SAT-149 The Metabolic Impairments Caused by Fructose and Prednisolone Intake Are Reversible After the Interruption of Exposure

Regular ingestion of fructose and continuous glucocorticoid (GC) treatment, separately, may result in metabolic adverse effects (1,2), but their combined impact is not yet understood. Thus, we aimed to evaluate the impact of a combination of fructose and prednisolone ingestion on glucose and lipid metabolism as well as the effect of the interruption of this combined treatment. Male Wistar rats were divided into five groups as follows: control (C) group, fructose (F) group (20% fructose in the drinking water), prednisolone (P) group (12.5 μg/mL prednisolone in the drinking water), fructose plus prednisolone (FP) group (a combination of fructose and prednisolone in the drinking water as for F and P groups) for 90 consecutive days. Half of the rats (group R) from the FP group were maintained for 90 more days with a discontinuation of fructose and prednisolone to monitor the parameters. The combination of fructose and GC intake led to an increase in the circulating triacylglycerol from the fourth week of treatment until the end of treatment (P<0.05, n=10). The FP group also exhibited higher abdominal adiposity and plasma insulin values, reduced insulin sensitivity, increased uricemia, and impaired hepatic redox balance that paralleled with augmented fat content in the liver (p<0.05, n=10). No major impact on blood glucose or glucose tolerance was observed in the FP group. These results observed in the FP group were associated with increased beta-cell mass (p<0.05, n=8). Moreover, the combination of sugar and GC treatment led to a reduction in the total hepatic protein kinase B (PKB) content and to a reduction in the phosphorylated 5’ AMP-activated protein kinase (AMPK) content in the epididymal adipose tissue (p<0.05, n=6). Combination of fructose and GC intake did not impact on proinflammatory protein contents in the adipose tissue. Complete cessation of treatments resulted in the normalization of plasma triacylglycerol and uric acid levels in the R group (p<0.05, n=10). Interruption of sugar and GC treatments also led to normalization of the peripheral insulin sensitivity, hepatic fat content and the hepatic redox state (p<0.05, n-10). We conclude that the combination of fructose and prednisolone intake induces a metabolic syndrome-like phenotype and that interruption of fructose and GC intake recover practically all metabolic impairments. These findings point to the risk of associating GC-based therapies with a regular intake of sweetened beverages and draws attention to the plasticity of the organism and the benefits of removing the causal factors, whenever possible. Reference: (1) Zhang et al., Nutrients. 2017 Mar 29;9(4). pii: E335. (2) Pasieka et al., Metabolites. 2016 Aug 3;6(3). pii: E24. Sources of Research Support: CNPq and CAPES.