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Randomized Controlled Trial
. 2010 Jul;33(7):1591-7.
doi: 10.2337/dc10-0013.

Effects of acute insulin-induced hypoglycemia on indices of inflammation: putative mechanism for aggravating vascular disease in diabetes

Rohana J Wright  1 , David E Newby, David Stirling, Christopher A Ludlam, Ian A Macdonald, Brian M Frier
Affiliations
Randomized Controlled Trial

Effects of acute insulin-induced hypoglycemia on indices of inflammation: putative mechanism for aggravating vascular disease in diabetes

Rohana J Wright et al. Diabetes Care. 2010 Jul.

Abstract

Objective: To examine the effects of acute insulin-induced hypoglycemia on inflammation, endothelial dysfunction, and platelet activation in adults with and without type 1 diabetes.

Research design and methods: We studied 16 nondiabetic adults and 16 subjects with type 1 diabetes during euglycemia (blood glucose 4.5 mmol/l) and hypoglycemia (blood glucose 2.5 mmol/l). Markers of inflammation, thrombosis, and endothelial dysfunction (soluble P-selectin, interleukin-6, von Willebrand factor [vWF], tissue plasminogen activator [tPA], high-sensitivity C-reactive protein [hsCRP], and soluble CD40 ligand [sCD40L]) were measured; platelet-monocyte aggregation and CD40 expression on monocytes were determined using flow cytometry.

Results: In nondiabetic participants, platelet activation occurred after hypoglycemia, with increments in platelet-monocyte aggregation and P-selectin (P <or= 0.02). Inflammation was triggered with CD40 expression increasing maximally at 24 h (3.13 +/- 2.3% vs. 2.06 +/- 1.0%) after hypoglycemia (P = 0.009). Both sCD40L and hsCRP (P = 0.02) increased with a nonsignificant rise in vWF and tPA, indicating a possible endothelial effect. A reduction in sCD40L, tPA, and P-selectin occurred during euglycemia (P = 0.03, P <or= 0.006, and P = 0.006, respectively). In type 1 diabetes, both CD40 expression (5.54 +/- 4.4% vs. 3.65 +/- 1.8%; P = 0.006) and plasma sCD40L concentrations increased during hypoglycemia (peak 3.41 +/- 3.2 vs. 2.85 +/- 2.8 ng/ml; P = 0.03). Platelet-monocyte aggregation also increased significantly at 24 h after hypoglycemia (P = 0.03). A decline in vWF and P-selectin occurred during euglycemia (P <or= 0.04).

Conclusions: Acute hypoglycemia may provoke upregulation and release of vasoactive substances in adults with and without type 1 diabetes. This may be a putative mechanism for hypoglycemia-induced vascular injury.

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Figures

Figure 1
Figure 1
A: Blood glucose concentrations during hyperinsulinemic hypoglycemic and euglycemic clamp studies. B: Epinephrine responses to experimental procedures.i. nondiabetic subjects; ii. subjects with type 1 diabetes.
Figure 2
Figure 2
Platelet activation in response to experimental hypoglycemia and euglycemia. A: Platelet-monocyte aggregation. B: Soluble P-selectin, i. Nondiabetic subjects, ii. Subjects with type 1 diabetes.
See this image and copyright information in PMC

Comment in

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