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Editorial
January 15, 2014

Insights From Monogenic Diabetes and Glycemic Treatment Goals for Common Types of Diabetes

Author Affiliations
  • 1Center for Human Genetic Research, Massachusetts General Hospital, Boston
  • 2Diabetes Research Center, Diabetes Unit, Massachusetts General Hospital, Boston
  • 3Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts
  • 4Department of Medicine, Harvard Medical School, Boston, Massachusetts
JAMA. 2014;311(3):249-251. doi:10.1001/jama.2013.283981

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 microvascular24 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.

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