Insulin resistance in uraemia. An insulin receptor or an intracellular defect?
The present study was designed to determine the participation of a decreased insulin binding versus that of a post-binding defect in uraemic insulin resistance and to examine the possible effect of dialysis treatment. This was done by constructing an in vivo insulin dose-response curve using the euglycaemic clamp technique. We found that the maximal responsiveness to insulin was decreased in uraemic patients. Long-term dialysis treatment improved the maximum glucose metabolism significantly (7.7. +/- 0.7 mg/kg/min versus 10.7 +/- 0.6 mg/kg/min, p less than 0.01). On the contrary we found no clearcut alteration of the half-maximal insulin concentrations in relation to dialysis. In conclusion, this report indicates that the insulin resistance in uraemia is primarily due to post-binding defects, i.e. an impaired intracellular glucose metabolism or an abnormal glucose transport system.
D000328:Adult; D000368:Aged; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007333:Insulin Resistance; D008875:Middle Aged; D011972:Receptor, Insulin / Q000378:metabolism; D006435:Renal Dialysis; D014511:Uremia / Q000378:metabolism* / Q000628:therapy
D011972:Receptor, Insulin; D005947:Glucose