糖尿病及糖耐量减低合并冠心病患者的超声心动图特点

目的　探讨糖尿病及糖耐量减低合并冠心病患者的超声心动图的特点。方法　回顾我院经冠状动脉造影确诊为冠心病患者 10 4例 ,分为糖尿病组 4 4例、糖耐量减低组 15例和糖耐量正常组 4 5例。观察上述三组超声心动图差异。结果　三组间左室重量 (LVM )、体质量指数 (BMI)、射血分数 (EF)、二尖瓣血流最大流速E峰和A峰比值(E/A)、右室内径 (RV)之间差异有统计学意义 (P <0 .0 5～ 0 .0 1) ;而左房内径 (LA)、左室内径 (LV)、室间隔 (IVS)、左室后壁 (LVPWD)差异无统计学意义。结论　糖尿病及糖耐量减低患者合并冠心病时 ,左室功能明显减退。     

Insulin and C-peptide levels, pancreatic beta cell function, and insulin resistance across glucose tolerance status in Thais

Impaired pancreatic beta cell function and insulin sensitivity are fundamental factors in the pathogenesis of type 2 diabetes; however, the predominant defect appears differ among ethnic groups. We conducted a cross-sectional study to evaluate the contribution of impaired beta cell function and insulin sensitivity at different stages of the deterioration of glucose tolerance in Thais. The study involved 420 urban Thais of both sexes, 43-84 years old. A 75-g oral glucose tolerance test was performed on all of the subjects. Indices of insulin resistance and beta cell function were calculated with the use of a homeostasis model assessment. The subjects were classified as having normal glucose tolerance (NGT), isolated impaired fasting glucose (IFG), isolated impaired glucose tolerance (IGT), combined IFG and IGT, or type 2 diabetes mellitus according to the American Diabetes Association (ADA) criteria. There were no differences between groups with regard to gender and age. The percentage of obesity was significantly greatest in the diabetic group. Fasting serum insulin and C-peptide levels progressively increased from the NGT to the diabetic subjects. Serum C-peptide was more strongly associated with newly diagnosed diabetes than insulin, and was an independent factor associated with newly diagnosed diabetic subjects. The insulin resistance index progressively increased when the glucose tolerance stage changed from NGT through diabetic subjects. Beta cell function did not change significantly in any other group compared to the NGT group. An increase in fasting serum C-peptide may be a risk factor for type 2 diabetes. Obesity and insulin resistance are the predominant features in the deterioration of glucose tolerance in Thais.     

Inverse association between fish intake and risk of glucose intolerance in normoglycemic elderly men and women.

OBJECTIVE: To examine the association of fish intake with the subsequent risk of impaired glucose tolerance and diabetes mellitus (glucose intolerance). RESEARCH DESIGN AND METHODS: In 1971, information about food intake was obtained by the cross-check dietary history method on 175 men and women aged 64-87 yr who were normoglycemic and free of clinical diabetes. During the follow-up period from 1972 to 1975, an oral glucose tolerance test was performed annually, and in 59 of 175 elderly people a diagnosis of glucose intolerance was made at least once. RESULTS: In 1971, approximately 60% of the subjects usually ate fish, with a mean daily intake of 24.2 g. In fish eaters, the incidence of glucose intolerance was significantly lower compared with nonfish eaters (odds ratio [OR] 0.40, 95% confidence interval [CI] 0.21-0.77). With logistic regression analysis, this inverse association could not be explained by taking into account age and sex or possible confounding baseline characteristics, such as the prevalence of myocardial infarction, body mass index, energy intake per kilogram body weight, or intake of carbohydrates (OR 0.47, 95% CI 0.23-0.93). Baseline characteristics of the oral glucose tolerance test and serum triglyceride levels could also not account for this result. CONCLUSIONS: These results suggest that, in an elderly population, the habitual consumption of a small amount of fish may protect against the development of impaired glucose tolerance and diabetes mellitus.     

