WHAT IS THE FREQUENCY OF CARBOHYDRATE METABOLISM DISORDER IN CKD?

Objective: The objective of this paper is to detect the incidence of insulin resistance (IR) in Chronic Kidney disease (CKD) patients and the presence of impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and diabetes mellitus (DM) in patients with/without IR. Methods: We enrolled 113 patients with CKD. Biochemical parameters were investigated. Results: IFG was found 59.3% of patients with CKD. Age (p = 0.012), BMI (p = 0.036), TG (p = 0.008), HbA1c(p = 0.002), hs‐CRP (p = 0.015) levels were higher in patients with IFG. According to the results of Oral glucose tolerance test (OGTT), 69% of patients with CKD had a detected carbohydrate metabolism disorder, 9.7% had DM, 59.3% had IGT. In patients with IFG 13.6% had DM, 31.8% IGT, in patients without IFG 4.2% had DM and 29.8% IGT. The mean HOMA‐IR and insulin levels were 3.03 ± 1, 97/11.9 ± 7.13. IR was detected 23% of patients with CKD. In patients with IR; FBG (p = 0.003), serum insulin (p = 0.001), TG (p = 0.05) and HbA1c (p = 0.004) levels were elevated. 31.3% of patients with IFG were found to be IR. Conclusion: Carbohydrate metabolism disorder and insulin resistance are found in patients with CKD. Most patients with CKD who are elderly, obesity or overweight offer targets for additional risk factors. For these reasons, screening for DM may be recommended.     

Comparison between beta-cell function and insulin resistance indexes in prepubertal and pubertal obese children

Several methods have been developed to assess insulin resistance (IR), insulin secretion, and sensitivity: some of them, such as the homeostasis model assessment (HOMA) for IR (HOMA IR) and for insulin secretion (HOMA beta cell) and the quantitative insulin sensitivity check index (QUICKI) are based on fasting levels of glucose (fasting G) and insulin (fasting I); others, such as the pancreatic insulin response to glucose (IRG) and the insulin sensitivity index (ISI) are derived from the glycemic and insulinemic responses to the oral glucose tolerance test (OGTT). The aim of the study was to compare these indexes in a large group of prepubertal and pubertal obese subjects and verify whether the data from fasting samples were enough for evaluating IR and insulin secretion or if OGTT was mandatory. A total of 405 obese subjects (221 boys and 184 girls) was studied. Ninty-three were prepubertal (Tanner stage I), 98 early pubertal (stage II to III) and 214 late pubertal (stage IV to V). In each subject, a 120-minute OGTT was performed, and the glycemic (mean blood glucose [MBG]) and insulinemic (mean serum insulin [MSI]) responses, expressed as AUC/120, as well as IRG and ISI were calculated. The fasting I/fasting G ratio (FIGR), HOMA IR, HOMA beta cell, and QUICKI were then measured. FIGR and HOMA IR increased in both sexes during puberty, but in girls, the increase was already evident from stage I to stage II to III, while in boys, it was evident only from stage II to III to stage IV to V. QUICKI decreased in girls at the onset of puberty and was lower than in boys in stage II to III; on the other hand, HOMA beta cell did not show any variation. IRG increased throughout puberty, although it was higher in boys than in girls in stages II to III and IV to V, while ISI decreased at the onset of puberty in boys; HOMA IR correlated with MSI and IRG, and HOMA beta cell with MSI in pubertal subjects only. In conclusion, the indexes deriving from fasting samples, such as FIGR and HOMA IR, proved to be enough for evaluating IR in prepubertal and pubertal obese subjects, as did QUICKI for insulin sensitivity, However, OGTT is still useful for assessing insulin secretion, because IRG is more sensitive in depicting the pubertal variations of IR than HOMA beta cell.     

