Aims/hypothesis: The aim of this prospective study was to investigate predictors of deteriorating glucose tolerance in subjects of British extraction. Methods: A total of 156 non-diabetic subjects (86 with a family history of type 2 diabetes) underwent a 75-g OGTT and anthropometric assessment at baseline and 5 years later. Pancreatic beta cell function and whole-body insulin sensitivity were studied by model assessment. Subjects were classified as progressors if glucose tolerance moved one or more steps from normal, impaired fasting glucose, impaired glucose tolerance and diabetes over the follow-up period. Results: At baseline, the progressors (n=22) had increased adiposity and a higher proportion of familial diabetes and abnormal glucose tolerance than non-progressors. Baseline pancreatic beta cell sensitivity to changes in glucose (p<0.02) and whole-body insulin sensitivity (p<0.0001) were decreased in the progressors. Logistic regression revealed that baseline and follow-up changes in beta cell glucose sensitivity and insulin sensitivity, rather than the classical clinical predictors (adiposity, familial diabetes and glucose levels), were the key independent predictors of progression (explaining over 50% of the progression). Conclusions/ interpretation: Impaired pancreatic beta cell glucose sensing and whole-body insulin sensitivity predict progression to hyperglycaemia. Strikingly, these pathophysiological changes override the importance of the clinical risk factors and highlight potential metabolic targets for prevention strategies.

Unfortunately the values given for insulin sensitivity and disposition index (DI) in Tables 2 and 3 of this article were incorrect. The corrected tables are reproduced here. There was also a mistake in the legend for Figure 3 which should have read: 'Data points and bars are mean ± SE for insulin sensitivity and for beta cell glucose sensitivity', instead of 'Data points and bars are mean ± SE for insulin sensitivity and median ± SE for beta cell glucose sensitivity'. Data appear as the mean ± SD or as the median and interquartile range (the difference between the 75th and 25th percentile numbers). ISR Insulin secretion rate; IS insulin secretion; DI disposition index; NS not significant Units for each measurement as described in Tables 1 and 2. Data appear as the mean ± SD or as the median and interquartile range (the difference between the 75th and 25th percentile numbers)

We report an unusual case of recurrent, painful, unilateral gynaecomastia (GM) in an elderly male with relapsing Graves' hyperthyroidism and co-existing primary hypogonadism. This patient presented to the Breast Clinic with a 4-month history of painful, right GM. Malignancy was excluded but T3 was noted to be raised at 7.3 pmol l(-1) (normal 3.5-5.5) with a suppressed thyroid-stimulating hormone. Testosterone, luteinizing hormone and follicle-stimulating hormone were consistent with primary hypogonadism. He was later referred to physicians with night sweats and painful right GM. FT3 was 7.4 and carbimazole was commenced. Within 4 months, the night sweats and right GM had resolved but he became hypothyroid. When carbimazole was stopped, right GM recurred together with hyperthyroidism. The male breast, which is sensitive to subtle changes in T/E2 ratio, is more likely to be stimulated in an elderly male with hyperthyroidism and pre-existing hypogonadism, and hence recurrence of GM with relapsing hyperthyroidism. Recognition of this association is clinically relevant to avoid unnecessary investigations and undue patient anxiety, and to facilitate appropriate early diagnosis and treatment.

the consumption of wheat products, rye products, sugar, vegetables, roots, legumes, fruits, berries, butter, whole fat milk, pork, beef, sausages or fish, or the intake of starch, sucrose, available carbohydrates, or protein into the model, but the result remained unchanged.These cross-sectional findings are in line with earlier observations suggesting untoward effects of potato intake on glucose metabolism [2,3]. The present finding of a relationship between the intake of potatoes and glucose levels and insulin resistance in men only, who consumed approximately 50% more potatoes per day than women, suggests that one needs to exceed a certain threshold of potato intake before an untoward effect on glucose metabolism becomes manifest.It could also be argued that potatoes might only be a marker of a dietary pattern associated with disordered glucose metabolism. A 'conservative' dietary pattern, characterized by consumption of butter, potatoes and whole milk, has been associated with increased risk for Type 2 DM [8]. In that population, however, the consumption of potatoes was also independently associated with the risk of diabetes [2]. In the men in the present study, the consumption of potatoes was significantly directly correlated with fibre intake, but inversely correlated with total and saturated fat intake. As a diet characterized by high intake of fibre but low intake of fat and saturated fat seems to be associated with improved rather than impaired glucose metabolism, and as potatoes and fibre remained independent predictors of insulin resistance in the present analyses, our results suggest an independent role for potatoes in glucose metabolism.