Influência de uma dieta normolipídica à base de óleo de coco 44 sobre o perfil sérico e hepático de ácidos graxos e sua relação 45 com a sensibilidade à insulina

Abstract

Introduction: The increasing consumption of coconut oil is due, in part, to its composition in medium-chain fatty acids, which are seen as safe and which, supposedly, would result in health benefits. However, it is an oil that is also rich in saturated fatty acids (SFA) and poor in mono and polyunsaturated fatty acids and free from essential fatty acids. The excess of SFA and the deficiency of mono- and polyunsaturated fats contribute to the pathogenesis of insulin resistance, inflammation and nonalcoholic fatty liver. Objective: To evaluate the influence of a normolipid diet based on coconut oil on the serum and hepatic profile of fatty acids (FA) and its relationship with insulin sensitivity in rats. Methods: Male Wistar rats, with an initial age of 30 days, were randomly assigned to three groups: SO, SO + CO and CO, formed from animals fed, respectively, with an AIN-93G diet, based on soybean oil. (SO, 70 g/kg); diet containing a mixture of soybean oil (35 g/kg) and coconut oil (35 g/kg) (SO + CO); and diet based on coconut oil (CO, 70 g/kg) for 60 days. At 90 days of life, indicators of insulin sensitivity and inflammatory markers (Glycemia, Insulin, HOMA-IR, AST, ALT and CRP), the protein content of PEPCK, GSK, SCD-1, PPAR-alpha and CPT- 1, histological analysis of the liver and the serum and liver fatty acid profile, as well as the percentage of fatty acids in the diets. Results: The CO diet showed a high percentage of SFA (93%), mainly lauric acid (40.4% among medium chain GA) and myristic (20.94% among long chain GA). The CO and SO + CO diets were similar regarding the predominance of lauric acid (40.4% and 23.8%, respectively) and myristic (20.9% and 11.8%, respectively) and low concentration of oleic acid. (5.9% and 14.9%, respectively). A deficiency of essential FA in the CO diet was observed and this reflected in the presence of mead in the serum and liver of the animals in this group. In addition, the CO group showed high serum concentrations of saturated fats and MUFAS and low concentrations of PUFAS, especially stearic, elaidic and mead acids. In the SO+CO group, the serum concentrations of stearic and elaidic acids were similar to the CO group. Total food intake was higher in the CO group compared to the SO and SO + CO groups. Absolute and relative liver fat were lower in the CO group compared to SO and SO + CO, while serum TG was higher in the CO group compared to SO and the SO + CO group did not differ from the others. Blood glucose did not differ between the groups, but insulinemia was lower in the CO group compared to SO+CO and both did not differ from the SO group. The highest HOMA-IR was observed in the SO+CO group, while the CO and SO groups were similar to each other. ALT and CRP were higher in the SO+CO group compared to the SO, and the CO group did not differ from these two groups. The protein level of SCD1 was lower in CO compared to the others, while glycogen synthetase was lower in the SO+CO group than 15 in the SO and both were equal to the CO group. The SO+CO group showed no changes in liver architecture. On the other hand, animals treated with coconut oil showed an increase in the number of vessels in the portal space region, accumulation of type 1 collagen fibers, as well as an increase in glycogen reserve. Conclusion: The CO diet resulted in an intense hepatic inflammatory process, possibly due to the excess of serum saturated fatty acids and absence of essential fatty acids in serum and liver, which culminated in tissue damage without the presence of insulin resistance. The presence of essential fatty acids in the SO+CO group seems to have attenuated the inflammatory process, delaying the derangement of the liver structure, however, without protecting it from the effects of hepatic insulin resistance