Postabsorptive muscle protein metabolism in type 1 diabetic patients afterpancreas transplantation

Citation
L. Luzi et al., Postabsorptive muscle protein metabolism in type 1 diabetic patients afterpancreas transplantation, ACT DIABETO, 37(4), 2000, pp. 219-224
Citations number
18
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
ACTA DIABETOLOGICA
ISSN journal
09405429 → ACNP
Volume
37
Issue
4
Year of publication
2000
Pages
219 - 224
Database
ISI
SICI code
0940-5429(200012)37:4<219:PMPMIT>2.0.ZU;2-3
Abstract
Insulin was shown to induce protein anabolism in vivo mainly by inhibiting proteolysis. Heterotopic pancreas transplantation in type 1 diabetes mellit us is characterized by peripheral hyperinsulinemia due to systemic rather t han portal insulin delivery. Therefore, we studied the postabsorptive muscl e protein metabolism in type 1 diabetic patients with or without pancreas t ransplantation. The forearm balance technique was performed in 9 type 1 dia betic patients on exogenous insulin treatment, in 4 type 1 diabetic patient s following successful pancreas transplantation and in 6 healthy volunteers . Labelled leucine and phenylalanine were infused to quantify whole-body an d muscle protein synthesis, respec tively. In the postabsorptive state, who le-body protein synthesis (leucine kinetics) was similar in pancreas-transp lanted patients and controls. In contrast, muscle protein synthesis tended to be less negative in pancreas-transplanted patients with respect to type 1 diabetic patients and healthy volunteers. The present data suggest that r ecipients with peripheral insulin delivery and chronic hyperinsulinemia are characterized by a preferential stimulation of protein synthesis in muscle rather than in the splanchnic district. When insulin was infused acutely, while maintaining euglycemia, the whole-body and muscle protein synthesis r ates were approximately halved in type 1 diabetic patients with and without pancreas transplantation. We conclude that pancreas transplantation is abl e to normalize basal and insulin-stimulated protein metabolism. Chronic hyp erinsulinemia counteract steroid-induced protein degradation by means of a mild, but persistent stimulation of muscle protein synthesis.