Uric acid,impaired fasting glucose and impaired glucose tolerance in youth with overweight and obesity

Background and aimThe relationships between uric acid (UA) and prediabetes is poorly explored in youth. We investigated the association between UA, impaired fasting glucose (IFG), impaired glucose tolerance (IGT), insulin resistance (IR) and low insulin sensitivity (IS) in youth with overweight/obesity (OW/OB).Methods and resultsA cross-sectional study was performed in 2248 youths with OW/OB (age 5–17 years). The sample was stratified in sex-specific quintiles (Q1 to Q5) of UA and the associations with fasting (FG), 2-h post-load glucose (2H-PG), IR and low IS were investigated. IR and low IS were estimated by assessment model of insulin resistance (HOMA-IR) and whole-body IS index (WBISI), respectively. IFG was defined as FG ≥ 100 < 126 mg/dL, IGT as 2H-PG ≥140 < 200 mg/dL, IR as HOMA-IR ≥75th percentile and low IS as WBISI ≤25th percentile by sex. Age, body mass index z-score, 2H-PG, HOMA-IR and WBISI, increased across sex-quintiles of UA while FG did not. The prevalence of IFG and IR were significantly increased in Q5 vs Q1 (reference quartile, P < 0.025). The prevalence of IGT increased from Q3 to Q5 vs Q1 (P < 0.025–0.0001) and that of low IS from Q2 to Q5 vs Q1 (P < 0.005–0.0001).ConclusionsIn youth with OW/OB, rates of IGT and low IS increased progressively across quintiles of UA. On the contrary, IFG and IR were associated only with the highest quintile of UA. Our data suggest that UA is a biomarker of impaired glucose metabolism prevalently in post–challenge condition rather than in fasting state.     

不同糖耐量人群血浆脂肪酸谱与胰岛素抵抗

目的　研究不同糖耐量人群血浆脂肪酸谱与胰岛素抵抗 (IR)之间的关系。方法　将受试者根据口服葡萄糖耐量试验 (OGTT)结果分为正常糖耐量组 (NGT) ,糖耐量受损组 (IGT )及 2型糖尿病组(DM )。采用毛细血管气相色谱法测定血浆脂肪酸谱 ,用胰岛素敏感指数 (IAI)评估IR。结果　DM组及IGT组血浆软脂酸 (C16:0 )、硬脂酸 (C18:0 )、二十二烷酸 (C2 2 :0 )、二十四烷酸 (C2 4:0 )和饱和脂肪酸浓度较NGT组明显升高 (P <0 .0 5～P <0 .0 1) ;花生四烯酸 (C2 0 :4)分别从NGT、IGT和DM组依次升高 ,差异有显著性 (P <0 .0 5～P <0 .0 1) ;血浆饱和脂肪酸 (SFA)从NGT、IGT、DM亚组依次升高 (P <0 .0 5～P <0 .0 1) ;NGT组的多不饱和脂肪酸 (PUFA)与饱和脂肪酸 (SFA)的比率高于IGT组和DM组 (均P <0 .0 5 ) ;血浆C16:0、C2 0 :4、C2 2 :0、SFA与IAI呈负相关 (P均 <0 .0 1)、PUFA/SFA与IAI呈正相关 (P <0 .0 1)。结论　不同糖耐量者血浆脂肪酸谱不同 ,糖耐量减低与 2型糖尿病患者SFA浓度升高 ,PUFA/SFA下降 ,且与胰岛素抵抗密切相关     

不同糖耐量水平人群血清真胰岛素和胰岛素原水平的临床意义

目的 探讨不同糖耐量者血清真胰岛素（ＴＩ）及胰岛素原（ＰＩ）水平的变化及临床意义。方法 用特异的单克隆抗体夹心放大酶联免疫分析法（ＢＡ－ＥＬＩＳＡ）检测１３５例正常糖耐量（ＮＧＴ）、８６例糖耐量低减（ＩＧＴ）及１０１例Ⅱ型糖尿病（ＤＭ）者口服葡萄糖耐量试验（ＯＧＴＴ）各点血清ＴＩ及ＰＩ水平。结果 ３组血清空腹ＴＩ差异无显著性（Ｐ〉０．０５）,免疫反应胰岛素（ＩＲＩ）Ⅱ型ＤＭ组明显升高（Ｐ〈０．０１     

Diabetes and impaired glucose tolerance prevalences in Turkish patients with impaired fasting glucose

