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The Characterization of Catecholamine Stimulation of Glucose Transport by Rat Adipocytes and Isolated Plasma Membranes^*

CARL LUDVIGSEN, LEONARD JARETT and JAY M. McDONALD

Division of Laboratory Medicine, Departments of Pathology and Medicine, Washington University School of Medicine and Barnes Hospital St. Louis, Missouri 63110

Abstract

These studies were designed to resolve the controversy over the ability of catecholamines to stimulate glucose transport per se and not just glucose utilization in adipocytes. Glucose transport assays were performed using a dual label (3- O-[³H]methylglucose and L-[¹⁴C]glucose) procedure. Fifteenminute preincubations of intact adipocytes with epinephrine produced a 15% increase in specific 3-O-methylglucose transport at 5 x 10^–8 M, while a maximal stimulation of twice the control level was reached at 2.5 x 10^–7 M. This stimulation of glucose transport was inhibited 95% by 10^–5 M propranolol. Isoproterenol (10^–7 M) also stimulated 3-O-methylglucose transport, and this effect was completely blocked by 10^–5 M propranolol. Phenylephrine at maximal doses (5 x 10^–6 M) produced a marginal (20–30%) stimulation of transport which was only partially (50%) inhibited by phentolamine. Epinephrine and insulin stimulation of 3-O-methylglucose transport were compared, and the maximal stimulation of transport by epinephrine was 65% of that caused by 100 µU/ml insulin. Both insulin and epinephrine were capable of stimulating glucose transport in Krebs-Ringer bicarbonate buffers, but only insulin was effective in a Krebs-Ringer phosphate buffer.

Kinetic analysis was performed on specific D-glucose uptake at 1 sec into plasma membrane vesicles isolated from control or epinephrine-treated adipocytes. This revealed that epinephrine stimulation of glucose transport was due to a change in V_max (maximum velocity) with no change in the Km (substrate concentration producing V_max) of transport. (Endocrinology 106: 786, 1980)

Footnotes

^* Presented in part at the annual meeting of The Endocrine Society,Annaheim, CA, 1979. This work was supported by NIH Grants AM-11892, AM-20097, AM-20579, and GM-07200.

To whom requests for reprints should be addressed.

Received May 4, 1979.

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