenotypes of male offspring born to dams consuming diets containing either 30% fructose, 9.9% coconut fat and 0.5% cholesterol (F + SFA) or 30% glucose, and 11% corn oil (C), 1 month before conception and during gestation and nursing. METHODS: Proven male and female Sprague Dawley breeders were fed ad libitum with either F + SFA or C diet throughout the study. At weaning, five male pups from each group were sacrificed for determining morphological phenotypes. The other five male offspring from each group were rehabilitated to the C diet for an additional 12 weeks. At the age of 15 weeks, morphological phenotypes and blood biochemistries [glucose, insulin, growth hormone (GH), insulin-like growth factor-1 (IGF-1), corticosterone, and testosterone] of male adult offspring were then assessed. RESULTS: Body weight (BW) and body length of the F + SFA male adult offspring was slightly smaller than the C. The BW-adjusted epididymal and retroperitoneal fat depots of the F + SFA adult offspring were significantly 18 and 44% smaller than the C, respectively. GH and IGF-1 were not different in adult offspring between groups. Fasted plasma insulin of the F + SFA adult offspring was 64% larger than the C (P <or= 0.0001) and homeostasis model assessment value was 55% larger (P = 0.004). There were negative correlations between fat depot sizes and plasma insulin in adult offspring. CONCLUSIONS: Our results suggest that, through fetal programming, an early exposure to both fructose and saturated fats may cause hyperinsulinemia and insulin insensitivity in the nonobese male rats later in life.
BACKGROUND: Early exposure to suboptimal nutrition during perinatal period imposes risk to metabolic disorders later in life. Fructose intake has been associated with increases in de novo lipogenesis, dyslipidemia, insulin resistance, and obesity. Excess consumption of saturated fat is associated with metabolic disorders. AIM OF THE STUDY: Objective of this animal study was to investigate morphological, metabolic, and endocrine phenotypes of male offspring born to dams consuming diets containing either 30% fructose, 9.9% coconut fat and 0.5% cholesterol (F + SFA) or 30% glucose, and 11% corn oil (C), 1 month before conception and during gestation and nursing. METHODS: Proven male and female Sprague Dawley breeders were fed ad libitum with either F + SFA or C diet throughout the study. At weaning, five male pups from each group were sacrificed for determining morphological phenotypes. The other five male offspring from each group were rehabilitated to the C diet for an additional 12 weeks. At the age of 15 weeks, morphological phenotypes and blood biochemistries [glucose, insulin, growth hormone (GH), insulin-like growth factor-1 (IGF-1), corticosterone, and testosterone] of male adult offspring were then assessed. RESULTS: Body weight (BW) and body length of the F + SFA male adult offspring was slightly smaller than the C. The BW-adjusted epididymal and retroperitoneal fat depots of the F + SFA adult offspring were significantly 18 and 44% smaller than the C, respectively. GH and IGF-1 were not different in adult offspring between groups. Fasted plasma insulin of the F + SFA adult offspring was 64% larger than the C (P <or= 0.0001) and homeostasis model assessment value was 55% larger (P = 0.004). There were negative correlations between fat depot sizes and plasma insulin in adult offspring. CONCLUSIONS: Our results suggest that, through fetal programming, an early exposure to both fructose and saturated fats may cause hyperinsulinemia and insulin insensitivity in the nonobese male rats later in life.
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