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Effects of Insulin-Induced Hypoglycemia on β₂-Adrenoceptor Density and Proliferative Responses of Human Lymphocytes^*

Zentrum für Innere Medizin, Medizinische Klinik und Poliklinik, Abteilung für Nieren- und Hochdruckkrankheiten, and the Institut für Immungenetik (H.G.-W., M.H.), Universität Essen D-4300 Essen
the Institut für Arterioskleroseforschung an der Universität Munster (H.J.B.) D-4400 Munster, West Germany

Address all correspondence and requests for reprints to: Dr. Otto-Erich Brodde, Biochemisches. Forschungslabor, Meditinische Klinik und Poliklinik, Abteilung für Nieren- und Hochdruckkrankheiten, Universität Essen, Hufelandstr. 55, D-4300 Essen 1, West Germany.

We studied the effects of insulin (0.1 IU/kg BW, iv)-induced hypoglycemia on lymphocyte β₂-adrenoceptor function, lymphocyte subset distribution, and proliferative response to mitogen stimulation in 10 healthy volunteers. Thirty minutes after insulin injection plasma glucose levels were markedly decreased; concomitantly, plasma epinephrine levels had increased about 10-fold; plasma norepinephrine levels, however, increased only moderately. Lymphocyte β₂-adrenoceptor density and the cAMP response to 10 µmol/L isoproterenol stimulation were elevated; lymphocyte T_8/c-cells had increased, whereas T_h-cells had decreased, resulting in a decrease in the T_h-/T_8/c-cell ratio from 1.7 to 1.0. These changes were accompanied by a significantly reduced lymphocyte proliferative response (measured as [³H]thymidine uptake) to mitogen stimulation. Two hours after insulin injection plasma catecholamines, lymphocyte β₂-adrenoceptor function, lymphocyte subset distribution, and proliferative responses had returned to nearly preinsulin levels. We conclude that acute vigorous increases in endogenous epineph-rine evoked by insulin-induced hypoglycemia are associated with increases in lymphocyte β₂-adrenoceptor function, redistribution of lymphocyte subsets, and an (at least transiently) attenuated in vitro immune responsiveness.

^* This work was supported by the Gesellschaft zur Erforschung und Bekämpfung des hohen Blutdrucks (Essen, West Germany).

Received December 6, 1989.