Glucose modulation of gap junctions in the islets of Langerhans of protein malnourished rats.
Indian J Pathol Microbiol
;
1989 Jan; 32(1): 7-15
Artigo
em Inglês
| IMSEAR
| ID: sea-75484
ABSTRACT
It is believed that protein deficiency causes decreased insulin release in response to a glucose stimulus. We have recently shown that in prolonged protein deficiency, decreased insulin response to glucose is directly proportional to a decrease in the islet volume, suggesting no apparent defect in the insulin secretory mechanism in protein deficiency. It is documented that glucose-stimulated insulin release is closely related to an increase in the gap junctions of stimulated islet beta cells. In the present study, we show that the gap junctions of islets obtained from rats fed on a 4% protein diet were increased both in number and size following glucose treatment. This provided further proof that the mechanism to respond to glucose is not compromised in the endocrine tissue of the severely protein malnourished rats.
Texto completo:
DisponíveL
Índice:
IMSEAR (Sudeste Asiático)
Assunto principal:
Deficiência de Proteína
/
Ratos
/
Ratos Endogâmicos
/
Masculino
/
Ilhotas Pancreáticas
/
Técnica de Fratura por Congelamento
/
Glucose
/
Junções Intercelulares
/
Animais
Idioma:
Inglês
Revista:
Indian J Pathol Microbiol
Ano de publicação:
1989
Tipo de documento:
Artigo
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