A G Beckett

Cerebral blood flow in diabetes mellitus: evidence of abnormal cerebrovascular reactivity.

Cerebral blood flow (CBF) was studied at normocapnia and after a challenge with 5% CO2 in 59 diabetic patients and 28 controls. There was a significant age-related decline in CBF in both groups, which suggests that diabetes does not affect the rate of decrease of CBF with age. After CO2 challenge CBF increased in most of the controls; in the patients CBF increased in 23, decreased in 26, and remained stable in 10. Thus the reactivity of cerebral blood vessels in diabetics is altered. Diabetics have diminished cerebrovascular reserve and are thus at increased risk of cerebrovascular disease because they are unable to compensate when necessary with an increased CBF.

Exocrine pancreatic function in diabetes mellitus.

An investigation of serum immunoreactive trypsin concentration and pancreatic isoamylase activity in patients with diabetes mellitus has shown that exocrine pancreatic deficit is maximal in insulin dependent diabetics, intermediate in those controlled with sulphonylureas, and absent in patients controlled with biguanides or diet or both. A significant correlation between the serum concentrations of both these pancreatic enzymes and C peptide was found. Serum pancreatic enzyme concentrations were not related to glycosylated haemoglobin concentrations, the dosage of insulin, or the age of onset of diabetes. The concentration of immunoreactive trypsin was found to be low in most of the insulin dependent diabetics in whom this enzyme was measured at the time of the clinical onset of diabetes. Thus exocrine pancreatic deficit in diabetes closely parallels the endocrine beta cell deficit and occurs concurrently with, or antedates, the clinical presentation of type I diabetes. It is therefore possible that in type I diabetes similar mechanisms are entailed in the pathogenesis of impaired endocrine and exocrine pancreatic function.

INSTABILITY OF CEREBRAL BLOOD-FLOW IN INSULIN-DEPENDENT DIABETICS

Cerebral blood-flow (CBF) was measured in 23 insulin-dependent diabetics before and 2--3 h after insulin/breakfast. In 10 of these patients CBF changed significantly during the day, with a significant fall in 9. In 3 patients who had the greatest falls in CBF there was a concomitant sensation of an impending faint. Thus CBF is unstable in insulin-dependent diabetics in contrast to control subjects in who there is little or no variation. Sudden falls in CBF in insulin-dependent diabetics may explain the symptoms of impending faint without hypoglycaemia; such falls would also be relevant to the pathogenesis of strokes in these patients.

Low pancreatic lipase in insulin-dependent diabetics.

Serum samples obtained from 20 insulin-dependent diabetics (IDD), 23 non-insulin-dependent diabetics (NIDD) and 30 controls were assayed for their pancreatic lipase activity, immunoreactive trypsin concentration and glycosylated haemoglobin (HbA1) respectively. The distribution of serum pancreatic lipase activity in normal subjects and diabetics was nonparametric. The median serum lipase activity in IDDs (86 U/l) was significantly lower that that in controls (131 U/l, p less than 0.002) and NIDDs (126 U/l, p less than 0.001). There was a significant correlation between serum pancreatic lipase activity and serum IRT concentration (r = 0.65, p less than 0.001). Neither pancreatic lipase activity nor IRT was related to HbA1 concentrations. These data show for the first time that serum pancreatic lipase activity is diminished in IDDs.