SUN-117 Neuroendocrine Mechanisms Responsible for the Hydromineral Control in Rats with Obesity Induced by High Fat Diet (HFD)

Abstract

Besides being studied regarding cardiovascular diseases and metabolic disturbances, little is known about how obesity might modulate the hydroeletroctrolytic balance. Some studies suggest that such modulation might exist. This current study has the objective of clarify the neuroendocrine mechanisms of salt and water homeostasis in obese rats under normal and osmotic challenge conditions. Wistar male rats weighting 100 grams were used; they were divided into two groups, one submitted to high fat diet (HFD) and the other submitted to normal diet, both for 9 weeks. After that they were kept in a metabolic cage for three days in order to measure food, water and sodium intake and urinary volume. After 24 or 48 hour fluid deprivation, they were given back water, in the first hour, and water and saline (1,8% NaCl), in the second hour, determining the ingestion of both fluids. One week later, the rats were submitted again to 24 or 48 hour fluid deprivation and then euthanized to obtain blood samples and tissues. During the basal period, the obese rats drank less water and ate less food than the non-obese rats. After the 24 or 48 hour dehydration, the obese rats drank less water than the non-obese. Besides that, the dehydrated obese rats also had a reduced hematocrit, reduced plasma osmolality, and reduced levels of K⁺ in plasma, a tendency to bigger levels of Na⁺ in plasma when compared to dehydrated non-obese rats. It was possible to observe an adipose tissue mass reduction in obese dehydrated rats when compared to obese hydrated rats. Accordingly, we were able to see that obesity indeed changes the hydroelectrolytic balance and there is the hypothesis that obese rats might use fat as a water reserve through of beta oxidation of lipids, which is an issue still under investigation. Sources of Research Support: Sao Paulo Research Foudation (FAPESP) Grant #2013/09799-1; Fapesp Grant #2018/10920-3.