Cd36 gene expression in adipose and hepatic tissue mediates the lipids accumulation in liver of obese rats with sucrose-induced hepatic steatosis.

Obesity is considered a global epidemic and is mainly associated with the development of diabetes, cardiovascular diseases and Non-Alcoholic Fatty Liver (NAFLD). The pathogenesis between obesity and hepatic steatosis is partially known, but could involve differentiated or tissue-specific participation of the expression of Cd36 mRNA that codes for a receptor which is a transporter of free fatty acids (FFA) in different tissues, favoring the lipids storage. This relative expression was evaluated in adipose and liver tissue in rats with steatosis after consumption of sucrose for 30 and 40 weeks. Ten Wistar rats were divided into two experimental groups (St-30 and St-40), which received a standard diet plus 30 % sucrose in their water intake. These rats showed a significant increase in abdominal fat, serum biochemical determinations, HOMA-IR; as well as, changes in adipocytes size and mild portal hepatitis and grade 2 hepatic steatosis. The relative expression of Cd36 mRNA increased in liver tissue after 30 (4.5-fold) and 40 (8.5-fold) weeks of sucrose ingestión but no in adipose tissue; with respect to control group (P < 0.05). This expression was associated with a significant increase in the levles of sCD36 in serum, which is indicator of the presence of the FFA transporter in the hepatocyte membrane causing lipids accumulation. The above shows the link between the adipose and hepatic tissue for the accumulation of steatotic fat in the liver through time, mediated by the relative expression of cd36 mRNA that encodes for the FFA transporter.

Dietary sucrose regulates the expression of the Cd36 gene in hepatic tissue of rats with obesity and Non Alcoholic Fatty Liver Disease (NAFLD).

AIM: To evaluate the mRNA expression levels of Cd36 in adipose and hepatic tissues, in rats with NAFLD after the consumption of sucrose for 10 and 20 weeks. METHODS: Twenty Wistar rats, all nearly 21 days old were divided into two experimental groups (NAFLD-10 and NAFLD-20), that received a standard diet (2014 Teklad Global) plus 30% sucrose in their drinking water for 10 and 20 weeks and the control groups (C Groups). Variables such as body weight, food intakes, and serum parameters were measured. Adipose and hepatic tissues were extirpated; some tissue was preserved in formalin and some at -70 °C until analysis. Histological analysis was carried out, and the Cd36 mRNA expression levels were determined. RESULTS: The rats in the NAFLD-10 and NAFLD-20 groups showed a significative increase in abdominal fat, triglycerides, free fatty acids, insulin, AST, ALT, uric acid and HOMA index; as well as changes in the cellular dynamics in adipose tissue, (adipocytes hypertrophic: >1500 µm2) with respect to the control groups (P<0.05). The histological analysis showed development of mild portal hepatitis in rats of the NAFLD-10 group and grade 1 hepatic steatosis with mild portal inflammation in rats of the NAFLD-20 group. Finally, Cd36 mRNA expression levels were significantly increased in hepatic tissue after 10 (1.5-fold) and 20 (3.5-fold) weeks of sucrose ingestion (P<0.05). CONCLUSION: mRNA expression is a molecular mechanism involved in the development of NAFLD associated with obesity in rats consuming sucrose. However, there was increased Cd36 mRNA expression only in hepatic tissue while in hypertrophic adipose tissue mRNA levels remained unchanged.