This project examines the hypothesis that kidney failure causes patients to react so that they are more catabolic, i.e. loss more body protein in response to the stress of fasting than normal people. It also examines how hormones - insulin, adrenalin, and adrenal steroid hormones - act to control muscle protein in uremia. The proposed studies use an experimental model we have developed in which rat muscle from one leg can be perfused ndependently of the other. Because these two behave the same under control conditions, we can be much more precise in measuring hormone regulation of muscle metabolism. We will examine specifically insulin control over glucose and amino acid uptake by muscle and its control of protein synthesis over a range of insulin levels so that a dose response curve can be developed for normals and a comparative one developed for uremic rats. Adrenalin and adrenal steroid will be studied in the same way a) without and b) with insulin.
NIH ExPorter
NIH ExPorter