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The present study was designed to explore whether L-carnitine (CA) regulates insulin signaling and modulates the changes in liver in a well-characterized insulin resistant rat model. Adult male Wistar rats were divided into 4 groups. 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 i.p). After a period of 60 days hepatic tyrosine phosphorylation status was determined by assaying protein tyrosine phosphatase (PTP) and protein tyrosine kinase (PTK) activities. Oxidative damage was monitored by immunohistochemical localization of 4-hydroxynonenal (4-HNE), 3-nitrotyrosine (3-NT) and dinitrophenol (DNP)-protein adducts. In addition protein kinase C beta II (PKC beta II) expression, propidium iodide staining of isolated hepatocytes and histology of liver tissue were determined to examine liver integrity. Fructose-fed rats displayed reduced insulin action, increased expression of PKC beta II, altered histology, fragmentation of hepatocyte nuclear DNA, and accumulation of oxidatively modified proteins. Simultaneous treatment with CA alleviated the abnormalities associated with fructose feeding. In summary the data suggest that elevated oxidative damage and PKC expression could in part induce insulin resistance and CA has beneficial impact on liver during insulin resistance with modulatory effects at the post-receptor level.

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.

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 ofl-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. [ABSTRACT FROM AUTHOR]

Recently we showed that the administration of intraperitoneal L-carnitine (CA) has insulin-sensitizing effects in the high fructose-fed Wistar rat, a widely used model of metabolic syndrome. The present study was conducted to examine the regulatory effects of CA on blood pressure (BP) and related pressor mechanisms. Fructose-fed rats (FFR) showed elevated BP, cardiac hypertrophy, glucose intolerance, and increases in plasma glucose, insulin, free fatty acids (FFA), and angiotensin-converting enzyme (ACE) activity. They also showed increased protein kinase C βII (PKC βII) expression and oxidative stress in cardiac tissue. In plasma, decreased kallikrein enzyme activity and nitric oxide metabolites were observed, compared to control. Simultaneous treatment with CA (300 mg/Kg) mitigated these alterations. PKC βII expression was similar to that of control; the rats displayed normal BP and ACE activity, enhanced antioxidant protection, and close to normal values of metabolic parameters. The BP-lowering effect of CA was abolished when CA-treated rats were administered L-nitroarginyl methyl ester (L-NAME 6g/Kg). These observations suggest that the BP-lowering action of CA in this model could be attributed to multiple and interrelated mechanisms, such as an increase in NO and kinin availability, reduction in PKC action, and antioxidant protection. [ABSTRACT FROM AUTHOR]