糖耐量受损:心血管疾病的重要危险因子

学术背景:糖耐量受损阶段的异常血糖水平已导致机体组织器官损害,尤其是心血管病变.此阶段心血管疾病的患病率和死亡率均显著高于正常糖代谢人群,其心血管病变的危险性已接近糖尿病.目的:探讨糖耐量受损发生心血管疾病的危险性及其伴随的相关危险因素.检索策略:由该论文的研究人员应用计算机检索Pubmed、Blackwell Synergy数据库1997-01/2007-06的相关文献,检索词“impaired glucose tolerance,diabetes mellitus,cardiovascular disease“,并限定文章语言种类为English.同时计算机检索中国期刊全文数据库1998-01/2007-06的相关文献,检索词为“糖耐量受损,糖尿病,心血管疾病,血糖漂移“,并限定语种为中文.共检索到109篇文献,对资料进行初审,纳入标准:评估糖代谢状况的检测方法,糖耐量受损与2型糖尿病,糖耐量受损与心血管疾病.排除标准:重复性研究.文献评价:文献的来源主要是通过对糖耐量受损的定义、流行病学特点、评估方式及其危害性进行汇总分析.所选用的36篇文献中,6篇为综述,其余为临床或基础实验研究.资料综合:糖耐量受损与正常血糖者相比,已呈现明显的糖代谢紊乱.糖耐量受损进展为糖尿病的风险增大,且常合并一系列的心血管危险因子,致发生心血管疾病的危险性亦显著增加,糖耐量受损阶段心血管疾病的危险性已接近糖尿病.结论:糖耐量受损是心血管疾病的重要危险因子.有必要进一步研究及评估糖耐量受损阶段高血糖对机体的损害,早期采取干预措施,能降低及延缓心血管疾病的发生、进展.     

糖尿病和糖耐量异常患者在急性缺血性脑血管病中的调查研究

目的 探讨糖尿病和糖耐量异常患者在急性缺血性脑血管病中的流行情况.方法 选择急诊内科病房及神经内科住院的115例短暂性脑缺血发作(TIA)、496例急性脑梗死患者进行空腹血糖、糖化血红蛋白检测,登记患者的临床资料,对既往未诊断糖尿病而空腹血糖在6.1～6.9 mmol/L的患者中进行口服葡萄糖耐量试验(OGTT),糖代谢分类采用2003年美国糖尿病学会建议标准.结果 611例急性缺血性脑血管病患者住院前糖尿病的诊断率18.8%,住院后系统检查发现糖尿病新的患病率45.0%,糖耐量异常18.6%;212例空腹血糖在6.1～6.9 mmol/L的患者中,OGTT发现其中33.5%患者可诊断为糖尿病,53.8%提示糖耐量异常.结论 63.8%的急性缺血性脑血管病患者合并糖尿病或糖耐量异常;空腹血糖在6.1～6.9 mmol/L的患者应常规做OGTT检查来筛查糖代谢异常患者.     

Early postpartum metabolic assessment in women with prior gestational diabetes.