Impaired fasting glucose (IFG) like impaired glucose tolerance (IGT) has increased risk of progressing to diabetes mellitus (DM). The aim of the study was to evaluate prevalance of IGT and type 2 DM with oral glucose tolerance test (OGTT) in Turkish patients who had fasting glucose of 110 and 125 mg/dl. Hundred and forty-eight (67.3%) women and 72 (32.7%) men (30-65 years old with mean age of 51.3 +/- 8.7 year) who had fasting glucose range 110-125 mg/dl were evaluated with OGTT. Seventy-two patients had IGT (32.8%), 74 (33.6%) patients had type 2 diabetes and 74 (33.6%) patients had normal glucose tolerance (NGT). Mean fasting glucose and insulin levels were higher in the IGT group than in the NGT group. Mean level of total cholesterol was higher in DM than that in NGT and IGT groups. Mean triglyceride (TG) (P = 0.476), high-density lipoprotein (HDL) (P = 0.594), low-density lipoprotein (LDL) (P = 0.612), Apoproteine A (P = 0.876), Apoproteine B (P = 0.518), uric acid (P = 0.948) and ferritin (P = 0.314) were found higher in diabetic patients. Lipoproteine a (P = 0.083), fibrinogen (P = 0.175) and hsCRP (P = 0.621) levels were higher in IGT. Mean HOMA S% levels of NGT, IGT and DM were found to be 65.0 +/- 13.0%, 60.9 +/- 16.0% and 50.1 +/- 11.1%, respectively. HOMA B% levels were measured to be 80.4 +/- 29.1% in NGT, 85.3 +/- 14.59% in IGT and 60.1 +/- 10.1% in DM. Significant difference was found between IFG and DM (P = 0.043) groups. The prevalences of diabetes and IGT were found to be 33.63 and 32.7% in IFG, respectively.     

不同血糖状态下血清超敏C反应蛋白、纤溶酶原激活物抑制物-1水平的变化及与胰岛素抵抗的关系

目的检测不同血糖状态人群空腹血清超敏C反应蛋白（hs—CRP）、纤溶酶原激活物抑制物-1（PAI-1）水平,探讨hs—CRP、PAI-1与胰岛素抵抗之间的关系。方法选取健康对照组、糖耐量减低组、2型糖尿病组受试者各30例,测定受试者空腹血清hs—CRP、PAI-1、血脂、空腹胰岛素等项目,应用稳态模型评估法评价胰岛素抵抗。结果2型糖尿病组、糖耐量减低组、对照组依次比较,hs—CRP、PAI-1、胰岛素抵抗指数均有显著升高（P均〈0．05）;多元逐步回归分析显示体重指数、hs—CRP、PAI-1是影响胰岛素抵抗的重要危险因素。结论2型糖尿病人群、糖耐量减低人群存在明显的胰岛素抵抗,hs—CRP、PAI-1、BMI是加重胰岛素抵抗的危险因素;糖调节受损时期即可能存在慢性炎症反应,并出现大血管病变的一些病理生理改变。     

Early insulin secretion failure leads to diabetes in Chinese subjects with impaired glucose regulation

Background Both beta‐cell dysfunction and decreased insulin sensitivity are involved in the pathogenesis of impaired glucose tolerance (IGT) and impaired fasting glucose (IFG), while their relative contribution in the progression to type 2 diabetes still remains controversial. The aim of the present study is to clarify this process in Chinese subjects by using cross‐sectional method. Methods 2975 Chinese subjects were classified into: normal glucose tolerance (NGT), impaired glucose regulations (IGR), and diabetes mellitus (DM) based on oral glucose tolerance test (OGTT). The IGR group was sub‐classified as isolated IFG, isolated IGT and combined glucose intolerance (CGI). The DM group was sub‐classified as normal fasting plasma glucose and 2‐hour hyperglycemia (N0D2), fasting hyperglycemia and normal 2‐hour plasma glucose (D0N2), and both fasting and 2‐hour hyperglycemia (D0D2). Results As far as insulinogenic index (IGI) was concerned, there was no difference between IFG and IGT in either gender, however, HOMA2‐B% (homeostasis model assessment for beta‐cell function) of IGT was higher than that of IFG and CGI in both male and female (P < 0.05). In the diabetic sub‐groups, IGI of N0D2 was higher than that of D0N2, and both deteriorated compared with those of IGT and IFG, respectively. HOMA2‐B% of N0D2 was still higher than that of D0N2 and D0D2. No significant difference was detected in OGIS and HOMA2‐S% (homeostasis model assessment for insulin sensitivity) between IFG and IGT, and this was the case between N0D2 and D0N2. OGIS and HOMA‐IR of IGR sub‐groups were not different from those of their diabetic counterparts. Conclusion Failure of beta‐cell function might be the main reason for both IGT and IFG developing into diabetes instead of aggravated insulin resistance. Copyright © 2008 John Wiley & Sons, Ltd.     

