Deleterious effect of maternal consumption of a fructose rich diet during pregnancy or lactation, on metabolic-endocrine functions in the male offspring.

ALZAMENDI A; CASTROGIOVANNI D; GAILLARD RC; SPINEDI E; GIOVAMBATTISTA A

Washington DC, USA

Congreso; 91 th. American Endocrine Society Meeting; 2009

ESO

Obesity represents a major health problem affecting the population from both developed and developing countries. Human epidemiologic and experimental animal studies suggest that an adverse environment during the critical gestation or early neonatal life periods alters normal growth and predispose the individual for the development of severe metabolic disorder, such as obesity, insulin resistence and type 2 diabetes. The aim of the present study was to evaluate the impact of the consumption of an iso-caloric fructose rich diet (FRD) by mothers, during pregnancy or lactation, on adipocyte and other metabolic functions in the male offspring. Pregnant Sprague-Dawley rats fed with standard chow diet ad libitum were divided into groups: a) one receiving FRD (10 % F, w/v) in the drinking water during pregnancy (FRD-P); b) other consuming FRD during lactation (FRD-L), and c) a third drinking tap water served as a control one (CTR). Body weight, and food and drink intake were daily registered in male animals from the first offspring, from weaning (day 21) and up to day 60 of age (experimental day). Circulating levels of glucose (GLU), triglyceride (TG), total cholesterol (TC), insulin (INS) and leptin (LEP) were evaluated. Retroperitoneal (RP) adipose tissue pads were dissected out and kept frozen until quantification of ob mRNA expression. FRD-P male rats showed increased (P < 0.05 vs. CT) body weight throughout the study, and revealed and enhanced (P < 0.05 vs. CTR) daily food intake between days 49 and 60. Circulating levels of GLU, TG and TC were similar in FRD-P and CTR male animals. Conversely, FRD-P male rats developed an increase (P < 0.05 vs. CTR rats) in insulin and leptin peripheral levels. While FRD-L and CTR male rats displayed similar circulating levels of TC, INS and LEP, FRD-L rats were characterized by diminished (P < 0.05 vs. CT animals) plasma levels of GLU and TG. Finally, RP fat ob mRNA abundance was not modified in FRD-P male rats, and FRD intake during lactation (FRD-L) resulted in male rats bearing an increased (P < 0.05 vs. CTR animals) ob mRNA expression in RP fat pads. It is concluded that excessive fructose consumption during either pregnancy or lactation period resulted in severe metabolic-endocrine disorders of the first male offspring. These abnormalities could be responsible, at least in part, for the enhanced susceptibility of the adult male individual for the development of metabolic syndrome, obesity or/and type 2 diabetes.