Effect of Curcuma longa L. on hepatic mitochondrial beta-oxidation and on progression of frutose-induced hepatic steatosis

Abstract

Obesity is a condition that is growing worldwide. Increased body fat is associated with various metabolic complications, including insulin resistance, type 2 diabetes, cardiovascular diseases, renal and hepatic alterations. One of the factors responsible for increase in the number of obese people is the consumption of foods high in fat and sugar, especially fructose in the form of corn syrup. Fructose is highly used by the food industry to sweeten their products. However, the chronic consumption of this fructose is one of the factors responsible for the development of nonalcoholic fatty liver disease (NAFLD), characterized by the accumulation of triglycerides in the hepatocytes, and what may develop into more serious conditions, even cirrhosis. Also, it can affect hepatic beta-oxidation by reducing activation of Peroxisome Proliferator-Activated Receptor- alpha (PPAR-±). In addition to the conventional treatments, the use of food components has received increasing attention. Curcuma longa, commonly known as turmeric, has in its composition curcumin (80%), a polyphenol that has shown benefits in cases of obesity and its comorbidities. Thus, the main goal of this study is to test the effect of Curcuma longa on NAFLD induced by chronic consumption of fructose. We will study 48 male Wistar rats initially divided into two groups that will receive a standard diet (SD) or standard diet + fructose in drinking water (30% fructose) ad libitum for 15 weeks. Then they will be divided into four groups (n = 12 animals / group), which will receive placebo or turmeric for 12 weeks. We will be evaluating body weight, calorie intake, adiposity index, blood glucose and fasting and OGTT, triglycerides. The protein quantification of PPAR-± will be made by western blot technique. Steatosis will be identified by histological analysis and determination of liver triacylglycerol. (AU)