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Effects of Nonselective and β-1-Selective Blockade on Glucose Metabolism and Hormone Responses during Insulin-Induced Hypoglycemia in Normal Man^*

Medical Department C, Bispebjerg Hospital, Copenhagen, Denmark; and Department of Internal Medicine and Endocrinology, Herleu Hospital, Herleu, Denmark

Address requests for reprints to: Dr. J. Lyngsee, Medical Department C, Bispebjerg Hospital, 2400 Copenhagen NV, Denmark.

The effects of nonselective β-blockade (propranolol) and β-1-selective blockade (atenolol) on glucose metabolism during insulin-induced hypoglycemia were studied in eight normal subjects during constant infusion of 3-[³H]glucose. Propranolol and to a lesser extent atenolol prolonged the hypoglycemic response to insulin. After maximal hypoglycemia a significant increase in glucose uptake rate was seen after propranolol and a corresponding trend was found in the atenolol experiments. The two β-blockers did not influence glucose production rate after insulin administration.

FFA concentration declined rapidly after insulin. Propranolol delayed the subsequent normalization of FFA whereas atenolol had no significant effect.

Propranolol increased epinephrine and GH responses to hypoglycemia, whereas atenolol had no effect. Neither of the two β-blockers influenced the concentrations of glucagon, norepinephrine, and PRL.

It is concluded that nonselective β-blockade prolongs the hypoglycemic response to insulin through an increased tissue uptake of glucose which is not counteracted by an increased glucose production. It is suggested that nonselective β-blockade increases muscle glucose uptake by lowering FFA concentrations. β-Blocker inhibition of the antiinsulin effect of epinephrine on glucose uptake in muscle can, however, not be excluded. (J Clin Endocrinol Metab 56: 876, 1983)

^* This study was supported by grants from ICI.

Received January 6, 1982.

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