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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #249119
Title: Fructose and saturated fats predispose hyperinsulinemia in lean male rat offspring

Author
item CHEN, CHUNG-YEN (OLIV - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item CROTT, JIMMY - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item LIU, ZHENHUA - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item SMITH, DONALD - Jean Mayer Human Nutrition Research Center On Aging At Tufts University

Submitted to: European Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/20/2010
Publication Date: 9/20/2010
Citation: Chen, C.E., Crott, J., Liu, Z., Smith, D. 2010. Fructose and saturated fats predispose hyperinsulinemia in lean male rat offspring. European Journal of Nutrition. 49(6):337-343.

Interpretive Summary: Nutrition during pregnancy and lactation may have a significant impact on health of offspring later in life. Since Western diet containing high amounts of fructose and saturated fats is associated with metabolic disorders, we hypothesized rats born to mothers consuming a chow containing high amounts of fructose and saturated fats that will have abnormal metabolic and anatomical phenotypes. Parental rats were fed with either fructose plus saturated fat diet or normal diet during pregnancy and lactation. At weaning, five male pups from each group were killed for determining morphological phenotypes. The other 5 male offspring from each group were fed the normal diet for an additional 12 wks. Body weight (BW) and body length of the male adult offspring born to mothers fed the fructose and saturated diet was slightly smaller than the normal diet. Further, they had lower fat accumulation. However, overnight fasted plasma insulin of the adult offspring born to mothers fed the fructose and saturated fat diet was 64% larger than the normal diet. Our results suggest that mothers consuming a diet high in fructose and saturated fat may increase risk of metabolic syndrome in their offspring.

Technical 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 lipogensis, 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), one 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 5 male offspring from each group were rehabilitated to the C diet for an additional 12 wks. At the age of 15 wks, morphological phenotypes and blood biochemistries (glucose, insulin, growth hormone, insulin like growth factor-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. Growth hormone and insulin like growth factor-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 =0.0001) and HOMA 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.