Data/hora: 13/06/2024 08:20:03

Provedor de dados: | 56
País: | Brazil
Título: | A high-fructose diet induces changes in pp185 phosphorylation in muscle and liver of rats
Autores: | Ueno,M.; Bezerra,R.M.N.; Silva,M.S.; Tavares,D.Q.; Carvalho,C.R.; Saad,M.J.A.
Data: | 2000-12-01
Ano: | 2000
Palavras-chave: | Fructose; Insulin receptor; Pp185 phosphorylation.
Resumo: | Insulin stimulates the tyrosine kinase activity of its receptor resulting in the tyrosine phosphorylation of pp185, which contains insulin receptor substrates IRS-1 and IRS-2. These early steps in insulin action are essential for the metabolic effects of insulin. Feeding animals a high-fructose diet results in insulin resistance. However, the exact molecular mechanism underlying this effect is unknown. In the present study, we determined the levels and phosphorylation status of the insulin receptor and pp185 (IRS-1/2) in liver and muscle of rats submitted to a high-fructose diet evaluated by immunoblotting with specific antibodies. Feeding fructose (28 days) induced a discrete insulin resistance, as demonstrated by the insulin tolerance test. Plasma glucose and serum insulin and cholesterol levels of the two groups of rats, fructose-fed and control, were similar, whereas plasma triacylglycerol concentration was significantly increased in the rats submitted to the fructose diet (P&lt;0.05). There were no changes in insulin receptor concentration in the liver or muscle of either group. However, insulin-stimulated receptor autophosphorylation was reduced to 72 ± 4% (P&lt;0.05) in the liver of high-fructose rats. The IRS-1 protein levels were similar in both liver and muscle of the two groups of rats. In contrast, there was a significant decrease in insulin-induced pp185 (IRS-1/2) phosphorylation, to 83 ± 5% (P&lt;0.05) in liver and to 77 ± 4% (P&lt;0.05) in muscle of the high-fructose rats. These data suggest that changes in the early steps of insulin signal transduction may have an important role in the insulin resistance induced by high-fructose feeding.
Tipo: | Info:eu-repo/semantics/other
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2000001200004
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/S0100-879X2000001200004
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.33 n.12 2000
Fonte: | info:eu-repo/semantics/openAccess