Plasma free fatty acid concentrations (FFA) in chronic schizophrenia before and after insulin stimulation

Abstract

NUMEROUS investigations have suggested various abnormalities of carbohydrate metabolism in schizophrenic patients. A number of authorsclp”) have described a delayed or decreased response of blood glucose to injected insulin in schizophrenic patients. Others have noted decreased oral glucose tolerance,( l, O) or intravenous glucose tolerancecl, i, in certain patients. Two studiesc4, 5, have described abnormal Exton-Rose glucose tolerance tests in schizophrenic patients resembling diabetic curves after the second glucose load. In 1942, an anti-insulin effect of the plasma of certain schizophrenic patients was described(s) in which rabbits injected with insulin plus the plasma of schizophrenic patients had a smaller drop in blood glucose than did animals given equal amounts of insulin and normal plasma. Extracts of urine of schizophrenic subjects injected into rabbits intraperitoneallyc”) appeared to cause sustained elevation of blood glucose over a 4-hr period in the majority of animals while such sustained elevation was not observed when the same animals received extracts of normal urine. WALKER and MAYER-GROSS(‘@ in 1951 confirmed this hyperglycemic factor and associated the potency of the extract with the amount of amino acids in it. MORGAN and PILGRIM in 1952(ll) again confirmed the presence of a hyperglycemic factor in schizophrenic urine. MEDUNA and MCCULLKK(~~) defined a subgrouping of schizophrenia called “oneirophrenia” by certain psychiatric and physiologic criteria. Confusion and clouding of the sensorium clinically separated the patient with “oneirophrenia” from other schizophrenic patients. Moreover, three abnormalities were noted typically within this group: delayed or decreased glucose response to injected insulin, the urinary hyperglycemic factor, and decreased tolerance to oral and intravenous glucose. MAYER-GROSS(~) in 1952 confirmed the presence of these abnormalities in many schizophrenic patients, but could not demonstrate that they were more frequent in any clinical subtype or that they occurred together with more than random frequency. Other changes have been noted in the carbohydrate metabolism of schizophrenic patients. HENNEMAN et NI.(~:~) described abnormal changes in citric acid, a-ketoglutaric acid, inorganic