Protein, amino acid metabolism and therapy: Edited by Erich Roth and Paul B. PencharzEffect of insulin on whole body protein metabolism in children with type 1 diabetesCaso, Giuseppe; McNurlan, Margaret A Author Information Department of Surgery, Stony Brook University Medical Center, Stony Brook, New York, USA Correspondence to Giuseppe Caso, MD, PhD, Department of Surgery, HSC T19-048, Stony Brook University Medical Center, Stony Brook, NY 11794-8191, USA Tel: +1 631 444 1790; fax: +1 631 444 8947; e-mail: [email protected] Current Opinion in Clinical Nutrition and Metabolic Care: January 2010 - Volume 13 - Issue 1 - p 93-96 doi: 10.1097/MCO.0b013e328333294d Buy Metrics Abstract Purpose of review Untreated type 1 diabetes (T1D) is associated with abnormalities in protein metabolism, leading to protein loss. These alterations can be particularly detrimental in children, affecting both normal growth and development. A better understanding of the effects of insulin on protein metabolism in children with T1D is essential for optimizing therapy and minimizing consequences of the disease. The aim of the present review is to outline the effects of insulin on whole body protein metabolism in T1D, focusing particularly on studies in children with T1D. Recent findings Whole body protein degradation and amino acid oxidation are enhanced in children with T1D. Insulin reduces the rates at which body proteins are degraded. Whole body protein synthesis is either unaffected or reduced by insulin, even when insulin is administered together with amino acids to prevent insulin-dependent hypoaminoacidemia. Provision of insulin with oral nutrients improves protein balance by inhibiting whole body protein degradation, but does not affect protein synthesis. Summary In children with T1D the anticatabolic effects of insulin on whole body protein metabolism are mainly exerted through a reduction in rates at which body proteins are degraded. Nutritional factors enhancing the anabolic effect of insulin need to be further elucidated. © 2010 Lippincott Williams & Wilkins, Inc.