Showing papers by "K. G. M. M. Alberti published in 1990"

Determining diabetes prevalence: a rational basis for the use of fasting plasma glucose concentrations?

Abstract: The World Health Organization and the National Diabetes Data Group each recommend a diagnostic cut-off point for diabetes of 7.8 mmol l−1 for fasting plasma glucose concentrations as part of the diagnostic criteria for epidemiological studies. However, this cut-off has been shown to be insensitive compared with a screening test based on 2-h plasma glucose levels. In thirteen Pacific populations, from four ethnic groups (Asian Indian, Melanesian, Micronesian, and Polynesian), we have examined whether a different cut-off point for fasting plasma glucose would be more accurate for obtaining an estimate of the prevalence of diabetes when compared with 2-h levels. A fasting plasma glucose diagnostic cut-off of 7.0 mmol l−1 gave an estimate of prevalence not significantly different from that based on the 2-h plasma glucose in 12 of the 13 populations (mean difference 0.27, range −1.51 to +2.44,%). On the other hand, when a cut-off of 7.8 mmol l−1 for fasting plasma glucose was used, the resulting prevalence over-estimated the 2-h glucose prevalence in all populations (mean difference 1.91, range 0.14–5.80,%). Thus for Pacific populations, a fasting plasma glucose cut-off of 7.0 mmol l−1 provides estimates of prevalence that are equivalent to those based on 2-h plasma glucose levels. In epidemiological studies designed to estimate diabetes prevalence, we recommend use of a fasting plasma glucose cut-off of 7.0 mmol l−1 in preference to a detection level of 7.8 mmol l−1, if glucose loading is not possible. The low sensitivity associated with the 7.0 mmol l−1 cut-off however, precludes its use as a definitive screening test for diabetes, particularly in the clinical setting.

Impaired glucose tolerance precedes but does not predict insulin-dependent diabetes mellitus: a study of identical twins.

Abstract: Non-diabetic identical twins of insulin-dependent diabetic patients were studied within five years of the diagnosis of their index twin in order to determine whether changes in intermediary metabolism precede the onset of insulin-dependent diabetes mellitus. Two studies were performed: a cross-sectional study of 12 non-diabetic twins and a prospective study of a separate group of 41 non-diabetic twins. Ofthe 12 twins tested in the cross-sectional study six developed insulin-dependent diabetes and six did not; the six who developed diabetes were given an oral glucose load a mean of 10 months before diagnosis; they then had normal fasting blood glucose levels but worse glucose tolerance than control subjects (120 min post-load (mean±SD) blood glucose 8.5±3.5 vs 4.9±0.9 mmol/l respectively, p<0.05). However, blood lactate, pyruvate, alanine, glycerol, 3-hydroxybutyrate and serum insulin levels were similar. In contrast, the six twins in this cross-sectional study who did not develop diabetes and are now unlikely to do so, as a group, had no significant changes compared with the control subjects though one had impaired glucose tolerance. To determine the predictive value of impaired glucose tolerance a separate group of 41 non-diabetic twins was studied prospectively for 8 to 22 years having a total of 147 glucose tolerance tests in this period; in this group six developed diabetes. Eight of the 41 had impaired glucose tolerance; impaired glucose tolerance was found in four of the six who developed diabetes as compared with only four of the 35 who did not (p<0.01). Impaired glucose tolerance in these non-diabetic identical twins had a positive predictive value of33% for developing diabetes. The four twins with impaired glucose tolerance who remain nondiabetic now have normal glucose tolerance. We conclude that impaired glucose tolerance may precede the onset of insulin-dependent diabetes mellitus by many months but the change does not specifically predict the disease even in identical twins of diabetic patients. These observations are consistent with the possibility that in some twins the disease process can occur yet remit without leading to diabetes.

The spectrum of pancreatic exocrine and endocrine (beta-cell) function in tropical calcific pancreatitis.

Abstract: Exocrine pancreatic marker (immunoreactive-trypsin) and endocrine Beta-cell function (plasma insulin and C-peptide during an oral glucose tolerance test) were studied in 40 subjects with tropical-calcific-pancreatitis [seven non-diabetic, seven with impaired-glucose-tolerance and 26 diabetic (fibro-calculous-pancreatic-diabetes)]. In non-diabetic and impaired-glucose-tolerance subjects there was evidence of active pancreatitis in some and exocrine function was partially preserved. Fibro-calculous-pancreatic-diabetic subjects showed severely diminished exocrine pancreatic function; none showed ‘pancreatitic’ elevation of immunoreactive-trypsin. Beta-cell function was preserved in non-diabetic and impaired-glucose-tolerance subjects; diabetic subjects showed variable Beta-cell function but it was severely diminished in more than 75%. Immunoreactive-trypsin and C-peptide were directly correlated (rs=0.55, p<0.01). This cross sectional study demonstrates, for the first time, that the Beta-cell loss in tropical-calcific-pancreatitis is related to the exocrine loss. It suggests that diabetes in tropical-calcific-pancreatitis is either secondary to pancreatitis or that a common factor(s) acts simultaneously on both components.

Total-body potassium in insulin-dependent diabetes mellitus.

Abstract: 1. Total-body potassium and fat-free mass have been measured in 31 insulin-dependent diabetic patients and 31 age- and sex-matched normal volunteers. 2. Body mass index was significantly higher in the insulin-dependent diabetic patients (24.7 +/- 0.5 vs 23.3 +/- 0.4 kg/m2; P = 0.05). 3. Total-body potassium, uncorrected and corrected for weight and for fat-free mass, was not significantly different in the two groups (3281 +/- 141 mmol, 47.3 +/- 1.3 mmol/kg body weight, 60.9 +/- 1.0 mmol/kg fat-free mass, and 3315 +/- 143 mmol, 48.6 +/- 1.0 mmol/kg body weight, 60.4 +/- 0.8 mmol/kg fat-free mass, respectively, in diabetic patients and non-diabetic subjects). There was no relationship between blood glucose control, as assessed by glycated haemoglobin concentrations, and total-body potassium. 4. These results suggest, by contrast with previous reports, that in insulin-dependent diabetic patients, showing varying degrees of glycaemic control (glycated haemoglobin range 6.1-15.3%, mean 9.0%) that: (a) there is no significant abnormality of body potassium homoeostasis, and (b) there is no relation between total-body potassium and glycaemic control.

The metabolic effects of aspirin in fasting and fed subjects: relevance to the aetiology of Reye's Syndrome

Abstract: As a possible model for the mechanism of precipitation of Reye's Syndrome in children the metabolic effects of oral aspirin were studied in normal subjects in the fasted and fed states, to determine whether aspirin altered fatty acid oxidation. Starvation increased blood 3-hydroxybutyrate concentrations, but aspirin had no effect on this or other metabolite concentrations in either the fasted or fed states.