The “glucose hypothesis,” which held that bringing ambient glucose levels into the near-normal range would help prevent the onset of diabetic complications, was first supported by findings from the Diabetes Control and Complications Trial.1 Intensive glucose control resulting in a mean glycated hemoglobin (HbA1c) level near 7% had discernible and sustained effects on both microvascular2-4 and macrovascular5 end points. An appeal of type 1 diabetes as a model for studying hyperglycemic effects is its clear-cut phenotype, in which autoimmune destruction of pancreatic beta cells causes hyperglycemia as the main triggering vascular insult at disease onset, typically unconfounded by other potential or established cardiovascular risk factors such as hyperinsulinemia, hyperlipidemia, and hypertension.
Florez JC. Insights From Monogenic Diabetes and Glycemic Treatment Goals for Common Types of Diabetes. JAMA. 2014;311(3):249–251. doi:10.1001/jama.2013.283981
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