Glycogen synthase and phosphofructokinase protein and mRNA levels in skeletal muscle from insulin-resistant patients with non-insulin-dependent diabetes mellitus.

In patients with non-insulin-dependent diabetes mellitus (NIDDM) and matched control subjects we examined the interrelationships between in vivo nonoxidative glucose metabolism and glucose oxidation and the muscle activities, as well as the immunoreactive protein and mRNA levels of the rate-limiting enzymes in glycogen synthesis and glycolysis, glycogen synthase (GS) and phosphofructokinase (PFK), respectively. Analysis of biopsies of quadriceps muscle from 19 NIDDM patients and 19 control subjects showed in the basal state a 30% decrease (P < 0.005) in total GS activity and a 38% decrease (P < 0.001) in GS mRNA/microgram DNA in NIDDM patients, whereas the GS protein level was normal. The enzymatic activity and protein and mRNA levels of PFK were all normal in diabetic patients. In subgroups of NIDDM patients and control subjects an insulin-glucose clamp in combination with indirect calorimetry was performed. The rate of insulin-stimulated nonoxidative glucose metabolism was decreased by 47% (P < 0.005) in NIDDM patients, whereas the glucose oxidation rate was normal. The PFK activity, protein level, and mRNA/microgram DNA remained unchanged. The relative activation of GS by glucose-6-phosphate was 33% lower (P < 0.02), whereas GS mRNA/micrograms DNA was 37% lower (P < 0.05) in the diabetic patients after 4 h of hyperinsulinemia. Total GS immunoreactive mass remained normal. In conclusion, qualitative but not quantitative posttranslational abnormalities of the GS protein in muscle determine the reduced insulin-stimulated nonoxidative glucose metabolism in NIDDM.     

Diabetic nephropathy in patients with type 1 diabetes mellitus.

Proteinuria has been recognized in association with diabetes mellitus as early as the 18th century. This form of renal disease is known as diabetic nephropathy. It is now clear that diabetic nephropathy is the principal cause of end stage renal disease (ESRD) in the western world. According to reports by the United States Renal Data System (USRDS), in the past two decades there has been a continual increase in the incidence of ESRD among patients with diabetes. Many patients have diabetes that progresses to diabetic nephropathy, which is often not discovered until overt nephropathy is present. Many of the complications of diabetes could be minimized if patients received a comprehensive health maintenance program that includes vigorous cardiac risk reduction, routine eye examinations; routine foot examinations; screening and treatment for microalbuminuria, optimal hypertension management; and improved glycemic control. Hence, the key is not only prudent screening of these patients, but referral as well. Using a case study approach, this article illustrates the care of patients with diabetic nephropathy in type 1 diabetes mellitus.     

Hyperlipoproteinemia with albumin-lipid complex: a novel type of hyperlipoproteinemia associated with insulin-resistant diabetes mellitus

We describe a new phenotype of hyperlipoproteinemia in two members of a family with a high degree of consanguinity. Both have a history of uncontrolled diabetes mellitus without ketoacidosis, and a family history of coronary artery disease at a relatively early age. A high degree of insulin resistance was found. The abnormal lipoprotein(s) has alpha-lipoprotein mobility on cellulose acetate electrophoresis and has a relative density of less than 1.006 as determined by ultracentrifugation of serum collected after a short fast. The fraction isolated by ultracentrifugation contains about half of the serum cholesterol and triglycerides and most of the phospholipids; the major protein component is albumin. Immunoelectrophoresis showed low concentrations of beta-lipoproteins in both sera, and two abnormal precipitin bands against monospecific antiserum to antilipoprotein A; a third member of the family showed only one abnormal precipitin band against the same antibody. We tentatively propose an abnormal gene(s) as the underlying mechanism. The insulin-resistant diabetes mellitus, probably inherited separately, may aggravate the hyperlipidemia.     

