Alterations of cerebral metabolism in patients with diabetes mellitus studied by proton magnetic resonance spectroscopy.

To evaluate possible pathophysiologic links between cerebral changes in diabetic patients detected by proton magnetic resonance spectroscopy and clinical as well as laboratory parameters. The brains of 30 patients with diabetes mellitus and 30 healthy volunteers were examined using a STEAM sequence (TR 1500 ms, TE 20 ms). We measured in occipital gray matter and parietal white matter in a 1.5-Tesla magnet. Laboratory parameters were acquired before and after the examination. In diabetic patients a significant elevation of the myo-inositol/creatine ratio in gray and white matter was present (p = 0.006). Choline/creatine ratio in gray matter was elevated compared to normal controls (p = 0.002). No correlation with laboratory parameters was detected. Myo-inositol was even more elevated in patients with polyneuropathy (p = 0.024). No correlation with age or sex was detected. The changes found in diabetes are similar to those found in patients with Alzheimer's disease, dialysis, and after renal transplant, suggesting a similar etiology. Elevated myo-inositol may not only indicate osmolar changes in glial cells but also glial cell alteration due to amyloid or amylin deposition with formation of neurofibrillary tangles, especially as these changes are found in all of these diseases and no correlation to osmolar deterioration exists.     

Changes of arterial hemodynamics in patients with type 2 diabetes mellitus or impaired glucose tolerance.

AIM: The aim of our study was to evaluate the arterial hemodynamics in patients with type 2 diabetes mellitus or impaired glucose tolerance without clinical or Doppler evidence of peripheral arterial disease, in order to early detect vascular damage. METHODS: We studied 20 subjects (12 men and 8 women, aged between 48 and 62 years) with type 2 diabetes mellitus (Group 1), 20 subjects (11 men and 9 women, aged between 49 and 61 years) with reduced glucose tolerance (Group 2), and 20 normal subjects (10 men and 10 women, aged between 48 and 62 years) (Group 3). Each subject underwent strain-gauge plethysmography and the following parameters were evaluated: rest flow (RF); peak flow (PF); PF/RF ratio; time to peak flow (tPF); half-time (t 1/2) and total time (tT) of hyperemic response; basal vascular resistances (BVR) and minimal vascular resistances (MVR). RESULTS: There was no difference among groups in RF, but maximal postischemic flow was reduced in patients with diabetes and with impaired glucose tolerance. The MVR showed a similar behavior, while the basal ones were increased only in the diabetic group. Finally, the t1/2 and the tT of the hyperemic response, that reflect arteriolar reactivity, were significantly reduced, if compared with controls. No significant differences between Group 1 and 2 were found. CONCLUSIONS: These results confirm the presence of hemodynamic modifications in the vascular bed of both diabetics and patients with impaired glucose tolerance, as compared with normal subjects.     

Measurement of cerebral oxidative glucose consumption in patients with type 1 diabetes mellitus and hypoglycemia unawareness using C nuclear magnetic resonance spectroscopy

The aim of the present study was to use ¹³C nuclear magnetic resonance (NMR) to measure the cerebral oxidative metabolic rate of glucose (CMRglc[ox]) in patients with diabetes and to compare these measurements with those collected from matched controls. We elected to study a group with type 1 diabetes mellitus and hypoglycemia unawareness because we had previously found such patients to have higher brain glucose concentrations than healthy volunteers under steady-state conditions. We sought to determine if this difference in steady-state brain concentrations could be explained by a difference in CMRglc(ox). Time courses of ¹³C label incorporation in brain amino acids were measured in occipital cortex during infusion of [1-¹³C]glucose. These time courses were fitted using a 1-compartment metabolic model to determine CMRglc(ox). Our results show that the tricarboxylic acid cycle (TCA) cycle rate (V_TCA, which is twice CMRglc[ox]) in subjects with type 1 diabetes mellitus was not significantly different from that of healthy controls (0.84 ± 0.03 vs 0.79 ± 0.03 μmol/[g min], n = 5 in each group, mean ± SEM). We conclude that the changes in steady-state brain glucose concentrations that we observed in patients with type 1 diabetes mellitus in a previous study (J Neurosci Res. 2005;79:42-47) cannot be explained by changes in oxidative glucose consumption     

Plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus and impaired glucose tolerance

