Nutrient toxicity in pancreatic beta-cell dysfunction.
J Physiol Biochem
; 56(2): 119-28, 2000 Jun.
Article
em En
| MEDLINE
| ID: mdl-11014617
ABSTRACT
Nutrients, such as glucose and fatty acids, have a dual effect on pancreatic beta-cell function. Acute administration of high glucose concentrations to pancreatic beta-cells stimulates insulin secretion. In addition, short term exposure of this cell type to dietary fatty acids potentiates glucose-induced insulin release. On the other hand, long-term exposure to these nutrients causes impaired insulin secretion, characterized by elevated exocytosis at low concentrations of glucose and no response when glucose increases in the extracellular medium. In addition, other phenotypic changes are observed in these conditions. One major step in linking these phenotypic changes to the diabetic pathology has been the recognition of both glucose and fatty acids as key modulators of beta-cell gene expression. This could explain the adaptative response of the cell to sustained nutrient concentration. Once this phase is exhausted, the beta-cell becomes progressively unresponsive to glucose and this alteration is accompanied by the irreversible induction of apoptotic programs. The aim of this review is to present actual data concerning the development of the toxicity to the main nutrients glucose and fatty acids in the pancreatic beta-cell and to find a possible link to the development of type 2 diabetes.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Ilhotas Pancreáticas
/
Diabetes Mellitus Tipo 2
/
Ácidos Graxos
/
Glucose
Limite:
Animals
/
Humans
Idioma:
En
Revista:
J Physiol Biochem
Assunto da revista:
BIOQUIMICA
/
FISIOLOGIA
Ano de publicação:
2000
Tipo de documento:
Article
País de afiliação:
Espanha