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Biomedical subjects

G M Alberti

Publications and source records attributed to G M Alberti.

6 recordsLinked to original sources
PubMed1991

Study in Tanzania of impaired glucose tolerance. Methodological myth?

During a study of diabetes prevalence in six rural Tanzanian communities, a repeat oral glucose tolerance test (OGTT) was carried out in 514 subjects greater than or equal to 15 yr of age within 1 wk of an initial 75-g OGTT. In 498 subjects, blood glucose was measured 2 h after the glucose load on both occasions, and in 175 subjects, fasting blood glucose measurement was also repeated. Of the 498 subjects, 245 had normal glucose tolerance in the first test and were selected at random for further testing; 223 subjects had impaired glucose tolerance (IGT), and 30 had diabetic values. Diabetes and IGT were diagnosed on the basis of the 2-h blood glucose values. In the second test, 241 (98.4%) of the 245 subjects with normal tolerance continued in this category and 4 (1.6%) showed IGT. Of the 223 with IGT in the first test, 171 (76.2%) reverted to normal on the second test, 7 (3.1%) had diabetic values, and 45 (20.2%) persisted with IGT. Of the 30 subjects diagnosed as diabetic in the first test, 8 (26.7%) remained with diabetic values, 11 (36.7%) had IGT, and 11 (36.7%) were normal. Based on the second test, the population-prevalence rates of diabetes and IGT would have been 0.5 and 3.3% vs. 1 and 7.6% based on the first test. There was a significant downward trend in the mean 2-h blood glucose values in all three diagnostic groups. Regression toward the mean could not account for the downward shift in blood glucose values observed on retesting.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1977

Ketoacidosis in pancreatectomized man.

We investigated the importance of glucagon in the development of diabetic ketoacidosis by withholding insulin from six patients with juvenile-type diabetes and four totally pancreatectomized subjects. Patients were fasting and had previously been maintained on intravenous insulin for 24 hours. In diabetic patients plasma glucagon concentrations rose sharply after withdrawal of insulin, and the increases were accompanied by a rise in blood ketone concentration of 4.1+/-0.7 (S.E.M.) and blood glucose concentration of 12.5+/-1.8 mmol per liter by 12 hours. In the pancreatectomized patients, despite the absence of measurable glucagon, blood ketones rose by 1.8+/-0.8 and blood glucose by 7.7+/-1.5 mmol per liter. Thus, glucagon is not essential for the development of ketoacidosis in diabetes, as has previously been suggested, but it may accelerate the onset of ketonemia and hyperglycemia in situations of insulin deficiency.

Acetoacetates↗
PubMed1977

Decrease in postprandial insulin and glucose concentrations by guar and pectin.

Postprandila glycaemia and rise in serum insulin after carbohydrate-containing meals were reduced by the addition of guar flour or pectin, or both. After a liquid test meal (four subjects) the 30-min blood glucose was reduced from 6.33 +/- 0.19 mmol/litre (114 +/- mg/dl), mean +/- SEM, in the control subjects of 4.77 +/- 0.17 mmol/litre (86 +/- 3 mg/dl) by addition of guar gum (P less than 0.05). The mean insulin level was also significantly lower at 15 min. A breakfast test meal (bread, butter, marmalade, and tea) resulted in a mean 15-min blood glucose of 6.18 +/- 0.21 mmol/litre (111 +/- 4 mg/dl) in eight subjects; 10 g of pectin added to the marmalade reduced this level to 5.64 +/- 0.17 mmol/litre (102 +/- 3 mg/dl) (P less than 0.01). The insulin levels were significantly lower at 15, 30, and 45 min. A similar meal in which guar was added to the bread and pectin to the marmalade resulted in significant reductions of blood glucose at 15 min (P less than 0.002) and 30 min (P less than 0.01). The insulin values were also significantly lower throughout the first 90 min of the test. This action of unavailable carbohydrate may prove useful in the dietary control of diabetes.

Adult↗
PubMed1977

A kinetic spectrophotometric assay for rapid determination of acetoacetate in blood.

We describe an automated kinetic assay for acetoacetate in blood. Acetoacetate is enzymatically reduced to D-beta-hydroxybutyrate and the reaction is monitored for 60 s with a reaction-rate analyzer. This technique allows low concentrations of acetoacetate to be measured with good precision and overcomes many of the problems associated with other automated techniques. Our studies on the stability of acetoacetate emphasize the need for care in handling specimens. The use of a reaction-rate analyzer, an item of equipment common to most laboratories, allows for rapid handling of samples in small or large batches, depending on the needs of the laboratory.

Acetoacetates↗