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Effect of carnosine alone or combined with alpha-tocopherol on hepatic steatosis and oxidative stress in fructose-induced insulin-resistant rats
Giriþ, Murat; Doðru-Abbasoðlu, Semra; Kumral, Alkýn; Koçak-Toker, Necla; Uysal, Müjdat; Olgaç, Vakur.
Afiliação
  • Giriþ, Murat; Istanbul University. Institute for Experimental Medicine. Department of Neuroscience. Istanbul. Turkey
  • Doðru-Abbasoðlu, Semra; Istanbul University. Istanbul Faculty of Medicine. Department of Biochemistry. Istanbul. Turkey
  • Kumral, Alkýn; Istanbul University. Istanbul Faculty of Medicine. Department of Biochemistry. Istanbul. Turkey
  • Koçak-Toker, Necla; Istanbul University. Istanbul Faculty of Medicine. Department of Biochemistry. Istanbul. Turkey
  • Uysal, Müjdat; Istanbul University. Istanbul Faculty of Medicine. Department of Biochemistry. Istanbul. Turkey
  • Olgaç, Vakur; Istanbul University. Oncology Institute. Department of Pathology. Istanbul. Turkey
J. physiol. biochem ; 70(2): 385-395, jun. 2014.
Artigo em Inglês | IBECS | ID: ibc-122960
Biblioteca responsável: ES1.1
Localização: BNCS
ABSTRACT
A diet high in fructose (HFr) induces insulin resistance in animals. Free radicals are involved in the pathogenesis of HFr-induced insulin resistance. Carnosine (CAR) is a dipeptide with antioxidant properties. We investigated the effect of CAR alone or in combination with α-tocopherol (CAR + TOC) on HFr-induced insulin-resistant rats. Rats fed with HFr containing 60 % fructose received CAR (2 g/L in drinking water) with/without TOC (200 mg/kg, i.m. twice a week) for 8 weeks. Insulin resistance, serum lipids, inflammation markers, hepatic lipids, lipid peroxides, and glutathione (GSH) levels together with glutathione peroxidase (GSH-Px) and superoxide dismutase 1 (CuZnSOD; SOD1) activities and their protein expressions were measured. Hepatic histopathological examinations were performed. HFr was observed to cause insulin resistance, inflammation and hypertriglyceridemia, and increased triglyceride and lipid peroxide levels in the liver. GSH-Px activity and expression decreased, but GSH levels and SOD1 activity and expression did not alter in HFr rats. Hepatic marker enzyme activities in serum increased and marked macro- and microvesicular steatosis were seen in the liver. CAR treatment did not alter insulin resistance and hypertriglyceridemia, but it decreased steatosis and lipid peroxidation without any change in the antioxidant system of the liver. However, CAR + TOC treatment decreased insulin resistance, inflammation, hepatic steatosis, and lipid peroxidation and increased GSH-Px activity and expression in the liver. Our results may indicate that CAR + TOC treatment is more effective to decrease HFr-induced insulin resistance, inflammation, hepatic steatosis, and dysfunction and pro-oxidant status in rats than CAR alone
Assuntos
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Coleções: Bases de dados nacionais / Espanha Base de dados: IBECS Assunto principal: Carnosina / Síndrome Metabólica / Tocoferóis / Fígado Gorduroso Limite: Animais Idioma: Inglês Revista: J. physiol. biochem Ano de publicação: 2014 Tipo de documento: Artigo Instituição/País de afiliação: Istanbul University/Turkey
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Coleções: Bases de dados nacionais / Espanha Base de dados: IBECS Assunto principal: Carnosina / Síndrome Metabólica / Tocoferóis / Fígado Gorduroso Limite: Animais Idioma: Inglês Revista: J. physiol. biochem Ano de publicação: 2014 Tipo de documento: Artigo Instituição/País de afiliação: Istanbul University/Turkey
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