OBJECTIVE: To present the results of early postpartum metabolic assessment in women with gestational diabetes mellitus (GDM), to determine predictive factors for subsequent diabetes, and to investigate the association of postpartum glucose tolerance with other components of the metabolic syndrome. RESEARCH DESIGN AND METHODS: A total of 788 women were evaluated 3-6 months after a GDM pregnancy. A 75-g oral glucose tolerance test (OGTT) was performed. Cholesterol, HDL cholesterol, triglycerides, blood pressure, BMI, and body fat distribution were assessed. Clinical and obstetric history, baseline variables at the diagnosis of GDM, metabolic control during pregnancy, and index pregnancy outcome were compared in women with diabetes and women without diabetes (American Diabetes Association [ADA] criteria) after pregnancy. Multivariate logistic regression analysis was used to ascertain independent predictors of subsequent diabetes. Correlation coefficients were assessed between postpartum glucose tolerance and lipid levels, blood pressure, BMI, and body fat distribution. RESULTS: According to ADA criteria, 588 (74.6%) women were normal, 46 (5.8%) had impaired fasting glucose, 82 (10.4%) had impaired glucose tolerance, 29 (3.7%) had both impaired fasting glucose and impaired glucose tolerance, and 43 (5.4%) had diabetes. Prepregnancy obesity, recurrence of GDM, gestational age at diagnosis of GDM, glucose values in the 100-g OGTT, number of abnormal values in the 100-g OGTT, fasting C-peptide levels in pregnancy, C-peptide/glucose score in pregnancy, insulin requirement in pregnancy, 3rd trimester HbA1c levels, and macrosomia differed significantly in women with subsequent diabetes. Independent predictors of postpartum diabetes were prepregnancy obesity, C-peptide/glucose score during pregnancy, and the number of abnormal values in the 100-g diagnostic OGTT. The area under the postpartum glucose curve was positively associated with BMI, waist circumference, waist-to-hip ratio, triglycerides, and systolic and diastolic blood pressures. CONCLUSIONS: Low C-peptide/glucose score during pregnancy together with prepregnancy obesity and severity of GDM (number of abnormal values in the 100-g diagnostic OGTT) are independent predictors of subsequent diabetes. Our data suggest that regardless of obesity and severity of GDM, a beta-cell defect increases the risk of postpartum diabetes. The association of postpartum glucose tolerance with triglyceride levels, blood pressure, obesity, and regional distribution of body fat suggests that postpartum glucose intolerance anticipates a high-risk cardiovascular profile that comprises other risk factors besides diabetes.     

Receptor and postreceptor defects contribute to the insulin resistance in noninsulin-dependent diabetes mellitus.

We have assessed the mechanisms involved in the pathogenesis of the insulin resistance associated with impaired glucose tolerance and Type II diabetes mellitus by exploring, by means of the euglycemic glucose-clamp technique, the in vivo dose-response relationship between serum insulin and the overall rate of glucose disposal in 14 control subjects; 8 subjects with impaired glucose tolerance, and 23 subjects with Type II diabetes. Each subject had at least three studies performed on separate days at insulin infusion rates of 40, 120, 240, 1,200, or 1,800 mU/M2 per min. In the subjects with impaired glucose tolerance, the dose-response curve was shifted to the right (half-maximally effective insulin level 240 vs. 135 microunits/ml for controls), but the maximal rate of glucose disposal remained normal. In patients with Type II diabetes mellitus, the dose-response curve was also shifted to the right, but in addition, there was a posal. This pattern was seen both in the 13 nonobese and the 10 obese diabetic subjects. Among these patients, an inverse linear relationship exists (r = -0.72) so that the higher the fasting glucose level, the lower the maximal glucose disposal rate. Basal rates of hepatic glucose output were 74 +/- 4, 82 +/- 7, 139 +/- 24, and 125 +/- 16 mg/M2 per min for the control subjects, subjects with impaired glucose tolerance, nonobese Type II diabetic subjects, and obese Type II diabetic subjects, respectively. Higher serum insulin levels were required to suppress hepatic glucose output in the subjects with impaired glucose tolerance and Type II diabetics, compared with controls, but hepatic glucose output could be totally suppressed in each study group. We conclude that the mechanisms of insulin resistance in patients with impaired glucose tolerance and in patients with Type II noninsulin-dependent diabetes are complex, and result from heterogeneous causes. (a) In the patients with the mildest disorders of carbohydrate homeostasis (patients with impaired glucose tolerance) the insulin resistance can be accounted for solely on the basis of decreased insulin receptors. (b) In patients with fasting hyperglycemia, insulin resistance is due to both decreased insulin receptors and postreceptor defect in the glucose mechanisms. (c) As the hyperglycemia worsens, the postreceptor defect in peripheral glucose disposal emerges and progressively increases. And (d) no postreceptor defect was detected in any of the patient groups when insulin's ability to suppress hepatic glucose output was measured.     