Glucose intolerance,insulin resistance,and hyperandrogenemia in first degree relatives of women with polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is associated with hyperinsulinemia, insulin resistance (IR), increased risk of glucose intolerance, and type 2 diabetes. Family studies have indicated a genetic susceptibility to PCOS. The aims of this study were 1) to assess glucose tolerance status, gonadotropins, and androgens in first degree relatives of patients with PCOS; and 2) to assess IR in normal glucose tolerant (NGT) family members. One hundred two family members of 52 patients with PCOS [Mothers(PCOS) (n = 34; mean age, 46.5 yr; mean body mass index (BMI), 28.8 kg/m(2)), Fathers(PCOS) (n = 24; mean age, 50.4 yr; mean BMI, 27.5 kg/m(2)), Sisters(PCOS) (n = 19; mean age, 25.1 yr; mean BMI, 22.9 kg/m(2)), and Brothers(PCOS) (n = 25; mean age, 23.7 yr; mean BMI, 22.5 kg/m(2))] and 82 unrelated healthy control subjects without a family history of diabetes or PCOS (4 age- and weight-matched subgroups, i.e. Control(MothersPCOS), Control(FathersPCOS), Control(SistersPCOS), and Control(BrothersPCOS)) were studied. Glucose and insulin (at baseline and during a 75-g, 2-h oral glucose tolerance test) were measured. IR was assessed by fasting insulin (FI), fasting glucose to insulin ratio (FGI), homeostatic model assessment (HOMA IR), and area under the curve for insulin during the oral glucose tolerance test (AUC(insulin)) in NGT Mothers(PCOS), Fathers(PCOS), Sisters(PCOS), Brothers(PCOS), and matched control subgroups. Including the prestudy-diagnosed 3 mothers and 2 fathers with diabetes, diabetes and impaired glucose tolerance (IGT) were noted in 16% and 30% of Mothers(PCOS) and 27% and 31% of Fathers(PCOS), respectively. There was no diabetes in Sisters(PCOS) and Brothers(PCOS). IGT was found in 5% of Sisters(PCOS). Impaired fasting glucose was found in 3% of Mothers(PCOS) and 4% of Brothers(PCOS). The analysis of NGT family members showed that Mothers(PCOS) had higher FI (P < 0.05), HOMA IR (P < 0.05), and AUC(insulin) (P < 0.01) and lower FGI (P < 0.05) than Control(MothersPCOS), whereas all IR parameters were comparable between Fathers(PCOS) and their matched control subgroup. Sisters(PCOS) had higher FI (P < 0.05), HOMA IR (P < 0.01), and AUC(insulin) (P < 0.05) and lower FGI (P < 0.01), and Brothers(PCOS) had higher AUC(insulin) (P < 0.01) than their matched control subgroups, respectively. Mothers(PCOS) had higher testosterone levels than Control(MothersPCOS) (P < 0.01 and P < 0.05 for pre- and postmenopausal women, respectively). Sisters(PCOS) had higher LH (P < 0.01), testosterone (P < 0.001), androstenedione (P < 0.01), and dehydroepiandrosterone sulfate (P < 0.05) levels than Control(SistersPCOS). There was no difference in gonadotropin and androgen levels in Fathers(PCOS) compared with Control(FathersPCOS) or in Brothers(PCOS) compared with Control(BrothersPCOS). Our results suggest that 1) first degree relatives of patients with PCOS may be at high risk for diabetes and glucose intolerance; 2) NGT female family members have insulin resistance; and 3) mothers and sisters of PCOS patients have higher androgen levels than control subjects. We propose that the high risks of these impairments warrant screening in first degree relatives of patients with PCOS.     

