Programming of hepatic and intestinal metabolic alteration in the offpring of rats fed with a fatty diet

M. BELÉN MAZZUCCO; DAIANA FORNES; SABRINA ROBERTI; ALICIA JAWERBAUM; VERÓNICA WHITE

Santiago de Chile

Congreso; IPW 2013 Lawson joint meeting; 2013

International Postgraduate Workshop (IPW)

Metabolic alterations in overweight mothers promote lipid accumulation in the developing fetus leading to metabolic alterations in the fetus and the neonate, which are linked to oxidative stress and inflammation and to the generation of metabolic diseases in adulthood. Incretins are produced by the intestin and modulate metabolic homeostasis. Objectives: To study the impact of a saturated fat overload in the maternal diet on triglycerides levels, nitric oxide (NO) production and lipid peroxidation in the fetal and neonate liver and intestine and the intestinal expression of two incretins: GIP and GLP1. Methodology: Wistar rats were fed with standard diet (SD group, 5% lipids) or supplemented with 25% saturated fat (FD group) from 7 weeks prior to mating rats with SD males and until the end of lactation. One group of rats was sacrificed on day 21 of gestation to obtain the fetuses, the other finished the pregnancy and their neonates were sacrificed on day 2, 21 and 120 post-natal. Plasma triglycerides (TG) and colesterol were mesured using commercial kits. NO production (dosage of nitrate/nitrite) and TBARS levels were analyzed in liver and intestine. GIP and GLP1 expression was studied by PCR. Results: the FD group showed elevated TG levels in the fetus and offspring (50-83%, p less than 0.01), increased NO production in the fetal and offspring liver and intestine (p less than 0.05), elevated TBARS levels in the fetal and offspring liver (p less than 0.01) and in the offspring intestine (25%, p less than 0.05). GIP and GLP1 expression showed several developmental-stage alterations. Conclusions: a saturated fat overload in the maternal diet alters incretins expression and induces a pro-oxidant and pro-inflammatory environment in the fetal liver and intestine programming metabolic alterations that persist in the offspring.