血清C-反应蛋白与妊娠糖尿病的关系研究

目的探讨血清C-反应蛋白（C-reactive protein,CRP）水平与妊娠糖尿病（gestational diabetes mellitus,GDM）的关系。方法选取2002年6月至2006年6月本院门诊及住院患者经75g葡萄糖耐量试验（OGTT）确诊为妊娠期糖尿病患者（GDM）48例和糖耐量异常妊娠妇女32例,并随机选择同期相匹配的正常糖耐量妊娠妇女80例（作为对照组）,同时检测空腹血清CRP水平。结果GDM组C-反应蛋白水平明显高于另两组（P〈0.05）;CRP水平与孕前体重指数（BMI）、空腹血糖、空腹胰岛素呈正相关,相关系数分别为0.348、0.156和0.296,P值分别为0.0001、0.0178和0.0004。直线回归方程y=0.0741x1＋0.0147x2＋0.0397x3-1.457,r2=0.2469。结论C-反应蛋白与GDM密切相关,参与了其发病机制。     

Diagnosis of impaired glucose tolerance in hypertensive patients in daily clinical practice

Many patients with hypertension suffer from impaired glucose tolerance or type 2 diabetes mellitus. Although these diagnoses are generally simple and reliable, it is more difficult to diagnose impaired glucose tolerance. As the gold standard (oral glucose tolerance test (OGTT)) is complicated to perform, a simpler alternative would be useful. The aims of the Pre-Diabetes Score study are to correlate demographic and/or laboratory parameters that are clinically simple to determine with the results of the OGTT and to determine the diagnostic significance of the combinations of parameters with regard to impaired glucose tolerance. A total of 260 patients were included in the evaluation; 39% had impaired glucose tolerance and 12% had diabetes mellitus. A combination of HbA1c of > or =6%, a venous fasting glucose of > or =110 mg/dl, an age of > or =55 years, a systolic blood pressure of > or =140 mmHg and an enlarged waist size is highly predictive of impaired glucose tolerance.     

Relationship between serum lipoprotein ratios and insulin resistance in obesity

BACKGROUND: The fasting serum lipid profile [triglycerides (TGs), total cholesterol (TC), and LDL- and HDL-cholesterol (LDL-C and HDL-C)] is used to calculate lipid ratios (TC/HDL-C, LDL-C/HDL-C, TG/HDL-C) that allow identification of individuals at increased risk for cardiovascular disease. Because these individuals are also frequently insulin resistant, this study analyzed the relationships between lipid ratios and insulin sensitivity. METHODS: In 132 obese [mean (SE) body mass index, 37.5 (0.6) kg/m(2)] outpatients without known diabetes mellitus, fasting serum lipid profiles and 75-g oral glucose tolerance tests were performed. Insulin sensitivity was assessed from surrogate estimates for fasting (QUICKI) and dynamic (OGIS) conditions. RESULTS: After exclusion of other endocrine diseases (n = 35), the remaining patients were classified as glucose tolerant (n = 56), glucose intolerant (n = 22), or as having type 2 diabetes (n = 19). QUICKI and OGIS indicated severe insulin resistance in all individuals with type 2 diabetes and impaired glucose tolerance compared with glucose-tolerant individuals: QUICKI, glucose tolerant, 0.302 (0.002); glucose intolerant, 0.290 (0.002); type 2 diabetes, 0.281 (0.005); P <0.001; OGIS (mL . m(-2) . min(-1)), glucose tolerant, 343 (7), glucose intolerant, 293 (9); type 2 diabetes, 256 (12); P <0.001. Serum TG (P <0.005) and TG/HDL-C ratios (P <0.05) were increased in individuals with impaired glucose tolerance. TG/HDL-C ratios negatively correlated with QUICKI (r = -0.370; P < 0.001) and OGIS (r = -0.333; P < 0.005) in nondiabetic individuals (glucose tolerant plus glucose intolerant), but not in patients with type 2 diabetes (not significant). CONCLUSIONS: This study demonstrates that the TG/HDL-C ratio positively correlates with insulin resistance in severely obese nondiabetic individuals.     