Evaluation of insulin release and insulin sensitivity through oral glucose tolerance test: differences between NGT,IFG, IGT,and type 2 diabetes mellitus. A cross-sectional and follow-up study

Abstract. We evaluated both insulin release (IR) and insulin sensitivity (IS) through a single oral glucose tolerance test (OGTT) (blood samples at 0, 60, 120 min, as routinely performed in Europe) in subjects with normal and abnormal glucose tolerance. The value 1/HOMA was used as an index of IS and I/G at 60 min was used as an index of IR. In preliminary experiments, 1/HOMA correlated with glucose infusion rate (GIR) at euglycaemic insulin clamp (r=0.495) and with insulin sensitivity index (ISI) at LDIGIT (r=0.714). At OGTT with blood samples at 0, 30, 60 and 120 min, insulin levels at 30 min correlated with insulin levels at 60 min (I30 vs. I60, r=0.584) and I/G at 30 and at 60 min correlated (r=0.365). Values of 1/HOMA from 345 subjects with normal glucose tolerance (NGT), 32 with impaired fasting glucose (IFG), 186 with impaired glucose tolerance (IGT) and 72 with type 2 diabetic mellitus were divided into quartiles. For each quartile, mean (± SE) and 95% confidence intervals (CI) of I/G at 60 min were calculated, and subjects were represented by plotting IS vs. IR. Plots of NGT, IGT, and type-2 diabetes mellitus described different curves. Values of subjects with IFG, IGT and type 2 diabetes mellitus fell outside the 95% CI of NGT subjects in all quartiles of IS. To validate this finding, 113 morbidly obese subjects (basal OGTT: 55 NGT, 40 IGT, 18 T2DM) who underwent a major reduction of body weight through bariatric surgery received a second OGTT one year after surgery. Glucose tolerance improved in 40 patients, deteriorated in 8, did not change in 65; the new plots were concordant with the new class of glucose tolerance. OGTT can be used to evaluate both IR and IS in subjects with NGT, IFG, IGT, and type 2 diabetes mellitus in population studies and in follow-up studies. IFG, IGT and type 2 diabetes mellitus are characterized by reduced IR compared to IS.     

Insulin secretion and insulin sensitivity at different stages of glucose tolerance: a cross-sectional study of Japanese type 2 diabetes

To evaluate the factors causing glucose intolerance in type 2 diabetes in Japan, insulin secretion and insulin sensitivity were compared across the range of glucose tolerance. Subjects were divided into 3 groups: normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and type 2 diabetes (DM) according to the criteria of the World Health Organization (WHO). We examined insulin secretion and insulin sensitivity using fasting blood glucose and insulin levels and 75 g oral glucose tolerance test (OGTT). We used homeostasis model assessment (HOMA) beta-cell and insulinogenic index (30 minutes) to estimate insulin secretion and HOMA-insulin resistance (IR) and insulin sensitivity index (ISI) composite for insulin sensitivity. Although insulin resistance plays an important role in the development of diabetes in many ethnic populations, the differences in insulin sensitivity between NGT and IGT and between IGT and DM are small in Japanese patients. On the other hand, as glucose intolerance increases, insulin secretion decreases most remarkably both between NGT and IGT and between IGT and DM in Japanese patients. Decreasing insulin secretion and decreasing insulin sensitivity both occur in developing type 2 diabetes in Japanese patients, but decreased basal and early-phase insulin secretion had more pronounced contribution to glucose tolerance than the indices of insulin sensitivity. Japanese type 2 diabetic patients are characterized by a larger decrease in insulin secretion and show less attribution of insulin resistance.     

Thiazolidinediones increase hepatic insulin extraction in African Americans with impaired glucose tolerance and type 2 diabetes mellitus. A pilot study of rosiglitazone

