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The presence of glucagon receptors on human adipocytes has not yet been described. In this work we present an exceptional case of glucagon binding to human adipocytes taken from a malignant tumor of adipose tissue of a patient with a liposarcoma. Binding analysis revealed that the total number of glucagon receptors on liposarcoma-cells was 99,000 and the apparent receptor affinity (ED:50) was 5 x 10(-9) M. Despite the presence of these specific receptors, glucagon was unable to induce a lipolytic response, or to activate the adenylate-cyclase system in these liposarcoma-cells. Whether the induction of glucagon receptors is a specific process of the tumor biology remains to be elucidated.

Human adipocytes from patients with chronic endogenous hypercortisolism (Cushing's syndrome) showed a statistically significant decrease in insulin binding at low unlabelled-insulin concentrations but no change in receptor numbers (Cushing's 180,000 +/- 48,000 (3) receptors/cell and controls 189,000 +/- 30,000 (7)) together with a fourfold decrease in apparent receptor affinity (ED50: Cushing's 2.25 x 10(-9) M and controls 0.57 x 10(-9) M) and a decreased sensitivity to the antilipolytic effect of insulin. These events could represent the final situation of a chronic and endogenous regulation by high levels of cortisol of insulin receptors in human adipose tissue.

Insulin binding in adipocytes from patients with a phaeochromocytoma (PH) approached that of the controls (C) at low and higher concentrations of unlabeled insulin. The apparent receptor affinity was unchanged (ED50: PH 0.50 x 10(-9) M and C 0.60 x 10(-9) M). Scatchard analysis of the binding data using the negative cooperative model revealed a 46% decrease in the total number of receptors together with no changes in both K-e (PH 0.55 x 10(9) M-1 and C 0.36 x 10(9) M-1) and K-f (PH 0.13 x 10(9) M-1 and C 0.07 x 10(9) M-1). According to the two site model, an altered proportion in the two classes of insulin binding sites was detected. This was accompanied by a catecholamine-desensitization of the adipocytes to the antilipolytic action of insulin. These events could represent a final situation of a chronic and endogenous regulation by high levels of catecholamines of insulin receptors in human adipose tissue.