Insulin treatment increases skeletal muscle fibre area in patients with diabetes mellitus type 2

The effects of insulin treatment on skeletal muscle characteristics were studied in 18 patients (62 ± 11 years) with poorly controlled diabetes mellitus type 2 (mean duration 7·5 ± 6 years). Skeletal muscle biopsy samples were taken from the lateral portion of the quadriceps muscle before and after a period of insulin treatment of 40 ± 14 days. Enzyme activities (phosphofructokinase, 3‐hydroxyacyl‐CoA dehydrogenase, citrate synthase, lactate dehydrogenase and creatine kinase) and myoglobin content were assessed. In a subgroup of 11 patients (60 ± 11 years), skeletal muscle fibre type composition (type I, IIA, IIB and IIC) and fibre type cross‐sectional area were also analysed. Following insulin treatment there were 32 and 38% increases, respectively, in the cross‐sectional areas of type IIA and IIB fast‐twitch fibres (P<0·02). The fibre type distribution did not change. The myoglobin content in muscle decreased by 20% (P<0·01). Of the enzymes tested, the 3‐hydroxyacyl‐CoA dehydrogenase activity decreased by 10% (P<0·04). Serum glucose, HbA1_C and serum triglyceride levels decreased (P<0·001) and body weight and arm muscle circumference increased (P<0·02). In conclusion, insulin treatment of patients with poorly controlled non‐insulin‐dependent diabetes mellitus increased the fast‐twitch fibre area, reduced myoglobin levels and decreased muscle enzyme activity related to fatty acid oxidation.     

Incretin-based therapy in patients with type 1 diabetes mellitus

GLP-1 has multiple physiological functions including glucose-dependent insulin secretion and glucagon suppression, delay of gastic emptying, suppression of hepatic glucose production, stimulation of beta cell replication and neogenesis, inhibition of beta cell apoptosis. All of these actions are beneficial for the treatment of diabetes. Therefore, incretin-based therapy may be still worthwhile as evidenced by studies demonstrating that beta cell mass may be preserved or expand in animals and that residual insulin secretion may be elevated to reduce the risk of hypoglycemia in patients treated with intensive insulin therapy, although the effect of GLP-1R agonists and DPP-4 inhibitors(DPP-4is) on beta cells may be small because destruction of beta cells leads to absolute insulin deficiency by cell-mediated autoimmune attack. Recent report also showed that DPP-4i might ameliorate an autoimmune attack against beta cells by restoring or increasing the number of regulatory T lymphocytes. Furthermore, GLP-1R-mediated signals might suppress the expression of chemokine ligand CXCL10 which binds to newly identified receptor TLR4 (Toll-like receptor 4), and impairs beta cell function and viability in diabetes. Taken together, incretin-based therapy may be worth testing in patients with type 1 diabetes.     

Predictors of macrovascular disease in patients with type 2 diabetes mellitus.

OBJECTIVE: To assess the importance of classic and nonclassic risk factors in the development of coronary artery disease (CAD) or cerebrovascular disease (CVD) in patients with type 2 diabetes mellitus (DM). PATIENTS AND METHODS: In this community-based, prospective cohort study, quantitative measurements for cholesterol, triglycerides (TGs), glucose, and lipoprotein(a) detected as a sinking pre-beta-lipoprotein band on electrophoresis were obtained from 1968 through 1982 from 449 patients who were free of CAD and CVD but had type 2 DM. Demographic data and covariables obtained were age, body mass index, duration of diabetes, sex, smoking, and hypertension. The relationship of individual continuous factors to the development of CAD and CVD as well as multivariate models were evaluated with use of the Cox proportional hazards model. The primary outcome was to determine which risk factors are associated with development of CAD or CVD in patients with type 2 DM. RESULTS: After a mean follow-up of 13 years, 216 CAD and 115 CVD events had developed. The hazard ratio estimates with 95% confidence intervals (CIs) for CAD after multivariate analysis were significant for age, 1.45 (95% CI, 1.27-1.67); fasting glucose levels at enrollment, 1.63 (95% CI, 1.17-2.25); smoking, 1.45 (95% CI, 1.10-1.91); and TGs, 1.49 (95% CI, 1.15-1.92). The hazard ratio estimates for CVD were significant for age, 1.95 (95% CI, 1.59-2.38); hypertension, 1.89 (95% CI, 1.30-2.74); fasting glucose levels at enrollment, 1.69 (95% CI, 1.06-2.70); and smoking, 1.57 (95% CI, 1.07-2.30). CONCLUSION: In diabetic patients, age, fasting glucose levels, smoking, and TG levels are independent risk factors for development of CAD events. Age, hypertension, glucose, and smoking predicted development of CVD events.     