Peripheral insulin levels are determined by beta-cell secretion, insulin sensitivity, and hepatic insulin extraction (HIE). We have previously shown that whereas sulfonylureas reduce insulin extraction, metformin enhances HIE. However, the effects of thiazolidinediones (TZDs) on HIE remain uncertain. Thus, we investigated the potential contribution of hepatic insulin clearance to peripheral insulin levels during rosiglitazone therapy in African Americans with impaired glucose tolerance (IGT) and type 2 diabetes mellitus (DM). The study was composed of 12 first-degree relatives with IGT and 17 patients with newly diagnosed type 2 DM. Nineteen healthy relatives with normal glucose tolerance served as controls. Serum glucose, insulin, and C-peptide, and HIE (C-peptide-insulin molar ratios) were measured at t = 0 and 120 minutes during oral glucose tolerance test (OGTT) in all the subjects. The OGTT was performed before and after 3 months of rosiglitazone therapy (4 mg/d x 4 weeks and >8 mg/d x 8 weeks) in patients with IGT and type 2 DM. Insulin resistance index and beta-cell function were calculated in each subject using homeostasis model assessment (HOMA). Rosiglitazone therapy improved but did not normalize the overall glycemic control in the IGT and type 2 DM groups. After rosiglitazone therapy, the mean serum insulin and C-peptide levels at fasting remained unchanged. However, the 2-hour serum glucose and insulin were lower, whereas serum C-peptide was unchanged during 3 months of rosiglitazone treatment. Mean insulin resistance index of HOMA was reduced by 30% (4.12 +/- 1.95 vs 6.33 +/- 3.54, P < .05) in the type 2 DM group and by 21% (3.78 +/- 2.45 vs 4.81 +/- 3.49, P = NS) in the IGT group. Mean HIE values were significantly lower (70%) in the type 2 DM and IGT groups when compared with the normal glucose tolerance group. At 3 months, basal HIE was not significantly changed by rosiglitazone therapy in IGT and type 2 DM groups when compared with the baseline (0 month). However, rosiglitazone therapy was associated with increased HIE at 2 hours during OGTT by 40% and 30% in the IGT and type 2 DM groups, respectively, from the baseline (0 month) values. Furthermore, HIE inversely correlated with the insulin resistance index of HOMA (r = -.46, P < .05). We conclude that rosiglitazone therapy improved overall glucose tolerance and enhanced insulin sensitivity in patients with IGT and type 2 DM. Although basal HIE remained unchanged, rosiglitazone therapy increased postglucose challenge HIE in African Americans with IGT and type 2 DM. We speculate that TZDs increase insulin clearance or HIE after oral glucose challenge. This study suggests that in addition to insulin sensitization, rosiglitazone may be involved in insulin metabolism. The significance of the increased insulin clearance by TZD therapy remains uncertain and deserves further investigation in patients with insulin resistance and glucose intolerance.     

Insulin resistance and impaired glucose tolerance in obese children and adolescents referred to a tertiary-care center in Israel

OBJECTIVE: To establish the prevalence of insulin resistance and impaired glucose tolerance (IGT) and their determinants in a cohort of obese children and adolescents. METHODS: A retrospective design was used. The study group included 234 patients with a body mass index (BMI) greater than the 95th percentile for age and gender and 22 patients with a BMI between the 85th and 95th percentile for age and gender referred for evaluation to a major tertiary-care center in Israel. Ages ranged from 5 to 22 y. Estimates of insulin resistance (homeostatic model assessment (HOMA-IR)); insulin sensitivity (ratio of fasting glucose (GF) to fasting insulin (IF) (GF/IF), the quantitative insulin sensitivity check index (QUICKI)), and pancreatic beta-cell function (HOMA-derived beta-cell function (HOMA %B)) were derived from fasting measurements. An oral glucose tolerance test (OGTT) was performed in 192 patients to determine the presence of IGT. RESULTS: Insulin resistance was detected in 81.2% of the patients, IGT in 13.5%, and silent diabetes in one adolescent girl. Only two patients with IGT also had impaired fasting glucose (IFG). The prevalence of IGT was higher in adolescents than prepubertal children (14.7 vs 8.6%). GF/IF and QUICKI decreased significantly during puberty (P<0.005), whereas HOMA-IR and HOMA %B did not. Insulin resistance and insulin sensitivity indexes were not associated with ethnicity, presence of acanthosis nigricans or family history of type 2 diabetes. Patients with obesity complications had lower insulin sensitivity indexes than those without (P=0.05). Compared with subjects with normal glucose tolerance (NGT), patients with IGT had significantly higher fasting blood glucose (85.9+/-6.5 vs 89.2+/-10.6 mg/dl, P<0.05), higher 2-h post-OGGT insulin levels (101.2+/-74.0 vs 207.6+/-129.7 microU/ml, P<0.001), a lower QUICKI (0.323+/-0.031 vs 0.309+/-0.022, P<0.05), and higher fasting triglyceride levels (117.4+/-53.1 vs 156.9+/-68.9, P=0.002). However, several of the fasting indexes except QUICKI failed to predict IGT. There was no difference between the group with IGT and the group with NGT in fasting insulin, HOMA-IR, HOMA %B or the male-to-female ratio, age, BMI-SDS, presence of acanthosis nigricans, ethnicity, and family history of type 2 diabetes.CONCLUSIONS:Insulin resistance is highly prevalent in obese children and adolescents. The onset of IGT is associated with the development of severe hyperinsulinemia as there are no predictive cutpoint values of insulin resistance or insulin sensitivity indexes for IGT, and neither fasting blood glucose nor insulin levels nor HOMA-IR or HOMA %B are effective screening tools; an OGTT is required in all subjects at high risk. Longitudinal studies are needed to identify the metabolic precursors and the natural history of the development of type 2 diabetes in these patients.     

