Role of Ca2+ in adrenocorticotropic hormone-stimulated lipolysis in the perfused fat cell system.

The role of Ca2+ in adrenocorticotropic hormone (ACTH)stimulated lipolysis in rat adipocytes was investigated using perifused fat cells. With this system, it is possible to monitor minute-to-minute changes in glycerol release from adipocytes during both the activation and inactivation phases of hormone-induced lipolysis. The lipolytic response to ACTH was dose-dependent and 0.1 unit per ml of ACTH produced the maximal lipolytic response. Unlike the response observed with other lipolytic polypeptide hormones and with catecholamines, cessation of ACTH infusion did not result in a return of lipolysis to the basal value, rather, maximal rates of lipolysis were maintained. During this period of maintained lipolytic response after the termination of ACTH administration, the infusion of EGTA (1 mM), or the perifusion with Ca2f-free buffer caused the lipolytic rate to return to basal value. When the lipolytic response was tested in Ca2+-free buffer, the maximal rate of ACTH-stimulated lipolysis was decreased 45% and the rate returned to the basal value after the termination of ACTH infusion. On the basis of the present findings it is speculated that a part of the ACTH-stimulated lipolysis in rat adipocytes may be Ca2+-independent and that Ca2f exerts a role in the binding of ACTH to its membrane receptor.