No abstract

No abstract

No abstract

No abstract

SummaryMany mutagenic nitroso compounds are also diabetogenic. Betel-nut (Areca catechu) chewing populations have an increased incidence of foregut cancers related to betel-nut nitrosamines which suggests that betel consumption could be diabetogenic. Young adult CD1 mice with a low spontaneous incidence of diabetes were fed betel nut in standard feed for 2~5 days. Single point (90 min) intra-peritoneal glucose tolerance tests were used to follow glucose tolerance up to 6 months of age. Glucose intolerance was defined as over 3 SD above mean control values. Glucose intolerance was found in 3 of 51 male and 4 of 33 female adult mice which were fed the betel diet (p < 0.01). Studies on the progeny of these mice are presented separately for animals studied in Aberdeen (Group 1) and London (Group2). In matings of Group 1 betel-fed parents glucose intolerance was found in 4 of 25 male and 1 of 22 female F1 offspring, with significant hyperglycaemia in F1 males born to hyperglycaemic but not to normoglycaemic mothers (p < 0.01). In the F2 generation 4 of 23 males and 1 of 16 females and in the F3 generation 1 of 16 males and 0 of 20 females were glucose intolerant. In the Group 2 studies where betel-fed parents were mated to normal controls glucose intolerance was found in 10 of 35 male and 10 of 33 female F1 progeny (p < 0.005), and mean islet areas were increased in offspring of betel-fed parents (p < 0.001). The total incidence of glucose intolerance in F1 progeny from studies in Groups 1 and 2 was 14 of 60 males and 11 of 55 females (p < 0.005). Insulin dependence did not develop in the glucose-intolerant betel-fed animals or their descendants; affected animals appearing well built and active. The development of glucose intolerance in F1 offspring was not dependent on maternal glucose intolerance or on maternal betel-feeding, and 90-min glucose levels of F1 offspring were directly related to paternal but not to maternal glycaemia (p < 0.01). Our findings suggest that betelnut (Areca) consumption may be diabetogenic and induce an inheritable abnormality. The hypothesis is of interest in view of the widespread habit of betel consumption and of the strategies known to inhibit the induction of experimental diabetes by diabetogenic nitroso compounds. [Diabetologia (1994) 37: 49-55]

In a study of 10 diabetic patients, each of whom was in a severely decompensated state, notable alteration of blood flow properties was observed in those six patients who were hyperosmolar. In this form of diabetic decompensation, whole blood filtration was distinctly impaired. The additional impairment was shown to be due to an accumulation of solute within the erythrocytes occurring as a consequence of hyperosmolarity. The alterations in erythrocytes were revealed by Coulter blood count abnormalities and confirmed by osmotic fragility studies. When biochemical improvement was achieved in these patients, rapid resolution of the erythrocyte abnormalities occurred. Microvascular ischaemia due to such erythrocyte alterations may be a possible explanation for the characteristic cerebral disturbances of the hyperosmolar diabetic state. Altered blood flow properties would also promote vascular thrombosis, a common terminal event in the hyperosmolar non-ketotic syndrome with associated 50 per cent mortality. An improved design of the insulin and fluid replacement therapy for patients in hyperosmolar diabetic coma might be based on the findings of these and further studies.

No abstract

Antibodies to insulin were found in 92% of the 138 insulin-treated pregnant diabetic patients studied. No effect of pregnancy was shown on insulin antibody levels. Higher insulin antibody levels were significantly associated with the previous use of conventional insulins. Change from conventional to highly purified porcine insulin during pregnancy produced a significant reduction in insulin antibody levels. The combination of protamine zinc and soluble insulin used before pregnancy was found to be the most immunogenic. Insulin antibodies were freely transferred to the fetus but not detectable after the first 8 months of life. No insulin antibodies were found in the cord blood or during the next few weeks in the infants of mothers who had no antibodies to their injected insulin. There was a tendency for higher insulin antibody levels to be associated with indices of neonatal morbidity but not with percentile birth weights and C-peptide levels in cord sera.