Clinical evaluation of insulin resistance and β-cell function by the homeostasis model assessment in patients with systemic lupus erythematosus

The aim of this preliminary study was to evaluate insulin resistance and secretion using homeostasis model assessment (HOMA) in patients with systemic lupus erythematosus (SLE). The fasting glucose and insulin concentrations, HOMA insulin resistance (IR), HOMA -cell, antidouble-stranded DNA antibodies (anti-dsDNA), C3, C4, and SLE disease activity index (SLEDAI) were determined in a total of 58 female SLE patients. All patients were classified into subgroups according to the presence of anticardiolipin antibodies (aCL+ vs. aCL-) and SLEDAI scores (SLEDAI <3 vs. SLEDAI >3). Results showed that SLE patients with and without aCL had significantly higher fasting insulin levels, HOMA IR, and HOMA -cells than controls. Similar results were also found in SLE patients with different disease activities. Pearsons correlation analysis showed that there was a highly significant correlation of HOMA IR with fasting insulin concentration in the SLE patients and SLE subgroups overall. However, HOMA -cells were positively correlated with HOMA IR and fasting insulin level, but negatively correlated with fasting glucose concentration in SLE patients overall. In conclusion, SLE patients, regardless of the presence of aCL and different disease activities, had a higher risk of insulin resistance and abnormal insulin secretion than age-matched healthy controls, based on fasting insulin concentration, HOMA IR, and HOMA -cells.Abbreviations HOMA Homeostasis model assessment - IGT Impaired glucose tolerance - IR Insulin resistance - NGT Normal glucose tolerance - SLE Systemic lupus erythematosus - SLEDAI SLE disease activity index     

Ⅱ型糖尿病家系中一级亲属的脂质代谢紊乱与胰岛素抵抗

为研究II型糖尿病家系中一级亲属的脂质变化和胰岛素抵抗，对25个II型糖尿病家系中非糖尿病一级亲属，糖耐量减低者，糖尿病患者进行了空腹血糖，空腹胰岛素，总胆固醇，甘油三酯和高密度脂蛋白测定，根据公式计算低密度脂蛋白及胰岛素敏感指数，并与家系中非糖尿病非糖耐量减低同胞的配偶进行了比照，结果发现，一级亲属，糖耐量减低者，糖尿病患者甘油三酯较正常对照组高，高密度脂蛋白，胰岛素敏感指数较正常对照组低，此结果提示，II型糖尿病患者的一级亲属在未患糖耐量减低和糖尿病之前存在脂代谢紊乱和胰岛素抵抗。     

Abnormal glucose tolerance in young male patients with nonalcoholic fatty liver disease

Objective: The association of nonalcoholic fatty liver disease (NAFLD) with insulin resistance and metabolic syndrome has been documented for obese men and middle‐aged men. This study was designed to determine the relationship between NAFLD and the oral glucose tolerance test (OGTT) to predict preclinical diabetes in nondiabetic young male patients (<30 years old). Methods: A total of 75 male patients who had elevated liver enzymes and who were diagnosed with NAFLD were enrolled in this study. A standard 75 g OGTT was carried out on all patients. Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) were defined as a fasting plasma glucose (FPG) level ≥100 mg/dl but <126 mg/dl, and a 2‐h post‐load glucose on the OGTT of ≥140 mg/dl, but <200 mg/dl respectively. Results: According to the OGTT results, 24 (32%) patients were diagnosed as having IGT and 12 (16%) patients were diagnosed as having diabetes. Among the 48 patients with normal fasting glucose, 18 (37.6%) patients showed abnormal glucose tolerance (15 had IGT and three had diabetes). The NAFLD patients with abnormal glucose tolerance showed significant differences in age, weight, body mass index, waist–hip ratio, alanine aminotransferase, total bilirubin, total cholesterol, low‐density lipoprotein cholesterol, triglyceride, insulin, FPG and homeostasis model for insulin resistance (HOMA‐IR). Multiple regression analysis showed that age, FPG and HOMA‐IR were independent predictors of abnormal glucose tolerance. Conclusions: Although the patients were young men, an OGTT should be recommended for NAFLD patients with elevated liver enzymes and IFG to predict the risk of type 2 diabetes.     