Increased intracranial arterial resistance in patients with type 2 diabetes mellitus.

BACKGROUND: The majority of the studies investigating risk factors for stroke have focused on the atherosclerosis of extracranial carotid arteries. Risk factors for the involvement of intracranial arteries in patients with stroke have not been widely investigated so far. The pulsatility index reflects the vascular resistance of intracranial arteries and could therefore be used as an estimate of the severity of vascular damage. MAIN PURPOSE: The present study aimed to examine the influence of type 2 diabetes mellitus and some other atherosclerosis risk factors on intracranial vascular resistance in patients with a previous stroke or transient ischemic attack. METHODS: Transcranial doppler investigations were performed in 103 patients with previous stroke (31 with diagnosis of type 2 diabetes, 72 without diabetes), at least 3 months after stroke occurred. Blood flow velocities of anterior cerebral arteries, middle cerebral arteries, the intracranial part of vertebral arteries and the basilar artery, as well as of the extracranial part of the internal carotid artery were measured, and Gosling's pulsatility index was calculated. The maximal pulsatility index of intracranial arteries was defined to express the most pronounced damage. RESULTS: Diabetic patients had a significantly higher pulsatility index than non-diabetic patients in all examined intracranial arteries. The maximal pulsatility index was also significantly higher in diabetic patients than in non-diabetic patients (1.24 +/- 0.25 vs. 1.00 +/- 0.23; p < 0.0001). There was no significant difference in the pulsatility index between men and women and between groups of patients with or without hypertension. In the multivariate analysis, the presence of diabetes (p < 0.0001) and the age of patients (p < 0.0001) were the only factors significantly predicting maximal pulsatility index, and this relationship was independent on the presence of hypertension. CONCLUSIONS: Diabetic patients with previous stroke have a higher pulsatility index than non-diabetic patients with previous strokes, which indicates a higher increase in intracranial arterial resistance and more severe damage to cerebral blood flow in diabetes mellitus.     

Increased glucose effectiveness in normoglycemic but insulin-resistant relatives of patients with non-insulin-dependent diabetes mellitus. A novel compensatory mechanism.

20 normoglycemic first degree relatives of non-insulin-dependent diabetes mellitus (NIDDM) patients were compared with 20 matched subjects without any family history of diabetes using the intravenous glucose tolerance test with minimal model analysis of glucose disappearance and insulin kinetics. Intravenous glucose tolerance index (Kg) was similar in both groups (1.60 +/- 0.14 vs 1.59 +/- 0.18, x 10(-2) min-1, NS). However, insulin sensitivity (Si) was reduced (3.49 +/- 0.43 vs 4.80 +/- 0.61, x 10(-4) min-1 per mU/liter, P = 0.05), whereas glucose effectiveness (Sg) was increased (1.93 +/- 0.14 vs 1.52 +/- 0.16, x 10(-2) min-1, P < 0.05) in the relatives. Despite insulin resistance neither fasting plasma insulin concentration (7.63 +/- 0.48 vs 6.88 +/- 0.45, mU/liter, NS) nor first phase insulin responsiveness (Phi1) (3.56 +/- 0.53 vs 4.13 +/- 0.62, mU/liter min-1 per mg/dl, NS) were increased in the relatives. Phi1 was reduced for the degree of insulin resistance in the relatives so that the Phi1 x Si index was lower in the relatives (11.5 +/- 2.2 vs 16.7 +/- 2.0, x 10(-4) min-2 per mg/dl, P < 0.05). Importantly, glucose effectiveness correlated with Kg and with basal glucose oxidation but not with total glucose transporter 4 (GLUT4) content in a basal muscle biopsy. In conclusion we confirm the presence of insulin resistance in first degree relatives of NIDDM patients. However, insulin secretion was altered and reduced for the degree of insulin resistance in the relatives, whereas glucose effectiveness was increased. We hypothesize that increased glucose effectiveness maintains glucose tolerance within normal limits in these "normoinsulinemic" relatives of NIDDM patients.     