1157例体检者空腹血糖及糖耐量分析

目的 对1 157例体检者空腹血糖及糖耐量分析,掌握该区居民的血糖及其代谢情况.方法 采用人口成比例抽样(PPS)的方法,按经济条件分成3个层次,随机抽取1 157例研究对象采用葡萄糖氧化酶法测定空腹血糖,其中926例口服75 g无水葡萄糖2 h后测量血糖.结果 共计检出高血糖患者198例,检出糖耐量受损者117例,占12.63%,糖尿病患病率则为4.86%.结论 该区糖尿病患者及潜在者形势严峻,该区当前糖尿病防治应以经济较好的市区为重点向开发区辐射直至全区.     

Low birth weight, family history of diabetes, and glucose intolerance in Swedish middle-aged men.

OBJECTIVE: To investigate the association between low birth weight and glucose intolerance in relation to family history of diabetes. RESEARCH DESIGN AND METHODS: We conducted a population-based cross-sectional study of 2,237 men born in 1938-1957 in four municipalities in the outskirts of Stockholm, 50% of whom had a family history of diabetes (at least one first-degree or two second-degree relatives with diabetes). Oral glucose tolerance testing detected 35 cases of type 2 diabetes, 102 cases of impaired glucose tolerance, and 57 cases of impaired fasting glucose. RESULTS: In subjects without a family history of diabetes, low (< or = 3,000 g) birth weight was associated with an odds ratio of 2.3 (95% confidence intervals = 0.4-14.4) for diabetes, 1.8 (0.7-4.3) for impaired glucose tolerance, and 3.3 (1.0-10.4) for impaired fasting glucose. In subjects with a family history of diabetes, the corresponding figures were approximately similar, except for diabetes, for which the odds ratio was 5.4 (2.0-14.9). For men with low birth weight in combination with a family history of diabetes, the odds ratio was 10.9 (2.9-41.2) for diabetes, 2.4 (1.1-5.6) for impaired glucose tolerance, and 5.9 (2.1-16.3) for impaired fasting glucose. CONCLUSIONS: This study indicated that low birth weight is associated with type 2 diabetes, impaired glucose tolerance, and impaired fasting glucose in men. This finding was most pronounced in subjects with diabetes in the family, but it was also indicated in those without a family history of diabetes. Men with the combination of low birth weight and family history of diabetes seem to be at particularly high risk of developing type 2 diabetes.     

The effects of high haematocrit levels on glucose metabolism disorders

There has been only limited research investigating the possible association between raised haematocrit levels, glucose intolerance and type 2 diabetes. In the present study, we explored the association between high haematocrit levels and impaired glucose tolerance by performing oral glucose tolerance tests in 46 patients with chronic obstructive pulmonary disease and no previous history of diabetes mellitus or glucose intolerance. A glucose metabolism disorder was observed in 12 (26%) patients (type 2 diabetes in six patients and impaired glucose tolerance in a further six). There was a significant association between high haematocrit levels and the presence of a glucose metabolism disorder, which was independent of other risk factors. High haematocrit levels may be an independent risk factor for type 2 diabetes and impaired glucose tolerance.     

Diabetic nephropathy and proliferative retinopathy with normal glucose tolerance

A 61-yr-old man presented with the nephrotic syndrome and normal oral glucose tolerance. Renal biopsy showed the nodular (Kimmelstiel-Wilson) and diffuse glomerulosclerosis lesions characteristic of diabetes. Direct ophthalmoscopy and fluorescein angiography demonstrated a picture of advanced proliferative diabetic retinopathy. The patient had no history of diabetes mellitus and upon testing had normal glucose values in response to an oral glucose tolerance test. Insulin response to an intravenous glucose tolerance test was abnormally low. It is concluded that the nodular glomerulosclerosis lesions and proliferative retinopathy, thought to be specific for diabetes mellitus, may present in the absence of either overt clinical diabetes or impaired glucose tolerance.     