Visfatin, a new adipokine, facilitates adipogenesis and has insulin-mimetic properties. We aimed to investigate the plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus (T2DM) and impaired glucose tolerance (IGT), who had no obesity or hypertension. Twenty-two patients with T2DM, 18 subjects with IGT and 40 healthy controls were enrolled. Visfatin levels were measured along with the BMI, blood pressure, lipids, glucose, insulin, adiponectin and hsCRP levels, and HOMA-IR indexes. Age, sex and BMI were similar in all groups. Visfatin levels were higher in the diabetic group than the controls (p=0.01). There was no significant difference in the visfatin levels between the T2DM and IGT groups as well as IGT group and healthy controls. Plasma visfatin concentrations did not differ between men and women. Visfatin levels did not correlate with BMI, blood pressure, plasma adiponectin, insulin, hsCRP, glucose and lipid levels or HOMA-IR indexes in the three groups. These results indicate that hyperglycemia causes an increase in plasma visfatin levels and, as in people with T2DM but not with IGT, this increase gets more prominent as the glucose intolerance worsens.     

不同糖耐量人群及糖尿病患者血浆内脂素与血糖及胰岛功能的关系研究

目的探讨不同糖耐量人群血浆内脂素的变化及其与体重指数(BMI)、腰围、血糖、胰岛素抵抗指数、胰岛B细胞功能、血脂等的关系。方法2006年4月至2006年10月在南京医科大学第一附属医院门诊常规健康体检及糖尿病初次就诊者95名,按WHO1999糖尿病诊断标准分为初诊2型糖尿病组(53例)、糖耐量减退组(7例)、正常糖耐量组(35名);以WHO1998肥胖诊断标准分为超重或肥胖组(50名)、正常体重组(45名)。检测受试者BMI、腰围、血压,测定空腹血浆内脂素、血糖、血脂、胰岛素等。结果初诊2型糖尿病患者空腹血浆内脂素明显高于正常糖耐量组(P<0.01)。超重或肥胖组与正常体重组间血浆内脂素差异无显著性意义。人群中血浆内脂素与空腹血糖(r=0.338,P<0.01)、餐后2h血糖(r=0.340,P<0.01)、胰岛素抵抗指数(r=0.227,P<0.05)呈正相关,与胰岛素分泌指数(HOMA-B)呈负相关(r=-0.296,P<0.05)。在2型糖尿病组,血浆内脂素与糖化血红蛋白(HbA1c)呈正相关(r=0.356,P<0.01)。多元线性逐步回归分析表明,餐后2h血糖是影响血浆内脂素的独立相关因素。结论初诊2型糖尿病患者血浆内脂素显著升高,可能是机体针对体内血糖增高、胰岛功能受损所发生的一种代偿效应。     

Influences of statins on glucose tolerance in patients with type 2 diabetes mellitus

Atorvastatin is frequently administered for the treatment of hypercholesterolemia associated with type 2 diabetes mellitus. However, a marked deterioration of glycemic control has been reported in some patients treated with atorvastatin. No study has been done to determine whether atorvastatin adversely affects glycemic control. In this study, we retrospectively compared an atorvastatin-treated group (Group A, n = 76) with a pravastatin-treated group (Group P, n = 78) to examine the effects of the 2 statins on glycemic control from the onset of administration to 3 months thereafter. No change occurred in the antidiabetic drug dose in 62 patients of Group A and 68 patients of Group P. In those patients, arbitrary blood glucose levels increased from 147 +/- 50 (mean +/- SD) mg/dL to 177 +/- 70 mg/dL in Group A and from 140 +/- 38 mg/dL to 141 +/- 32 mg/dL in Group P. HbA(1c) increased from 6.8 +/- 0.9% to 7.2 +/- 1.1% in Group A and from 6.9 +/- 0.9% to 6.9 +/- 1.0% in Group P. The increase was significant only in Group A, and the extent of the increase was also significantly greater in Group A. These results suggest a predisposition to a deterioration of glycemic control in type 2 diabetic patients treated with atorvastatin.     

Endothelial dysfunction in impaired fasting glycemia, impaired glucose tolerance, and type 2 diabetes mellitus

The aim of this study was to evaluate whether abnormal endothelial function is present in early stages of diabetes, such as impaired glucose tolerance (IGT) and impaired fasting glucose (IFG). Endothelial function was assessed by measuring flow-mediated dilatation and nitrate-induced dilatation of the brachial artery using high-resolution ultrasound. Fasting serum lipid levels were determined, and glucose and insulin values in response to a 75-g oral glucose load were also measured. The results showed the following new findings: (1) compared with subjects with normal glucose tolerance, those with IFG and IGT had impaired flow-mediated dilatation, more remarkable in subjects with type 2 diabetes mellitus than those with IFG and IGT, and (2) flow-mediated dilatation was inversely and strongly related to the extent of hyperglycemia. In conclusion, endothelial dysfunction is present in subjects with IGT and IFG, indicating endothelial damage in these stages.     

