Please use this identifier to cite or link to this item:
Type: Artigo de periódico
Title: Increased L-cpt-1 Activity And Altered Gene Expression In Pancreatic Islets Of Malnourished Adult Rats: A Possible Relationship Between Elevated Free Fatty Acid Levels And Impaired Insulin Secretion
Author: de Barros Reis M.A.
Arantes V.C.
Cunha D.A.
Latorraca M.Q.
Toyama M.H.
Carneiro E.M.
Boschero A.C.
Abstract: Intrauterine growth restriction is associated with chronically elevated levels of serum fatty acids and reduced glucose-stimulated insulin secretion. Lipid metabolism in pancreatic β cells is critical for the regulation of insulin secretion, and the chronic exposure to fatty acids results in higher palmitate oxidation rates and an altered insulin response to glucose. Using a rat model of isocaloric protein restriction, we examined whether pre- and postnatal protein malnutrition influences the properties of pancreatic islet carnitine palmitoyltransferase-1 (liver isoform, L-CPT-1), a rate-limiting enzyme that regulates fatty acid oxidation in mitochondria. The activity of L-CPT-1 in pancreatic islets increased in the low protein (LP), although the L-CPT-1 mRNA levels were unaffected by malnutrition. The susceptibility of enzyme to inhibition by malonyl-CoA was unaltered and the content of malonyl-CoA was reduced in LP cells. Because the mitochondrial oxidation of fatty acids is related to the altered expression of a number of genes encoding proteins involved in insulin secretion, the levels of expression of insulin and GLUT-2 mRNA were assessed. A reduced expression of both genes was observed in malnourished rats. These results provide further evidence that increased L-CPT-1 activity and changes in gene expression in pancreatic islets may be involved in the reduced insulin secretion seen in malnourished rats. © 2008.
Rights: fechado
Identifier DOI: 10.1016/j.jnutbio.2007.01.005
Date Issue: 2008
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.