AimsTo examine patient and physician beliefs regarding insulin therapy and the degree to which patients adhere to their insulin regimens.MethodsInternet survey of 1250 physicians (600 specialists, 650 primary care physicians) who treat patients with diabetes and telephone survey of 1530 insulin-treated patients (180 with Type 1 diabetes, 1350 with Type 2 diabetes) in China, France, Japan, Germany, Spain, Turkey, the UK or the USA.ResultsOne third (33.2%) of patients reported insulin omission/non-adherence at least 1 day in the last month, with an average of 3.3 days. Three quarters (72.5%) of physicians report that their typical patient does not take their insulin as prescribed, with a mean of 4.3 days per month of basal insulin omission/non-adherence and 5.7 days per month of prandial insulin omission/non-adherence. Patients and providers indicated the same five most common reasons for insulin omission/non-adherence: too busy; travelling; skipped meals; stress/emotional problems; public embarrassment. Physicians reported low patient success at initiating insulin in a timely fashion and adjusting insulin doses. Most physicians report that many insulin-treated patients do not have adequate glucose control (87.6%) and that they would treat more aggressively if not for concern about hypoglycaemia (75.5%). Although a majority of patients (and physicians) regard insulin treatment as restrictive, more patients see insulin treatment as having positive than negative impacts on their lives.ConclusionsGlucose control is inadequate among insulin-treated patients, in part attributable to insulin omission/non-adherence and lack of dose adjustment. There is a need for insulin regimens that are less restrictive and burdensome with lower risk of hypoglycaemia.

The object of this work is to try to elucidate the role of genetic and environmental factors in the aetiology of diabetes by studying a series of identical twins.Concor&ince in identical (monozygotic) twins does not necessarily mean that a disease is genetic in origin. Twins usually live together in early life and thus share the same environment. Concordance could therefore be the result of genetic or environmental similarity. However, in later life most twins live apart and then concordance does suggest a genetic disease. Discordance, on the other hand, must indicate that a disease is due, at least in part, to nongenetic factors. We are therefore particularly interested in discordance in younger and concordance in older twins. Previous Twin StudiesThere have been five large studies of diabetic twins [1-5] but all have defects; none has categorised the twins as insulin dependent diabetics (IDDs) or noninsulin dependent diabetics (NIDDs) and in 0nly two were the unaffected twins examined by glucose tolerance.Then Berg [1] reported 47 identical twin pairs of whom 35 were over 43 years old. All of these were concordant for diabetes on history or glucose tolerance testing, but of the 12 younger twin pairs only 6 were concordant. White [2] found 16 of 33 pairs to be concordant but did not categorise them by age or type of diabetes. Gottlieb and Root [3] who, like White, worked at the Joslin Clinic but, we assume, were reporting on different patients, found seven out of 10 pairs in whom diabetes was diagnosed over the age of 40 were concordant, compared to only two out of 20 younger twins. Harvald and Hauge [4] ascertained twins from the Danish twin register. Of 47 "maturity-onset" pairs 26 were concordant, of 36 younger onset pairs only 12 were concordant but unaffected twins were not tested. Pollin et al [5] studied 53 identical twin pairs among US ex-service men aged 43 to 53 and found only three pairs were concordant but again unaffected twins were not tested.All but one of these studies have also reported concordance rates in non-identical twins. Then Berg [1] found nine out of 50 pairs of non-identical twins to be concordant, White [2] two out of 63, Gottlieb and Root [3] two out of 70 and Harvald and Hauge [4] 22 out of 158. The overall figure for concordance in nonidentical twin pairs in these four studies is 35 out of 341 (10%).In spite of the limitations of these studies three broad conclusions can be drawn. 1) Identical twins always show a higher concordance rate than non-identical twins irrespective of their age at diagnosis.2) Younger onset pairs of identical twins are often discordant for diabetes.3) Older onset pairs, on the other hand, are usually concordant for diabetes.Our own previous results [6] confirm these general conclusions. Of 96 pairs of identical twins 59 index twins became diabetic before the age of 40, 31 were concordant and 28 discordant; of the 37 pairs in which the index twin was diagnosed after the age of 40 all but three were concordant. Similar proportions were found as the study has...

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Glucocorticoids play an important role in the pathogenesis of obesity and insulin resistance. Impaired conversion of cortisone (E) to cortisol (F) by the type 1 isoenzyme of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) in obesity may represent a protective mechanism preventing ongoing weight gain and glucose intolerance. We have studied glucocorticoid metabolism in 33 male subjects with type 2 diabetes mellitus [age, 44.2 +/- 13 yr; body mass index (BMI), 31.1 +/- 7.5 kg/m(2) (mean +/- sd)] and 38 normal controls (age, 41.4 +/- 14 yr; BMI, 38.2 +/- 12.8 kg/m(2)). Circulating F:E ratios were elevated in the diabetic group and correlated with serum cholesterol and homeostasis model assessment-S. There was no difference in 11beta-HSD1 activity between diabetic subjects and controls. In addition, 11beta-HSD1 activity was unaffected by BMI in diabetic subjects. However, in control subjects, increasing BMI was associated with a reduction in the urinary tetrahydrocortisol+5alpha-tetrahydrocortisol:tetrahydrocortisone ratio (P < 0.05) indicative of impaired 11beta-HSD1 activity. The degree of inhibition correlated tightly with visceral fat mass. Changes in 11beta-HSD1 activity could not be explained by circulating levels of adipocytokines. Impaired E to F metabolism in obesity may help preserve insulin sensitivity and prevent diabetes mellitus. Failure to down-regulate 11beta-HSD1 activity in patients with diabetes may potentiate dyslipidemia, insulin resistance, and obesity. Inhibition of 11beta-HSD1 may therefore represent a therapeutic strategy in patients with type 2 diabetes mellitus and obesity.