An overload of saturated fat in maternal diet programs intestine impairments in incretin expression in the rat offspring

MARÍA BELÉN MAZZUCCO, MARTINA RADICE, EVANGELINA CAPOBIANCO, ALICIA JAWERBAUM, VERÓNICA WHITE

Mar del Plata

Congreso; LXI Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2016

We have previously found that fetuses from rats fed with a saturated-fat rich diet show high circulating levels of lipids and leptin, and resistance to leptin action in the liver. We have also found alterations in mRNA levels of 2 incretins: gastric inhibitory peptide (gip) and glucagon-like peptide (gcg) in the intestine from these fetuses. Leptin and nutrients are well-known stimulators of incretin production. We aimed to analyze whether an overload of saturated fat in the maternal diet induces impairments in leptin-induced intestine gip and gcg mRNA levels in the fetus and whether the anomalies persist in the offspring. Methods: Female Wistar rats were fed with either a standard (5% fat) (controls) or a saturated fat-rich diet (28% fat) from 6 weeks of age (SFD rats). After 8 weeks of diet, they were mated with control males. Control and SFD pregnant rats were euthanized at 21 days of gestation, fetal intestines obtained and either preserved or cultured (3 h) with or without leptin (100 ng/ml). Another group of control and SFD rats were allowed to deliver, their offspring euthanized at 140 days of age, and the proximal portion of their intestine obtained. gip and gcg mRNA levels were assessed by PCR. Results: Leptin addition to the culture induced an increase in gcg and gip mRNA levels (p