Smoking is associated with impaired long-term glucose metabolism in patients with type 1 diabetes mellitus

Background and AimsSmoking is known to negatively influence glucose metabolism both in healthy subjects and in patients with diabetes. The aim of this study was to compare glycemic control in patients with type 1 diabetes mellitus who were smokers with those who did not smoke during a prospective long-term follow-up.Methods and ResultsIn a single center, 763 patients with type 1 diabetes mellitus were included, 160 (21.0%) of them were smokers. Patients were treated with intensive insulin therapy according to existing guidelines. Glucose control was monitored quarterly, diabetes related complications and cardiovascular risk factors were assessed at least once a year. Glucose control in smokers was significantly worse than in non-smokers at baseline and during follow-up (mean HbA1c during 5047 patient-years of follow-up 7.9 ± 1.3% in smokers and 7.3 ± 1.1% in non-smokers, p < 0.001) despite a higher insulin dosage in smokers (0.71 ± 0.30 U/kg vs. 0.65 ± 0.31 U/kg in non-smokers, p = 0.046). HDL cholesterol was lower in smokers at baseline (1.53 ± 0.45 vs. 1.68 ± 0.51 in non-smokers, p = 0.048). Diabetes related complications tended to occur with a higher frequency in smokers, with a significant difference in macroalbuminuria (9.8% vs. 4.8% in non-smokers, p = 0.047).ConclusionSmoking is associated with worse glucose control in patients with type 1 diabetes mellitus despite the same treatment strategies as in non-smokers. Hyperglycemia, therefore, may contribute to an earlier incidence of diabetes related complications in these patients, in addition to direct toxic effects of smoking.     

Different pathophysiology of impaired glucose tolerance in first-degree relatives of individuals with type 2 diabetes mellitus

To assess whether an increased genetic predisposition for type 2 diabetes mellitus (T2DM) influences the contributions of insulin resistance and impaired insulin secretion to impaired glucose tolerance (IGT), 437 subjects not known to have T2DM underwent an oral glucose tolerance test and a 3-hour hyperglycemic clamp. Plasma insulin responses and insulin sensitivity were compared between all subjects (unselected for demographic or anthropometric characteristics) who had normal glucose homeostasis and no first-degree T2DM relative (n = 133), IGT with a first-degree T2DM relative (IGT/FH+, n = 74), or IGT without a first-degree T2DM relative (IGT/FH−, n = 50). Compared with those with normal glucose homeostasis, first- and second-phase plasma insulin responses were reduced approximately 45% and 30%, respectively (both P < .001), in IGT/FH+, whereas insulin sensitivity was only approximately 20% reduced (P = .011). In contrast, in IGT/FH−, first-phase plasma insulin responses were only approximately 20% reduced (P = .016), second-phase plasma insulin responses were not reduced, but insulin sensitivity was approximately 40% reduced (P < .001). The IGT/FH+ group differed significantly from the IGT/FH− group by having 25% to 30% lower first-phase plasma insulin responses (P = .026) and 25% to 30% greater insulin sensitivity (P = .027). Adjustment for obesity abolished the differences in insulin resistance but not plasma insulin responses. However, when the IGT groups were stratified into subgroups based on body mass index (BMI), first-phase plasma insulin responses were approximately 30% lower in IGT/FH+ with a BMI of at least 27 kg/m² (P = .018) but similar in IGT/FH+ with a BMI less than 27 kg/m² compared with the corresponding IGT/FH− subgroups. We conclude that, in IGT, an increased genetic predisposition for T2DM increases the contribution of impaired insulin secretion to its pathophysiology. This effect is enhanced by obesity.     

