Normal Plasma Glucose Levels Research Articles

INCREASED FREQUENCY OF DIABETES MELLITUS IN PATIENTS WITH HUNTINGTON'S CHOREA

Six of ten patients with documented Huntington's chorea had an unusual form of diabetes mellitus characterised by marked hyperglycæmia, resistance to ketosis, absence of glycosuria, and markedly elevated insulin levels in response to the administration of glucose or arginine. Four patients (group I) had normal fasting plasma glucose and insulin levels and a normal response to the glucose-tolerance test (G.T.T.). The other six (group II) had normal fasting glucose levels but slightly elevated fasting insulin levels; the G.T.T. was abnormal. In group I arginine resulted in normal glucose and insulin rise, and peak insulin at 30 minutes was 44·0±6·1 μU. per ml. In group II, despite a similar degree of glucose elevation after arginine, peak insulin at 30 minutes was 96·3±21·3 μU. per ml. Clinically no correlation other than duration of disease could be made with the metabolic findings. Whether these data may be explained by an abnormal genetic linkage between Huntington's chorea and carbohydrate intolerance, or by a primary imbalance of biogenic amines, is not yet established.

Reduced brain glucose with normal plasma glucose in salicylate poisoning.

After the intraperitoneal injection into young mice of 700-800 mg/kg of salicylate, brain glucose fell to one-third or less of control values despite normal plasma glucose levels; brain lactate was nearly doubled and there were small decreases in phosphocreatine (18%) and in glycogen (17%). ATP, pyruvate, alpha-ketoglutarate, and glutamate were unchanged. In liver, glycogen was reduced 79% and lactate was five times higher than in control animals; glucose, glucose-6-phosphate, and ATP were unchanged. Since salicylate uncouples oxidative phosphorylation, it is postulated that high energy phosphate in the brain is maintained near normal levels by a compensatory increase in cerebral glycolysis. Apparently the brain glucose level falls because the rate of utilization exceeds the rate at which glucose can be supplied from the blood. Concurrent administration of glucose with salicylate elevated brain glucose concentration and was associated with striking improvement in the condition and the increased survival of the animals. These findings stress the fact that in salicylate poisoning the supply of glucose to the brain may be inadequate even when blood glucose levels are normal.

Proximal tubular malfunction as a mechanism for diuresis after renal homotransplantation.

Four patients who received renal homografts were studied during the first 24 hours after operation to determine the mechanisms of the post-transplantation diuresis. The marked diuresis was associated with decreased tubular reabsorption of sodium and glucose. Fractional excretion of filtered sodium reached values as high as 0.12 to 0.21, and fractional excretion of glucose achieved values as high as 0.10 at normal plasma glucose levels. The marked natriuresis and glycosuria subsided or improved spontaneously despite meticulous replacement of all renal and extrarenal fluid and electrolyte losses. In two subjects who excreted a hypotonic urine, free water excretion during the natriuresis rose to values as high as 12 to 20 percent of the glomerular filtration rate. Excreted potassium exceeded filtered potassium in two subjects. The data indicate that the early post-transplantation diuresis is due primarily to intrinsic defects in the proximal tubular transport systems for sodium and glucose whereas the transport systems in the distal nephron are relatively intact.