title: Carbohydrate metabolism in uremia.
abstract: Abnormalities of insulin and glucose metabolism, namely glucose intolerance, inhibition of insulin secretion and insulin resistance, are present in children with chronic renal failure. Insulin resistance is universal among children with end-stage renal disease and may be caused by uremic toxins accumulated because of reduced renal function. The normal response of the beta cell is to enhance insulin secretion to overcome the insulin resistance. In patients with secondary hyperparathyroidism, this increase in insulin secretion is inhibited, resulting in glucose intolerance. Presence of glucose intolerance may be responsive for the growth retardation in uremic children. Improvements in glucose tolerance correlate with improvements in linear growth in uremic children. Further research should be directed towards investigation of the mechanisms by which abnormal energy utilization may affect growth in uremia and development of indices of glucose metabolism as predictors of growth in uremia.
authors.affiliation: Division of Nephrology, Childrens Hospital of Los Angeles, University of Southern California School of Medicine 90054-0700.
authors.forename: R H
authors.initials: RH
authors.lastname: Mak
mesh_terms: D001692:Biological Transport; D050260:Carbohydrate Metabolism; D002241:Carbohydrates / Q000502:physiology; D002648:Child; D002657:Child Development; D002675:Child, Preschool; D002149:Energy Intake; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism / Q000502:physiology; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D010281:Parathyroid Hormone / Q000378:metabolism; D011972:Receptor, Insulin / Q000378:metabolism; D014511:Uremia / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D002241:Carbohydrates; D007328:Insulin; D010281:Parathyroid Hormone; D011972:Receptor, Insulin; D005947:Glucose