We appreciate the comments of Dhatariya (1) in this issue of Diabetes Care. Clearly, insulin is the ultimate anabolic hormone that may not only keep inflammation at bay, but also regulate the appropriate utilization of metabolites such that it conserves protein and fat and prevents their breakdown. Its usefulness in preventing protein catabolism in the clinical setting was demonstrated in the 1980s. The key studies of Nair and colleagues (2,3) referred to by Dhatariya provide the scientific basis for this important insulin action. The next challenge is to determine how inflammation induces a state of protein catabolism and exactly how insulin exerts its beneficial effects against the background of inflammation.

It is also worth mentioning two other key actions of insulin described recently: 1) apo E−/− mice that develop atherosclerosis suppress this process when given insulin (4), and 2) insulin suppresses reperfusion-induced myocardial damage following ischemia in isolated rat heart, as well as reduces myocardial apoptosis (5).

We believe this is just the beginning of a new era in understanding insulin action beyond the conventional biochemical/metabolic paradigm that we have been accustomed to for the first 80 years of its life. As discussed in our commentary, as we understand more about these novel actions of insulin, its clinical application will expand.

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Dhatariya K: Hyperglycemia after myocardial infarction (Letter).
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Nair KS, Ford GC, Ekberg K, Fernqvist-Forbes E, Wahren J: Protein dynamics in whole body and in splanchnic and leg tissues in type I diabetic patients.
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Shamir R, Shehadeh N, Rosenblat M, Eshach-Adiv O, Coleman R, Kaplan M, Hamoud S, Lischinsky S, Hayek T: Oral insulin supplementation attenuates atherosclerosis progression in apolipoprotein E-deficient mice.
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