A b b re v i a t i o n s : C V, coefficient of variation; FPG, fasting plasma glucose; OHA, oral hypoglycemic agents; RR, relative risk; UKPDS, U.K. Prospective Diabetes Study.A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Fasting Plasma Glucose Va r i a b i l i t y P redicts 10 -Year Survival of Type 2 Diabetic PatientsThe Ve rona Diabetes Study O R I G I N A L A R T I C L E O B J E C T I V E -In the present study, we evaluated whether the coefficient of variation (CV) of fasting plasma glucose (FPG) over a 3-year period was a significant predictor of mort a l i t y in type 2 diabetic patients aged 56-74 years.RESEARCH DESIGN AND METHODS -All type 2 diabetic patients (n = 1,409) aged 56-74 years attending the Ve rona Diabetes Clinic and having at least two FPG determ i n a t i o n s in each of the years 1984-1986 were followed for 10 years (1987)(1988)(1989)(1990)(1991)(1992)(1993)(1994)(1995)(1996) to assess total and cause-specific mort a l i t y. Patients were grouped into tertiles of mean and CV of FPG during 1984FPG during -1986. These parameters as well as sex, age, diabetes duration, insulin treatment, smoking, hypertension, and hyperc h o l e s t e rolemia were included in multivariate survival analyses.R E S U LT S -During the follow-up, 468 patients died. The CV of FPG was an independent p redictor of total, card i o v a s c u l a r, and cancer mort a l i t y. Mean FPG was a predictor of total mortality only when the CV of FPG was not included in the analyses.C O N C L U S I O N S -L o n g -t e rm variability of fasting glucose is an independent predictor of m o rtality in patients with type 2 diabetes. The CV of FPG might be considered a useful additional parameter in the management of these patients. Diabetes E p i d e m i o l o g y / H e a l t h S e r v i c e s / P s y c h o s o c i a l R e s e a r c h 46DIABETES CARE, VOLUME 23, NUMBER 1, JANUARY 2000 Glucose variability and mortality in diabetesMain clinical characteristics at baseline of the cohort under study and subjects excluded from the analysis are summarized in Table 1. Marginal diff e rences were found in age, sex distribution, smoking habits, and number of FPG values 3.9 mmol/l, while slightly greater diff e rences were found with respect to diabetes duration, t h e r a p y, and mean FPG. Total and causespecific mortality was similar. FPG determinationsFPG was repeatedly measured in a consistent fashion in the three years preceding the m o rtality follow-up. Venous blood was withdrawn from an antecubital vein after a 10-h overnight fast, collected in tubes containing EDTA and fluoride and centrifuged within 2 h. Plasma glucose was assayed with a glucose-oxidase method (Boehr i n g e r, Mannheim, Germ a n y ) .The total number of FPG measurements during the years 1984-1986, which w e re available in the clinical re c o rds of patients under study and which were collected for analysis, was 16,184 (per-p a t i e n t mean ± SD 11.5 ± 3.6; median 11.0; ra...
OBJECTIVE -To examine the 10-year mortality and effect of diabetes duration on overall and cause-specific mortality in diabetic subjects in the Verona Diabetes Study (VDS).RESEARCH DESIGN AND METHODS -Records from diabetes clinics, family physicians, and a drug consumption database were used to identify 5,818 subjects Ն45 years of age with type 2 diabetes who were alive and residing in Verona, Italy, on 31 December 1986. Vital status of each subject was ascertained on 31 December 1996. Underlying causes of death were determined from death certificates. Death rates and death rate ratios (DRRs) were computed and standardized to the population of Verona in 1991.RESULTS -During the study, 2,328 subjects died; 974 deaths were attributable to cardiovascular disease, 517 to neoplasms, 324 to diabetes-related diseases, 134 to digestive diseases, 250 to other natural causes, and 48 to external causes. There were 81 subjects who died of unknown causes. Death rates from natural causes were higher in men than in women (DRR 1.4, 95% CI 1.2-1.5) and rose in both sexes with increasing duration of diabetes (P = 0.001). Among the natural causes of death, those for diabetes-related diseases were strongly related to diabetes duration (P = 0.001); a modest relationship with duration was also found for ischemic heart disease in men (P = 0.07).CONCLUSIONS -Cardiovascular disease was the principal cause of death among people with type 2 diabetes in the VDS. Rates for natural causes of death rose with increasing duration of diabetes. Deaths from diabetes-related diseases in both sexes and from ischemic heart disease in men were largely responsible for this increase.
