Abstract
Clinical trials investigating whether glucose lowering treatment reduces the risk of CVD in diabetes have thus far yielded mixed results. However, this doesn't rule out the possibility of hyperglycemia playing a major causal role in promoting CVD or elevating CVD risk. In fact, lowering glucose appears to promote some beneficial long-term effects, and continuous glucose monitoring devices have revealed that postprandial spikes of hyperglycemia occur frequently, and may be an important determinant of CVD risk. It is proposed that these short, intermittent bursts of hyperglycemia may have detrimental effects on several organ systems including the vasculature and the hematopoietic system collectively contributing to the state of elevated CVD risk in diabetes. In this review, we summarize the potential mechanisms through which hyperglycemic spikes may increase atherosclerosis and how new and emerging interventions may combat this.
Highlights
The pathophysiological mechanisms through which individuals develop type 1 and type 2 diabetes are different, both conditions are characterized by elevated blood glucose levels and share a similar elevated risk of cardiovascular mortality [1]
Evidence suggests some reduction in cardiovascular disease (CVD) risk by long-term glucose lowering treatments in people with diabetes
Epidemiological research suggests that postprandial high glucose “spikes” as opposed to high average glucose levels are a more important determinant in CVD development in diabetes
Summary
The pathophysiological mechanisms through which individuals develop type 1 and type 2 diabetes are different, both conditions are characterized by elevated blood glucose levels and share a similar elevated risk of cardiovascular mortality [1]. If these individuals were grouped into the lowest (69–107 mg dL−1) vs the highest (150–194 mg dL−1) PBG, there was a 27% increased risk of CVD in those that had poorer PBG control These studies suggest that this association is a continuum for PBG, while for fasting plasma glucose levels there seemed to be a threshold effect at 100 mg/dL (5.6 mmol/L) [16]. We made the discovery that hyperglycemia impaired atherosclerotic lesion regression by promoting enhanced monocyte production from the bone marrow, causing their persistent entry into the atherosclerotic plaque [31] (Figure 2) This suggests that inflammatory changes in at least type 1 diabetes models are largely mediated by hyperglycemia, and not merely by changes in insulin or lipid levels.
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