Influence of captopril on glucose and fatty acid oxidation in human thrombocytes and mononuclear leucocytes.
Captopril (CAS 62571-86-2) may be beneficial for the treatment of diabetes because of its activating effect on peripheral glucose consumption besides its well known blood pressure degradation. The glucose oxidation has been found to be activated by captopril in thrombocytes and mononuclear leucocytes, cell types which are usually considered to be independent from insulin. Because the oxidation of pyruvate labelled in position C-1 but not of 2-14C-pyruvate and of 1-14C-acetate was enhanced, captopril most probably stimulated the pyruvate decarboxylation reaction. The metabolism of glucose labelled in positions 1 and 6 was equally activated by captopril indicating another step which may be affected by captopril.
Haeckel
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R
Institut für Laboratoriumsmedizin, Bremen, Fed. Rep. of Germany.
Colic
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D
D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D002216:Captopril / Q000494:pharmacology*; D002245:Carbon Dioxide / Q000378:metabolism; D005227:Fatty Acids / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D066298:In Vitro Techniques; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism*; D010084:Oxidation-Reduction
D005227:Fatty Acids; D002245:Carbon Dioxide; D002216:Captopril; D005947:Glucose