A role for zinc in pancreatic islet ß-cell cross-talk with the α-cell during hypoglycaemia.
Diabetes Obes Metab
; 13 Suppl 1: 106-11, 2011 Oct.
Article
en En
| MEDLINE
| ID: mdl-21824263
Signalling by intraislet ß-cells to neighbouring α-cells was recognized almost 40 years ago, leading to the hypothesis that this is an essential mechanism to regulate the glucagon counterregulatory response to hypoglycaemia. The thesis was that during normoglycaemia or hyperglycaemia insulin secretion from ß-cells would enter the islet periportal circulation and travel downstream to α-cells to dampen glucagon secretion. As a corollary, during hypoglycaemia ß-cells would stop secreting insulin, which would permit α-cells to release glucagon into the hepatic portal circulation so it could travel to the liver to increase glucose production and thereby correct hypoglycaemia. This mini-review briefly mentions the early work that established this hypothesis and more extensively examines more recent work that has provided direct evidence supporting the hypothesis. A new twist has been introduced based on the fact that zinc is bound to insulin within ß-cells and co-secreted with insulin. Zinc is released from insulin when it reaches the higher pH of blood, and zinc has recently been shown to negatively regulate α-cell secretion. It is now suggested that a switch-off signal provided by a sudden cessation of zinc secretion from ß-cells during hypoglycaemia may play a critical role in stimulating glucagon secretion that is independent of the effect of insulin.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Zinc
/
Transducción de Señal
/
Comunicación Celular
/
Células Secretoras de Glucagón
/
Células Secretoras de Insulina
/
Hipoglucemia
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Diabetes Obes Metab
Asunto de la revista:
ENDOCRINOLOGIA
/
METABOLISMO
Año:
2011
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Reino Unido