Impact of glucagon response on postprandial hyperglycemia in men with impaired glucose tolerance and type 2 diabetes mellitus

Glucagon is the physiological antagonist of insulin. Postprandial (pp) hyperglycemia in impaired glucose tolerance (IGT) and in type 2 diabetes mellitus (T2DM) may also depend on irregularities in glucagon secretion. This study investigated the glucagon excursion after a lipid-glucose-protein tolerance test in subjects with different stages of glucose intolerance. We also analyzed the relationship between pp glucagon secretion and hyperglycemias. A total of 64 men (27 healthy subjects with normal glucose tolerance [NGT], 15 with IGT, and 22 with T2DM) were examined. Plasma glucose (PG), insulin, proinsulin, free fatty acids, and triglycerides were measured in the fasting state and at 30 minutes and 2, 3, 4, and 6 hours after the intake of the test meal, which contained 126 g carbohydrates, 92 g fat, and 17 g protein. Postprandial concentrations of metabolic parameters were calculated as area under the curve (AUC). Glucagon was measured in the fasting state and at 30 minutes and 2 and 4 hours pp. Early glucagon increment was defined as glucagon at 30 minutes minus fasting glucagon. The insulin response was quantified as insulin increment divided by PG increment in the corresponding time. Insulin resistance was calculated using lomeostasis model assessment (HOMA). Fasting glucagon was significantly increased in IGT vs NGT (P<.05), and early glucagon increment was significantly higher in T2DM vs NGT and IGT (P<.05). The 2-hour glucagon concentration after the load (AUC) was increased in IGT and T2DM vs NGT (P<.05). Early glucagon increment and the 2-hour AUC of glucagon were strongly correlated to pp glycemia (r=0.494 and P=.001, and r=0.439 and P=.003, respectively). An inverse correlation was observed between early glucagon increment and insulin response at 30 minutes and 2 hours after the meal load (r=-0.287 and P=.026, and r=-0.435 and P=.001, respectively). The 2-hour AUC of glucagon was significantly associated with insulin resistance (r=0.354, P=.020). Multivariate analysis revealed 2-hour insulin response and early glucagon increment as significant independent determinants of the AUC of PG in IGT (R=0.787). In T2DM, 2-hour insulin response, insulin resistance, and early glucagon increment were significant determinants of the AUC of PG (R=0.867). Our study suggests an important role for the irregularities in glucagon response in the pp glucose excursion after a standardized oral mixed meal in IGT and in T2DM. According to our data, a bihormonal imbalance starts before diabetes is diagnosed. Prospective studies are needed to evaluate the impact of glucagon on the progression of glucose intolerance and the possible effects of medicinal suppression of glucagon increment to prevent the progression of glucose tolerance.     

Early-stage atherosclerosis in newly diagnosed,untreated type 2 diabetes mellitus and impaired glucose tolerance

AimThe aim of this study was to investigate early-stage atherosclerosis in newly diagnosed, untreated type 2 diabetes mellitus (T2DM) and impaired glucose tolerance (IGT).MethodsThe study subjects underwent an oral glucose tolerance test (OGTT) and were then divided into three groups, according to plasma glucose level: those in the normal glucose tolerance (NGT) group had fasting plasma glucose (FPG) < 6.1 mmol/L and 2 h postload glucose (2hPPG) < 7.8 mmol/L; those in the IGT group had FPG < 6.1 mmol/L and 2hPPG ≥ 7.8 mmol/L; and those in the T2DM group had FPG ≥ 7.0 mmol/L or 2hPPG ≥ 11.1 mmol/L. Haemodynamic variables and brachial–ankle pulse-wave velocities (baPWV) in the three groups were compared.ResultsThe baPWV value increased with increases in plasma glucose, and was significantly and positively correlated to age, FPG, 2hPPG, systolic blood pressure (SBP), diastolic blood pressure (DBP), waist circumference and waist-to-hip ratio. Significant differences were found between the baPWV values in the NGT and IGT groups (1602 ± 347 vs 1707 ± 351 cm/s, respectively; P = 0.005), and between the NGT and DM groups (1602 ± 347 vs 1762 ± 381, respectively; P < 0.001). The results of multiple regression analyses showed that 2hPPG was closely related to baPWV as well as to SBP and DBP.ConclusionEarly-stage atherosclerosis is present in newly diagnosed, untreated T2DM and IGT patients, and it may be that its early assessment, along with good control of hypertension and hyperglycaemia, will help to delay its progression.     

