Uremic 'toxins' and blood platelet carbohydrate metabolism.
The effect of various small and middle molecular substances on blood platelet glycolysis was studied in vitro. Creatinine inhibited glucose utilization only at a concentration of 30 mg/dl; no effect of urea was found. o-Hydroxyphenolic acid and guanidinosuccinic acid, which were supposed to interfere with platelet function, inhibited glucose utilization at concentrations found in plasma of patients with chronic renal failure (CRF). Inhibitor of glucose utilization (IGU) peptide of middle molecular weight was found to inhibit glucose utilization without affecting glycogenolysis or lactate production. No additive or potentiating effects were found when interaction of different substances was tested. The only exception was a potentiation of IGU action on platelet glucose utilization by creatinine at a concentration of 15 mg/dl. Impaired glucose metabolism caused by 'uremic toxins' may contribute to the pathogenesis of bleeding in CRF by affecting platelet function.
D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D002478:Cells, Cultured; D003404:Creatinine / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism*; D006019:Glycolysis / Q000187:drug effects; D006801:Humans; D007773:Lactates / Q000096:biosynthesis; D010455:Peptides / Q000494:pharmacology; D014508:Urea / Q000494:pharmacology; D014511:Uremia / Q000378:metabolism*
D007773:Lactates; D010455:Peptides; C010169:glucose utilization inhibitor; D014508:Urea; D003404:Creatinine; D005947:Glucose