Volume 10, Issue 2 p. 171-180

Renoprotective action of l-carnitine in fructose-induced metabolic syndrome

P. Rajasekar

P. Rajasekar

Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Tamil Nadu, India

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P. Viswanathan

P. Viswanathan

Department of Pathology, Rajah Muthiah Medical College, Annamalai University, Tamil Nadu, India

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C. V. Anuradha

Corresponding Author

C. V. Anuradha

Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Tamil Nadu, India

Prof. Dr C. V. Anuradha, Department of Biochemistry and Biotechnology, Annamalai University, Annamalai Nagar-608 002, Tamil Nadu, India.
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cvaradha@hotmail.comSearch for more papers by this author
First published: 17 December 2007
Citations: 22

Abstract

Aim: Rats fed high dosage of fructose that form a well-known experimental model of the metabolic syndrome also display progressive renal disturbances. The present study evaluates the influence of l-carnitine (CA) administration on oxidant–antioxidant balance, protein damage and lipid levels in kidney of rats administered high dose of fructose.

Methods: Adult male Wistar rats were divided into four groups of 10 rats each. Groups I and IV animals received starch-based control diet, while groups II and III rats were fed a high-fructose diet (60 g/100 g). Groups III and IV animals additionally received CA (300 mg/kg/day) for 60 days. The extent of lipid peroxidation, enzymatic and non-enzymatic antioxidants and lipid levels were measured after 60 days. The accumulation of nitrated and oxidatively modified proteins in kidney was also measured by immunohistochemical study with specific antibodies.

Results: Fructose-fed rats exhibited increased levels of peroxidation end products, diminished antioxidant status, increased staining for the presence of 4-hydroxy-2-nonenal, 2,4-dinitrophenol and 3-nitrotyrosine protein adducts and lipid accumulation in kidney. CA administration attenuated these pathological renal alterations.

Conclusions: The benefits of CA in this model suggest the therapeutic use of CA to counter the kidney changes associated with metabolic syndrome.