OBJECTIVE:The relation between body weight and mortality in type II diabetic patients has not been fully elucidated. The aim of the present study was to evaluate the impact of body weight on mortality in a well-characterized type II diabetic cohort. RESEARCH DESIGN AND METHODS:We examined a cohort of 3398 type II diabetic patients, alive on December 1986 and followed up for 10 years, to assess mortality and its causes and to investigate the relationship between body mass index (BMI) and mortality from all and specific causes. For this purpose, survival in the different quartiles of BMI was evaluated by a Cox model, controlling for sex, age, treatment, smoking, duration of diabetes, hypertension, and fasting plasma glucose. The Cox model was applied either excluding (model 1) or including (model 2) the last three variables. RESULTS: During the 10 ys of follow-up, 1212 deaths (639 women, 573 men) occurred in the cohort under study. Since the interaction between BMI and age was statistically significant (P = 0.002), survival was studied separately in people aged o65 and Z65 y (median age of the cohort = 65.9 y). Under 65 y, a significantly higher all-cause mortality was observed in obese patients, that is, in the IV quartile (BMIZ30.9 kg/m 2 ; RR = 1.74; CI 95% = 1.26-2.40), in model 1. The inclusion of hypertension, duration of diabetes, and fasting plasma glucose in the model (model 2) slightly decreased the relative risk (RR = 1.52; CI 95% = 1.10-2.11). After 65 y, higher body weight was associated with a better outcome, especially in patients belonging to the IV quartile of BMI (RR = 0.74; CI 95% = 0.62-0.90). CONCLUSIONS: In older type II diabetic patients, a moderate excess weight predicts a better survival, while obesity is a negative prognostic factor in patients younger than 65 y. In the latter patients, the effect of obesity on mortality seems to be partly mediated by hypertension, duration of diabetes, and fasting plasma glucose.
Recent data suggest that insulin is a modulator of ovarian and adrenal steroidogenesis and that, in the ovary of hyperandrogenic women, hyperinsulinemia might cause dysregulation of cytochrome P450c17 alpha activity. To further assess in vivo the effects of insulin on adrenal steroidogenesis, ACTH stimulation was carried out in 21 hyperandrogenic women during a 3-h hyperinsulinemic (80 mU/m2-min) euglycemic clamp. In all of these women the procedure was repeated during saline infusion as n control. In nonamenorrheic patients, the tests were performed in the early follicular phase of two different menstrual cycles. Serum cortisol, progesterone, 17-hydroxypregnenolone (17-OHJPREG). 17-hydroxyprogesterone (17-OHP), dehydroepiandrosterone (DHEA), and androstenedione (A) were measured after 2 h of insulin or saline infusion (zero time) and, subsequently, 30 and 60 min after an iv bolus of 0.25 mg ACTH-(1-24). At zero time, no difference was found in the serum steroid concentrations between the two protocols. ACTH-stimulated serum 17-OHPREG and, to a lesser extent, 17-OHP were significantly higher during insulin than during saline infusion (peaks, 60.6 +/- 9.0 vs. 40.7 +/- 7.9 and 7.7 +/- 7.7 vs. 6.6 +/- 0.6 nmol/L; P < 0.005 and P < 0.01, respectively). Serum DHEA was also slightly higher during hyperinsulinemia, although only after 30 min (54.5 +/- 3.0 vs. 48.2 +/- 4.2 nmol/L; P < 0.05). No statistically significant difference in the cortisol, progesterone, or androstenedione response to ACTH was found between the two protocols. ACTH-stimulated 17-OHPREG/DHEA and 17-OHP/A molar ratios, indexes of apparent 17,20-lyase activity, were significantly higher during the clamp studies than during saline infusion (by ANOVA, F = 12.8; P < 0.001 and F = 6.7; P < 0.005, respectively), suggesting an impaired enzyme activity. These in vivo data support the hypothesis that insulin potentiates ACTH-stimulated steroidogenesis. This effect of insulin seems to be associated with a relative impairment of 17,20-lyase activity.
To assess whether androgen excess per se might impair insulin action, insulin sensitivity was measured by a two-step (20 and 80 mU/m2.min) hyperinsulinemic euglycemic clamp combined with indirect calorimetry and tracer glucose infusion in 43 women (13 obese and 30 nonobese) with normal glucose tolerance and clinical evidence of increased androgen action (hirsutism and/or polycystic ovary syndrome) as well as 12 age- and body mass index-matched healthy controls. Hyperandrogenic women were studied basally and after 3-4 months of antiandrogen treatment with 3 different drugs: spironolactone (n = 23), flutamide (n = 10), or the GnRH agonist buserelin (n = 10). Six women given spironolactone were also reexamined after 1 yr of therapy. At baseline, insulin-mediated glucose uptake was lower in hyperandrogenic women than in controls (by ANOVA, F = 14.3; P < 0.001). Insulin resistance was observed in both ovarian and nonovarian hyperandrogenism, as distinguished by acute GnRH agonist testing. After antiandrogen therapy, insulin action on glucose metabolism significantly increased for both the patients as a whole (F = 7.4; P < 0.01) and each treatment group separately. However, insulin action remained lower than in controls and showed no further improvement in patients reevaluated after I yr of treatment. Increases in both oxidative and nonoxidative glucose metabolism accounted for the improvement in substrate disposal induced by antiandrogen drugs. The increase in the effectiveness of insulin was greater in the lean subjects, whereas the change was small and not statistically significant in the obese women. Response to treatment was more pronounced in women with nonovarian hyperandrogenism, particularly at the low insulin infusion rate. Endogenous glucose production in hyperandrogenic patients was similar to that in healthy women and was unaffected by therapy. In conclusion, antiandrogen treatment partially reversed the peripheral insulin resistance associated with hyperandrogenism regardless of which antiandrogen was used. These data strongly suggest that in women, androgen excess per se contributes to impairment of insulin action.
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