化疗药物对头颈部鳞癌患者血糖代谢的影响

目的:探讨化疗药物对头颈部鳞癌患者血糖代谢的影响。方法:收集2000年1月~2005年12月收治的320例放化综合治疗及282例单纯放疗的头颈部鳞癌患者的血糖检验报告及相关临床资料,并对其进行回顾性分析。结果:320例放化综合治疗患者中,化疗前合并糖尿病6例,其余化疗前血糖水平正常。化疗后空腹血糖升高42例,占13.12%。42例中明确诊断为糖尿病11例,糖耐量减低14例,一过性血糖升高18例,分别占同期接受化疗的患者的3.43%、4.37%和5.62%。其中,接受以紫杉醇类药物为主的化疗患者123例,发生血糖异常24例,占同类化疗19.51%(24/123),占同期化疗7.50%(24/320);接受以铂类药物为主的化疗患者197例,发生血糖异常18例,占同类化疗9.13%(18/197),占同期化疗5.60%(18/320)。以紫杉醇类为主化疗与以铂类为主化疗引起的血糖异常的发生率相比较,差异有显著性(P<0.05)。而接受单纯放疗的282例患者中放疗前有12例糖尿病患者,放疗后没有新增病例。结论:头颈部恶性肿瘤患者接受化疗后可能会出现血糖异常,甚至发生糖耐量低减或糖尿病,以紫杉醇类为主的化疗方案治疗中这种情况更加常见。     

心内科住院患者糖代谢异常及相关因素分析

目的了解既往无糖尿病史的心内科住院患者糖代谢异常的发生情况以及与糖代谢异常有关的因素。方法413例心内科住院的非糖尿病患者为研究对象,进行生化、血脂、高敏C反应蛋白（hsCRP）、尿微量蛋白（尿蛋白肌酐比值）、糖化血红蛋白（HbA1c）、身高和体质量测定;根据简易口服葡萄糖耐量试验（OGTT）2小时血糖将患者分为正常糖耐量（NGT）组、糖调节受损（IGR）组和新诊断糖尿病（DM）组;记录患者心血管危险因素及心血管疾病。结果①413例患者中NGT占56．0％;IGR占29．5％;新诊断DM占14．5％;总的糖代谢异常率为44．0％。无冠心病的患者中32．4％存在糖代谢异常。②冠心病和超重患者IGR危险比（95％CI）增加,分别为2．04（1．20～3．47）和2．22（1．28～3．85）,新诊断DM危险比（95％CI）增加,分剐为2．77（1．36～5．62）和3．30（1．57～6．91）;随hsCRP水平增高,IGR和新诊断DM的危险比（95％CI）增加,分别为2．46（1．34～4．52）和2．24（1．01～4．98）。结论心内科住院的非糖尿病患者合并糖代谢异常比例较高,非冠心病患者也同样存在高血糖状态,并且多表现为餐后血糖增高,应将OGTT作为心内科所有住院非糖尿病患者的一项常规检查。     

Pathogenesis of NIDDM in Pima Indians

The Pima Indians of Arizona have the highest reported prevalence and incidence of non-insulin-dependent diabetes mellitus (NIDDM) of any population in the world. A cross-sectional and longitudinal study was begun in 1982 to determine the metabolic characteristic(s) that is (are) predictive of the development of NIDDM and to document the sequence of metabolic events that occur with the transition from normal to impaired glucose tolerance and then to diabetes. Preliminary analyses suggest that insulin resistance is a primary abnormality predisposing Pima Indians to develop impaired glucose tolerance, and that the development of diabetes occurs with subsequent pancreatic failure.     

Euglycemic clamp study in clozapine-induced diabetic ketoacidosis.