Glucose fluctuations in subjects with normal glucose tolerance, impaired glucose regulation and newly diagnosed type 2 diabetes mellitus

Objective Glycemic variability is poorly studied in the nondiabetic individuals and newly diagnosed patients with type 2 diabetes. The aim of the study is to investigate the characteristics of glucose fluctuations in subjects with normal glucose tolerance (NGT), impaired glucose regulation (IGR) and newly diagnosed, drug‐naïve type 2 diabetes mellitus (DM‐2). Design and patients This is a cross‐sectional study of three groups including 53 subjects with IGR, 56 DM‐2 patients and 53 NGT individuals. Monitoring by a continuous glucose monitoring system (CGMS^® System Gold^?) was performed for three consecutive days. Measurements Mean blood glucose (MBG), standard deviation of MBG (SDBG), largest amplitude of glycemic excursions (LAGE) and mean amplitude of glycemic excursions (MAGE) were calculated to estimate intraday blood glucose variability. Interday variability of glucose was evaluated by absolute means of daily differences (MODD). Postprandial glucose excursion (PPGE) was calculated to assess the influence of meals on glucose fluctuation. Results Twenty‐two percentage of NGT and 33·9% of IGR individuals experienced blood glucose ≥11·1 mmol/l; 49·1% of NGT, 50·9% of IGR and 30·8% of DM‐2 participants had hypoglycemic episodes (CGM values <3·9 mmol/l). The IGR and DM‐2 groups had greater SDBG (P = 0·010 and P < 0·001), LAGE (P = 0·014 and P < 0·001) and MAGE (P = 0·044 and P < 0·001) compared with the NGT group. Significantly greater MODD and PPGEs were found in the DM‐2 groups than in the IGR and NGT groups (P < 0·001). The DM‐2 patients had higher 72‐MBG and glucose levels overnight than the NGT and IGR subjects (P < 0·001). In the patients with diabetes, MAGE was positively associated with MODD (r = 0·558, P < 0·001) and PPGEs (r = 0·738–0·843, P < 0·001). Conclusions Glucose variability is present to an increasing degree from NGT to IGR and IGR to DM‐2. Compared with the NGT individuals, the IGR and DM‐2 subjects show more predominant intraday glucose fluctuations. The DM‐2 patients demonstrate increased PPGEs, higher glucose levels overnight and greater interday fluctuations.     

正常糖耐量、糖耐量受损及新诊断2型糖尿病人群胰岛β细胞功能的变化

胰岛β细胞功能自NGT到IGT再到T2DM呈进行性下降，所依证据是HOMA—β，△I30／△G30、前胰岛素和C肽的比值(PI／CP)。PI／CP可能是测定胰岛β细胞功能的较好指标。     

Detecting impaired glucose tolerance or type 2 diabetes mellitus by means of an oral glucose tolerance test in HIV‐infected patients

Objective

As a proactive diagnosis of diabetes mellitus (DM) may prevent the onset of severe complications, we used an oral glucose tolerance test (OGTT) to check for impaired glucose tolerance (IGT) and DM in patients with long‐standing HIV infection and long durations of exposure to antiretroviral drugs with normal fasting plasma glucose (FPG) levels.

Methods

This was a cross‐sectional, single‐centre study. The homeostatic model assessment for insulin resistance (HOMA‐IR) and 2‐h post‐load glucose levels were used to evaluate patients with known HIV‐1 infection since before 1988 and no previous diagnosis of DM for whom data on hepatitis C virus (HCV) and hepatitis B virus (HBV) infection were available.

Results

Eighty‐four Caucasian patients [67 (80%) male; median age 45.7 years; range 43.8–49.1 years] were able to be evaluated; 65 (77%) were coinfected with HCV, and seven (8%) were coinfected with HBV. Median (interquartile range [IQR]) exposure to antiretrovirals was 12.8 (10.4–16.5) years. Fifteen patients (18%) had a previous AIDS‐defining event, 64 (76%) had HIV RNA<50 copies/mL, and the median (IQR) CD4 count was 502 (327–628) cells/μL. The median [IQR] FPG was 81 mg/dL (4.5 mmol/L) [75–87 mg/dL (4.2–4.8 mmol/L)], and the median (IQR) HOMA‐IR was 2.82 (1.89–4.02). After OGTT, nine patients (11%) were diagnosed as having IGT (6) or DM (3). A first multivariable analysis showed that CD4 cell count (P=0.038) and HOMA‐IR (P=0.035) were associated with IGT or DM, but a second model including only the variables with a P‐value of <0.2 in the univariable analysis (CD4 cell count, HBV coinfection, and HOMA‐IR) found that only HOMA‐IR independently predicted IGT or DM.

Conclusions

In patients with long‐standing HIV infection and normal FPG levels, an OGTT can reveal IGT or DM.     

