The thermic effect of 1.67 MJ (400 kcal) of carbohydrate (glucose), fat, protein and mixed meal were examined in 11 lean and 11 obese subjects by indirect calorimetry. The changes in metabolic rate in response over 90 min period (30-120 min after the meal) to the different meals were compared with that seen after a similar volume of low calorie drink. The thermic effects of glucose and protein were not significantly different between lean and obese subjects. Obese subjects showed very little increase in metabolic rate following ingestion of fat (-0.9 +/- 2.0%, mean +/- SEM) and this was significantly different from that seen in lean subjects (14.4 +/- 3.4%). The thermogenic response to mixed meal was also significantly lower in obese subjects when expressed as percentage change (12.9 +/- 2.3% compared to 25.0 +/- 4.8%). There was no evidence for delay in gastric emptying times for glucose and fatty meal in the six obese subjects in whom these were measured. We conclude that obese subjects show a reduced thermogenic response to fat.
Many patients believe that their diabetes has been caused by stress or an adverse life event. Whereas there is strong evidence that psychological stress is related to a deterioration in glycaemic control in established diabetes, there is much less evidence that psychological stress can cause diabetes in humans de novo. It seems more likely that psychological stress produces a deterioration in glycaemia in the non-symptomatic patient which in turn makes diabetic symptoms and the diagnosis evident. The pathogenic mechanisms which have been suggested to relate psychological stress to diabetes are described and reviewed.
In a 12-month randomly allocated double-blind trial in 19 obese Type 2 diabetic patients, fluoxetine 60 mg daily compared to placebo produced a significant fall in median body weight after 3 months (3.8 kg), 6 months (6.5 kg), 9 months (7.1 kg) and at 1 year (5.8 kg). Median fasting blood glucose and HbA1c levels fell significantly after 3 months (1.9 mmol l-1) and 1.7%, respectively) and 6 months (1.8 mmol l-1 and 1.7%) but neither showed a significant difference to placebo after 9 or 12 months therapy with fluoxetine. There were no significant changes in serum cholesterol levels in the year but patients on fluoxetine showed a significant fall in serum triglyceride level (0.5 mmol l-1) after 3 months therapy but not thereafter. Compared to placebo there was a significant fall in median energy intake on fluoxetine after 3 months (257 kcal day-1) and 6 months (199 kcal day-1) but this difference was not significant at 9 or 12 months. There was also a significant fall in carbohydrate intake after 3 months (30 g day-1) and 6 months (23 g day-1) on fluoxetine as well as a significant fall in carbohydrate intake expressed as a percentage of the total daily energy intake; 5.9% at 3 months, 6.1% at 6 months, and 4.0% at 9 months. There were no significant effects on protein or fat intake except a significant increase in the intake of fat expressed as a percentage of daily energy intake, 5.9% after 6 months. Two of the nine patients on fluoxetine dropped out of the study due to gastrointestinal side-effects. Fluoxetine might prove to be a useful adjunct therapy in obese Type 2 diabetic patients where short-term weight loss and fall in carbohydrate intake and an improvement in glycaemia are indicated.
SUMMARY The prevalence of oral yeasts and humoral precipitating antibodies to candida was estimated in 204 unselected diabetic patients (172 outpatients and 32 inpatients). Yeasts, mainly Candida albicans, were isolated from the mouths of 41 % of the outpatients and precipitins were found in 17-5 % although none of the patients had clinically overt candidiasis. The extent of oral yeast colonisation and incidence of antibodies was not related to their antidiabetic treatment or to the duration of their diabetes. It was, however, related to the blood glucose and urine sugar levels at the time they were sampled, the highest incidence being among the diabetic inpatients with high blood glucose levels at the time of sampling and the lowest among outpatients with normal blood glucose levels at the time of sampling. There was no such correlation when diabetic control over the previous 12-month period was considered.
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