INCRETIN EXPRESSION IS ALTERED IN THE OFFSPRING OF RATS FED WITH A FATTY DIET: POSSIBLE ROLE OF LEPTIN

VERONICA WHITE; ALICIA JAWERBAUM; M. BELÉN MAZZUCCO

Buenos Aires

Congreso; Scientific IADPSG (International Association of the Diabetes and Pregnancy Study Groups) meeting; 2016

In a rat model of maternal overweight, induced by anoverload of saturated fat in the diet, we have previously found severalmetabolic alterations in mothers, fetuses and offspring, as well ashyperglycemia, hyperinsulinemia, hyperleptinemia and liver leptin resistance infetuses from these rats. Recently, we found alterations in the expression ofthe incretins gastric inhibitory peptide (GIP) and glucagon-like peptide (GLP)in the fetal intestine. Nutrients, as well as leptin, are well-knownstimulators of incretin production. We aimed to analyze whether an overload ofsaturated fat in the maternal diet induces impairments in leptin-inducedintestine GIP and GLP gene expression in the fetus and whether theseimpairments persist in the offspring?s later life. Methods: Female Wistar ratswere fed with either a standard (5% fat) (controls) or a saturated fat diet(28% fat) from 6 weeks of age (SFD rats). After 8 weeks of diet, they weremated with control males. Control and SFD pregnant rats were euthanized at 21days of gestation and fetal intestines obtained and either preserved orcultured (3 h) with or without leptin (100 ng/ml). Another group of control andSFD rats were allowed to deliver, their offspring euthanized at 21 or 140 daysof age and the proximal portion of their intestine obtained.  GIP and GLP expression were assessed by PCR. Results:The intestines from control male and female fetuses cultured with leptin showedhigher GIP and GLP expression (p