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.
Subject(s)
Animals , Freeze Fracturing , Glucose/pharmacology , Intercellular Junctions/drug effects , Islets of Langerhans/drug effects , Male , Protein Deficiency/pathology , Rats , Rats, Inbred StrainsABSTRACT
El número de uniones estrechas intercelulares fue cuantificado en islotes aislados de rata, incubados durante diferentes lapsos en un medio conteniendo distintas concentraciones de glucosa. El número de uniones estrechas aumentó en función de la duración de la incubación y de la concentración de glucosa en el medio. Estos resultados sugerirían la participación de las uniones estrechas en la regulación de la secreción de insulina en respuesta a la glucosa