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Beta-Adrenergic Blockade Effects on Glucose Counterregulation in Advanced T2DM and Beta-Cell Failure

At normoglycemia, beta-adrenergic blockade may cause increased insulin sensitivity…. 

Researchers theorized that beta-adrenergic blockade impairs glucose counterregulation in type 2 diabetes mellitus (T2DM) patients with advanced beta-cell failure, and tested this hypothesis by examining counterregulatory glucose kinetics in these patients.

Nine T2DM patients requiring insulin and six matched nondiabetic control subjects participated in this study. C-peptide response to arginine stimulation was used as a means of assessing their beta-cell function, and hyperinsulinemic euglycemic-hypoglycemic clamps with [3-3H] glucose infusion were used to assess their counterregulatory hormonal responses and glucose kinetics. The participants with T2DM were randomized to undergo two clamp experiments in a crossover method in which they were each infused with the beta-adrenergic antagonist propranolol once and normal saline once.

Results indicated that the T2DM patients had C-peptide responses to arginine stimulation that were decreased threefold in comparison with the control group. During the hypoglycemic clamp, glucagon responses were reduced significantly in the T2DM patients when compared to the control group, and endogenous glucose production (EGP) did not increase in the T2DM patients like it did in the control group however, systemic glucose disposal decreased normally, and other hormonal responses and the decrement in the required exogenous glucose infusion rate (GIR) from the euglycemic clamp to the hypoglycemic clamp were normal among both experimental and control groups. During the euglycemic clamp, beta-adrenergic blockade caused the GIR to increase in the T2DM patients by approximately 20% (p <0.01), but neither of the study groups had an increased GIR during the hypoglycemic clamp or a decreased decrement in GIR from the euglycemic clamp to the hypoglycemic clamp.

Based on these results, the researchers concluded that although the contribution of EGP was diminished in patients with advanced T2DM, their overall glucose conterregulation was preserved. At normoglycemia, beta-adrenergic blockade may cause increased insulin sensitivity, but it did not affect counterregulatory glucose kinetics in patients with T2DM, even if they were presenting with advanced beta-cell failure.

Practice Pearls:
  • This study indicates that glucose counterregulation was not impaired by beta-adrenergic blockade in patients with advanced type 2 diabetes mellitus and beta-cell failure.
  • However, beta-adrenergic blockade may decrease glucagon response and diminish endogenous glucose production in these patients.
  • At normoglycemia, beta-adrenergic blockade may also increase insulin sensitivity.

Bokhari S, Plummer E, Emmerson P, Gupta A, Meyer C. Glucose Counterregulation in Advanced Type 2 Diabetes Mellitus: Effect of beta-Adrenergic Blockade. Diabetes Care; 2014 Aug 4; pii: DC_140782 [Epub ahead of print].