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Renal Lipid Accumulation and Expression of the Proteins/Genes Responsible for Fatty Acid Synthesis in Rats with Fatty Liver Induced by Fructose Overconsumption
Liu Changjin3#, Liu Lei2#, Ke Dazhi4, Lin Xuemei2, Jiang Rong2, Xu Wenchun3, Zuo Guowei3*, Wang Jianwei1*
1College of Traditional Chinese Medicine, Chongqing Medical University; 2Faculty of Basic Medical Sciences,Chongqing Medical University; 3College of Laboratory Medicine, Chongqing Medical University;4Second Affi
Abstract: Chronically high consumption of fructose in rodents leads to fatty liver. However, it is still unknown whether fructose overconsumption affects renal lipid metabolism. Here, we found that treatment of rats with 10% fructose in drinking water over 5 weeks induced excess hepatic triglyceride deposition, further investigated the effects and mechanisms of fructose overconsumption on renal lipid metabolism by comparing to those in the liver in rats. Sixteen male SD rats were divided into two groups: (1) water control with free access to water; (2) fructose with free access to 10% fructose in drinking water (W/V, prepared daily). The duration of the experiment was 5 weeks. On day 35, animals were weighed, then blood samples were collected by retroorbital venous puncture under ether anesthesia for determination of plasma concentrations of glucose, insulin, total cholesterol and triglyceride. Immediately thereafter, animals were killed. Livers, kidneys, epididymal and perirenal white adipose tissues were collected and weighed. The indexes of lipid in liver and kidney were determined histologically and enzymatically. Gene expressions involved in lipid synthesis and oxidation were analyzed by Real time-PCR. Protein expressions of transcriptional regulators involved in lipid metabolism were analyzed by Western blot. The results showed that treatment of rats with 10% fructose in drinking water over 5 weeks induced excess hepatic triglyceride deposition, accompanied by increases in plasma concentrations of triglyceride and insulin, as well as adiposity. Further, hepatic mRNA and/or nuclear protein expressions of two key transcriptional regulators carbohydrate response element binding protein (ChREBP) and sterol regulatory element-binding protein (SREBP)1c, and their targeted genes responsible for de novo fatty acid synthesis, were activated. Surprisingly, the lipid content and expression of these proteins/genes in the kidneys were not altered by fructose feeding. Therefore, unlike the liver, fructose overconsumption does not alter renal lipid accumulation and expression of the proteins/genes responsible for de novo fatty acid synthesis in rats.