Rajasekar Panchamoorthy, Anuradha Carani Venkatraman
Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalai Nagar-608 002, Tamil Nadu, India.
Life Sci. 2007 Mar 6;80(13):1176-83. doi: 10.1016/j.lfs.2006.12.010. Epub 2006 Dec 23.
High fructose feeding (60 g/100 g diet) in rodents induces alterations in both glucose and lipid metabolism. The present study was aimed to evaluate whether intraperitoneal carnitine (CA), a transporter of fatty acyl-CoA into the mitochondria, could attenuate derangements in carbohydrate metabolizing enzymes and glucose overproduction in high fructose-diet fed rats. Male Wistar rats of body weight 150-160 g were divided into 4 groups of 6 rats each. Groups 1 and 4 animals received control diet while the groups 2 and 3 rats received high fructose-diet. Groups 3 and 4 animals were treated with CA (300 mg/Kg body weight/day, i.p.) for 30 days. At the end of the experimental period, levels of carnitine, glucose, insulin, lactate, pyruvate, glycerol, triglycerides and free fatty acids in plasma were determined. The activities of carbohydrate metabolizing enzymes and glycogen content in liver and muscle were assayed. Hepatocytes isolated from liver were studied for the gluconeogenic activity in the presence of substrates such as pyruvate, lactate, glycerol, fructose and alanine. Fructose-diet fed animals showed alterations in glucose metabolizing enzymes, increased circulating levels of gluconeogenic substrates and depletion of glycogen in liver and muscle. There was increased glucose output from hepatocytes of animals fed fructose-diet alone with all the gluconeogenic substrates. The abnormalities associated with fructose feeding such as increased gluconeogenesis, reduced glycogen content and other parameters were brought back to near normal levels by CA. Hepatocytes from these animals showed significant inhibition of glucose production from pyruvate (74.3%), lactate (65.4%), glycerol (69.6%), fructose (56.2%) and alanine (63.6%) as compared to CA untreated fructose-fed animals. The benefits observed could be attributed to the effect of CA on fatty acyl-CoA transport.
在啮齿动物中，高果糖喂养（60克/100克饮食）会引起葡萄糖和脂质代谢的改变。本研究旨在评估肉碱（CA），一种将脂肪酰基辅酶A转运到线粒体中的转运体，是否能减轻高果糖饮食喂养大鼠碳水化合物代谢酶的紊乱和葡萄糖过度生成。体重150 - 160克的雄性Wistar大鼠被分为4组，每组6只。第1组和第4组动物接受对照饮食，而第2组和第3组大鼠接受高果糖饮食。第3组和第4组动物用CA（300毫克/千克体重/天，腹腔注射）处理30天。在实验期结束时，测定血浆中肉碱、葡萄糖、胰岛素、乳酸、丙酮酸、甘油、甘油三酯和游离脂肪酸的水平。测定肝脏和肌肉中碳水化合物代谢酶的活性以及糖原含量。研究从肝脏分离的肝细胞在丙酮酸、乳酸、甘油、果糖和丙氨酸等底物存在下的糖异生活性。高果糖饮食喂养的动物表现出葡萄糖代谢酶的改变、糖异生底物循环水平升高以及肝脏和肌肉中糖原的消耗。仅用所有糖异生底物喂养高果糖饮食的动物肝细胞中葡萄糖输出增加。与果糖喂养相关的异常，如糖异生增加、糖原含量降低和其他参数，通过CA恢复到接近正常水平。与未用CA处理的果糖喂养动物相比，这些动物的肝细胞显示丙酮酸（74.3%）、乳酸（65.4%）、甘油（69.6%）、果糖（56.2%）和丙氨酸（63.6%）生成葡萄糖受到显著抑制。观察到的益处可能归因于CA对脂肪酰基辅酶A转运的作用。
