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SAT-226 Maternal Adiponectin Overexpression Decreases Fetal Growth and Alters Metabolic Functions

Abstract Abstract: Obese women who develop gestational diabetes show lower adiponectin levels across pregnancy than obese euglycaemic women suggesting that obese women with low adiponectin levels have an impaired capacity to handle the metabolic changes during pregnancy. Adiponectin acts on the placenta during pregnancy; this fact allows for the interesting possibility that adiponectin can exert endocrine effects on the developing fetus. The aim here was to investigate how adiponectin affects cellular and molecular mechanisms regulating fetal growth and metabolic functions during pregnancy. Wild type (wt) and adiponectin transgenic (APNtg) mice were fed normal chow or a high fat/high sucrose (HF/HS) diet for 8 weeks before mating with wt males. Fetus were dissected on pregnancy day 18.5. Maternal adiponectin overexpression decreased fetal body weight in dams on normal chow, and even more in dams on HF/HS diet. There was no difference in fasting glucose between the groups on normal chow and HF/HS diet, but APNtg animals had lower fasting glucose levels compared to wt. We also investigated the role of adiponectin on lipid uptake. Wild type dams fed HF/HS diet had decreased levels of circulating triglycerides but increased levels of liver triglycerides. However, APNtg dams were partly protected against the development of fatty liver confirming previous studies. In contrast, liver triglyceride levels were increased in fetuses from APNtg dams on HF/HS diet, suggesting an increased transport of lipids to the developing fetuses. To further investigate placenta function, we measured the expression of genes involved in placental nutrient transport. We found an increased expression of lipoprotein lipase (LPL), while IRS-1 expression was decreased in placentas from APNtg fetuses regardless of the dam’s genotype or diet. Adiponectin has previously been shown to decrease nutrient transport across placenta, with the assumption that the main nutrient transport is glucose. Our data opens up for the possibility that adiponectin may increases lipid delivery to the fetus. Sources of research support: Magnus Bergvall Foundation, Åke Wiberg Foundation, Hjalmar Svensson Foundation, Adlerbert Research Foundation, and Royal Society of Arts and Sciences in Gothenburg