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To the Editor: In his Commentary, Dr Unger¹ hypothesized that insulin therapy should be the treatment of last resort in patients with type 2 diabetes because exogenous hyperinsulinemia may increase ectopic lipid deposition in the skeletal muscle and other tissues in insulin-resistant states. The major mechanism proposed for this effect is the demonstration in leptin-deficient animals that insulin receptor substrate 2 is suppressed and the expression of sterol response element binding protein 1c (SREBP-1c) is increased in the liver by hyperinsulinemia. Unger concludes that these effects of insulin may contribute to insulin resistance and increased atherogenesis and potentially explain the higher mortality observed in the intensive arm of the ACCORD study.¹

In proposing this hypothesis, Unger did not consider that increased free fatty acids and not triglycerides are responsible for insulin resistance.² Insulin reduces concentrations of free fatty acids, and we are aware of no evidence that insulin leads to . . . [Full Text of this Article]

Paresh Dandona, MD, PhD
pdandona@kaleidahealth.org

Ajay Chaudhuri, MD; Husam Ghanim, PhD
Kaleida Health
Buffalo, New York

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Reinventing Type 2 Diabetes: Pathogenesis, Treatment, and Prevention
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