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.     

The patterns of glucose tolerance and insulin resistance among rural Chinese twin children, adolescents, and young adults

Pubertal insulin resistance (IR) is well recognized; but little data are available for glucose and insulin pattern from a large, unselected lean population. This report describes the age- and sex-specific distributions of glucose tolerance and IR in a rural Chinese twin population. This report includes 4488 subjects aged 6 to 24 years. The primary variables of interest are fasting plasma glucose, 2-hour postload plasma glucose (2-h PG), fasting serum insulin, 2-hour postload insulin, and the homeostatic model assessment for IR. Age- and sex-specific patterns for the primary variables are described using smoothing plot, arithmetic or geometric mean, and percentiles. There is an increase in fasting plasma glucose, 2-h PG, and IR during puberty (10-19 years) and a return to prepuberty level by the age of 20 years. Insulin resistance peaks at around the age of 14 years in girls and 16 years in boys. Two-hour postload plasma glucose and 2-hour postload insulin are higher in girls than in boys from early puberty, and the sex differences are more pronounced afterward. Moreover, the prevalence of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) increases after puberty and is higher in girls than in boys. In this community-based, nonobese rural Chinese twin population, we observed sex-specific remarkable pubertal surge of IR and modest increase in plasma glucose as well as increasing prevalence of IFG and IGT with age. Notably, females had higher 2-h PG and higher prevalence of IFG and IGT. Our study underscored that adolescence (even more so in females) is a critical period for developing IR and prediabetes.     

High prevalence of glucose metabolism disturbance in patients with lichen planus

AIM: To establish the prevalence of diabetes mellitus (DM) and insulin resistance in patients with lichen planus (LP), and to examine whether diabetic status showed any relation with the type of LP. PATIENTS AND METHODS: Thirty patients with LP and 30 age, weight, and sex matched volunteers were included. Serum fasting glucose, insulin, hemoglobin A1c levels were determined, a standard oral glucose tolerance test (OGTT) was performed. RESULTS: Of patients with LP, eight (26.7%) had DM (four newly diagnosed), however, only one (3.33%) diagnosed as DM in control group (p=0.007). Six patients (20.0%) with LP and four healthy persons (13.3%) had IGT (p>0.05). Glucose metabolism disturbance (DM+IGT) was detected in 14 (46.7%) of the patients and in 5 (16.7%) of the controls (p=0.026). HbA1c, fasting serum glucose, and insulin resistance (HOMA) were statistically higher in patients compared to controls. CONCLUSION: Our finding documented that approximately one half of the patients with LP had glucose metabolism disturbance, and one fourth had DM. We believe that further studies are needed to explain this close relationship between DM and LP.     

Betacellulin variants and type 2 diabetes in the Old Order Amish.

Betacellulin is a member of the epidermal growth factor (EGF) family and may play a role in islet neogenesis and regeneration. To evaluate whether polymorphisms in this gene are associated with type 2 diabetes (T2DM) and impaired glucose tolerance (IGT), we genotyped 7 previously identified betacellulin variants in Amish subjects with T2DM (n=150), IGT (n=148) and normal glucose tolerance (NGT) (n=361). There were no significant differences in the allele frequencies of the variants among the 3 groups. In an expanded set of 729 nondiabetic Amish subjects, there was no significant association between the betacellulin variants and levels of glucose or insulin either fasting or during a 3 h oral glucose tolerance test, HOMA or insulin secretion index. These results are consistent with previous studies in Caucasian populations and suggest that variants in the betacellulin gene do not play a major role in the development of T2DM in Caucasian populations.