糖代谢异常和糖尿病患者脉压的研究

目的:脉压与心脑血管疾病相关,糖代谢异常和2型糖尿病也是心脑血管疾病的危险因子,但是脉压与糖代谢异常、2型糖尿病的关系未见在我国人群中的研究报道。方法:对2 420例常规健康体检者进行血浆总胆固醇、甘油三酯、收缩压、舒张压、脉压和体重指数(BMI)测定,观察脉压与糖代谢异常和2型糖尿病的关系。为了避免年龄对脉压的影响,我们将所有被检查者以年龄分为3组(40~54岁组、55~69岁组和≥70岁组)。结果:40~54岁者脉压、收缩压、舒张压、BMI和甘油三酯在糖代谢异常和2型糖尿病组明显升高(P<0.01),总胆固醇在各组之间差异无显著性(P>0.05)。55~69岁者只有脉压在糖代谢异常和2型糖尿病组中明显升高(P<0.05)。年龄≥70岁组中,所有观察指标在各组之间差异均无显著性(P>0.05)。结论:脉压在年龄<70岁的糖代谢异常和2型糖尿病患者中升高。脉压升高预示着心脑血管疾病危险因素的存在。     

Association of sleep duration with type 2 diabetes and impaired glucose tolerance

Aims/hypothesis The aim of this study was to assess the relationship between sleep duration and type 2 diabetes or impaired glucose tolerance (IGT). Methods Anthropometric measurements and self-reported sleep duration were determined in a cross-sectional sample of 323 men and 417 women aged 21–64 years from the Quebec Family Study. Glucose homeostasis indicators were compared between short (5–6 h), ‘normal’ (7–8 h) and long (9–10 h) sleeper groups. Results Using adults with 7–8 h of sleep as a reference, the adjusted odds ratio for type 2 diabetes/IGT was 1.58 (1.13–2.31) for those with 9–10 h of sleep and 2.09 (1.34–2.98) for those with 5–6 h of sleep, after adjustment for potential confounding variables. The short and long sleepers presented significantly higher total insulin AUC (p < 0.05), whereas total glucose AUC was not different between the three sleeper groups in both sexes. The mean glucose area below fasting glucose concentrations was significantly higher in short (p < 0.01) and long sleepers (p < 0.05) compared with ‘normal’ sleepers, and significantly higher in short (p < 0.05) compared with long sleepers in both sexes. Conclusions/interpretation The present study provides evidence that short- and long-duration sleep times are associated with type 2 diabetes/IGT in adults, even after adjustment for several confounders. These results also showed that the lower glucose concentrations at the end of the OGTT were observed in short sleepers. According to the glucostatic theory of appetite control, this represents a stimulus that can trigger episodes of hunger and spontaneous food intake, which may explain at least in part the greater risk of overweight displayed by short sleepers, as shown in previous studies.     

Association of sleep time with diabetes mellitus and impaired glucose tolerance

BACKGROUND: Experimental sleep restriction causes impaired glucose tolerance (IGT); however, little is known about the metabolic effects of habitual sleep restriction. We assessed the cross-sectional relation of usual sleep time to diabetes mellitus (DM) and IGT among participants in the Sleep Heart Health Study, a community-based prospective study of the cardiovascular consequences of sleep-disordered breathing. METHODS: Participants were 722 men and 764 women, aged 53 to 93 years. Usual sleep time was obtained by standardized questionnaire. Diabetes mellitus was defined as a serum glucose level of 126 mg/dL or more (> or =7.0 mmol/L) fasting or 200 mg/dL or more (> or =11.1 mmol/L) 2 hours following standard oral glucose challenge or medication use for DM. Impaired glucose tolerance was defined as a 2-hour postchallenge glucose level of 140 mg/dL or more (> or =7.8 mmol/L) and less than 200 mg/dL. The relation of sleep time to DM and IGT was examined using categorical logistic regression with adjustment for age, sex, race, body habitus, and apnea-hypopnea index. RESULTS: The median sleep time was 7 hours per night, with 27.1% of subjects sleeping 6 hours or less per night. Compared with those sleeping 7 to 8 hours per night, subjects sleeping 5 hours or less and 6 hours per night had adjusted odds ratios for DM of 2.51 (95% confidence interval, 1.57-4.02) and 1.66 (95% confidence interval, 1.15-2.39), respectively. Adjusted odds ratios for IGT were 1.33 (95% confidence interval, 0.83-2.15) and 1.58 (95% confidence interval, 1.15-2.18), respectively. Subjects sleeping 9 hours or more per night also had increased odds ratios for DM and IGT. These associations persisted when subjects with insomnia symptoms were excluded. CONCLUSIONS: A sleep duration of 6 hours or less or 9 hours or more is associated with increased prevalence of DM and IGT. Because this effect was present in subjects without insomnia, voluntary sleep restriction may contribute to the large public health burden of DM.