Insulin action on glucose transport in isolated cardiac myocytes: signalling pathways and diabetes-induced alterations.

Cholera toxin, in contrast to its stimulatory action on adenylate cyclase, renders the insulin-stimulated adipose cell insensitive to the inhibitory actions of lipolytic agents such as isoprenaline, adrenocorticotropic hormone or glucagon. Conversely, pertussis toxin eliminates both the stirnulatory actions of the antilipolytic agents, such as adenosine, nicotinic acid, and prostaglandin E , , on insulin-stimulated glucose transport activity and the ability of these agents to block the inhibitory actions of the lipolytic agents. Such observations are consistent with a direct involvement of G-proteins in the regulation of insulin-stimulated glucose transport. In addition to these direct mechanisms for the regulation o f glucose transport activity, the sensitivity of both the insulin and PMA responses is enhanced by antilipolytic agents and diminished by lipolytic agents. Thus, the acute regulation of glucose transport activity in the isolated adipose cell is subject t o multiple hormonal inputs which elicit their rcsponscs by different, but interactive mechanisms.