OBJECTIVE: To describe the fifth case of clozapine-induced diabetic ketoacidosis (DKA) with complete resolution of abnormal glucose metabolism after discontinuation of clozapine as assessed by oral glucose tolerance testing (OGTT) and the first to be serially studied with markers of pancreatic autoimmunity; to demonstrate insulin resistance using the euglycemic clamp study and reduced pancreatic insulin reserve using intravenous glucose tolerance testing (IVGTT) in clozapine-induced diabetes mellitus and DKA, when the OGTT was normal; and to systematically review the previously described cases of clozapine-induced diabetes mellitus and DKA. CASE SUMMARY: A 33-year-old white man without past or family history of diabetes mellitus presented with DKA after eight months of clozapine therapy (50 mg twice daily). After treatment of DKA and discontinuation of clozapine, glucose tolerance and concurrent serum insulin concentrations reverted to normal as measured by two OGTT performed 60 and 320 days after resolution of DKA. DISCUSSION: Antiislet-cell antibodies, antiglutamic acid decarboxylase antibodies, and human insulin antibody were negative on two separate occasions. Euglycemic clamp study demonstrated insulin resistance manifested by a glucose disposal rate of approximately 55% of mean normal values. IVGTT demonstrated a low rate of glucose disappearance (KG = 0.95) and diminished first-phase insulin response when OGTT was normal, indicating impairment in insulin sensitivity and reduction in beta cell function 323 days after discontinuance of clozapine. This adverse reaction is considered probable according to the Naranjo probability scale. CONCLUSIONS: The occurrence of cases of DKA and new or worsening diabetes mellitus in patients using clozapine suggests a causal relationship. We hypothesize that the mechanism by which clozapine may produce glucose intolerance may require a preexisting latent defect in insulin secretion and insulin action. With the administration of clozapine, some of these patients may develop worsening insulin resistance and may fail to mount an appropriate compensatory beta cell insulin secretion for the degree of insulin resistance. As a consequence, hyperglycemia develops and its persistence results in glucose toxicity, further suppressing beta cell insulin secretion. Such combined defects in insulin secretion and sensitivity are known to be synergistic, leading to the development of abnormal glucose tolerance, which can be clinically manifested as a spectrum ranging from impaired glucose tolerance through severe hyperglycemia to DKA. Patients being started on clozapine should be carefully followed for the development or worsening of diabetes mellitus, regardless of the dose of the drug.     

Serum Uric Acid Levels Improve Prediction of Incident Type 2 Diabetes in Individuals With Impaired Fasting Glucose: The Rancho Bernardo Study

OBJECTIVE

To determine whether serum uric acid predicts incident type 2 diabetes by glucose tolerance status in older community-dwelling adults.

RESEARCH DESIGN AND METHODS

Participants without diabetes at baseline were evaluated for incident type 2 diabetes 13 years later. Baseline glucose tolerance status was defined as normoglycemia, impaired fasting glucose, and impaired postchallenge glucose tolerance.

RESULTS

A total of 566 participants were included (mean age 63.3 ± 8.6 years; 41% men). Regression models adjusted for age, sex, BMI, diuretic use, and estimated glomerular filtration rate showed that for each 1 mg/dl increment in uric acid levels, incident type 2 diabetes risk increased by ∼60%. When analyses were stratified by glucose status, uric acid levels independently predicted incident type 2 diabetes among participants who had impaired fasting glucose (odds ratio 1.75, 95% CI 1.1–2.9, P = 0.02).

CONCLUSIONS

Uric acid may be a useful predictor of type 2 diabetes in older adults with impaired fasting glucose.Increased levels of serum uric acid have been associated with insulin resistance (1) and with established type 2 diabetes (2). Previous studies demonstrated that uric acid is an independent predictor of incident type 2 diabetes in general populations (3,4), but whether uric acid predicts incident type 2 diabetes in individuals who have abnormal glucose tolerance is unknown. We examined whether baseline uric acid levels predict incident type 2 diabetes by glucose tolerance status in older adults.     

N-acetyl-beta-glucosaminidase isoenzymes in serum and urine of patients with diabetes mellitus

The isoenzyme pattern of N-acetyl-beta-glucosaminidase (NAG) in serum and urine was studied in two groups of patients with diabetes mellitus and in 30 control subjects. Total NAG activity was significantly (P less than 0.001) increased in the serum and urine of the 20 diabetics with vascular complications, but was insignificantly increased in the 20 diabetics without vascular complications. Ion-exchange chromatography demonstrated the presence of two major isoenzymes of NAG, A and B. The proportion of isoenzyme A activity always exceeded that of isoenzyme B. The proportion of isoenzyme B in serum of diabetics was lower than in controls; the reverse was true for urine of diabetics. The NAG isoenzymes pattern may provide additional diagnostic information regarding diabetic status and complications of diabetes.