Conjunctival flora in patients with type 1 or type 2 diabetes mellitus

Patients with diabetes mellitus (DM) are prone to infection because glucose in the skin, urine, mucous membranes, and tears promotes growth of microorganisms. Conjunctival flora develops soon after birth, and some saprophytic conjunctival flora play a pathogenic role when immune function is compromised, which can lead to serious infection. DM is one condition that may compromise immune status. In lacrimal function tests of DM patients, a decrease in breakup time (BUT) of lacrimal film and a decrease in Schirmer’s test results were seen. In the present study, conjunctival flora in patients with DM was compared with that in controls with regard to type and duration of diabetes and results of lacrimal function tests. Seventeen patients with type 1 DM (n=34 eyes), 66 patients with type 2 DM (n=132 eyes), and 50 control subjects (n=100 eyes) were included. The control group consisted of age-matched patients with no ophthalmologic problems other than refractive error. Clycosylated hemoglobin values were measured with highpressure liquid chromatography with the Hi-AUTOA1c analyzer (Kyoto Daiichi Kagatu Co., Ltd., Kyoto, Japan). Type and duration of diabetes and demographic data were recorded, and routine ophthalmologic examinations were performed; the BUT of lacrimal film was determined, and the results of Schirmer’s test were assessed. Microbiologic sampling was performed twice for both eyes with sterile cotton swabs. One sample was incubated in 2 mL of brain-heart infusion broth agar; the other was incubated for the presence of fungi in Sabouraud dextrose agar. Colony morphology, hemolysis, and Cram’s stain, as well as catalase, oxidase, and coagulase tests were performed. No growth was observed in 12 of 1 7 patients (35.4%) with type 1 DM, 28 of 66 patients (21.2%) with type 2 DM, and 25 of 50 control subjects (50%).Staphylococcus epidermidis (11.79%) andStaphylococcus aureus (11.7%) were the most frequently isolated organisms in the type 1 DM group, and Sepidermidis (24.2%) and Saureus (21.2%) were the predominant organisms in the type 2 DM group. In control subjects, Sepidermidis (22%), Saureus (12%), andCorynebacterium spp (10%) were the most frequently isolated organisms, and the number of eyes with growth of Saureus was significantly higher in the type 2 DM group than in the other groups (P<.01). Patients with diabetes are more prone to postoperative endophthalmitis than are nondiabetics, and preoperative application of antiseptic or antimicrobial agents to the conjunctiva may not sterilize the area. Impaired integrity of the posterior capsule may also increase the risk of endophthalmitis. Postoperative endophthalmitis is usually associated with gram-positive organisms (75%–80%); gram-negative organisms (15%–29%) and fungi (3%–13%) account for a smaller number of cases. A high rate of resistance to penicillin, ampicillin, and tetracycline was observed in Saureus isolates, although resistance to vancomycin was absent, rendering this molecule the most effective therapeutic option. In this study, Sepidermidis and Saureus were the 2 most frequently isolated organisms in patients with DM. It is concluded that the conjunctival flora in diabetic subjects differs from that in nondiabetic subjects. This should be considered preoperatively and postoperatively, and prophylactic and postoperative treatment should be administered accordingly to diabetic patients.     

Acute coronary syndrome in patients with type 2 diabetes mellitus

According to evidence obtained from large epidemiological studies, an incidence rate of acute coronary syndrome (ACS) in diabetics is 2-3 times higher than in general population. Relevant invalidity and mortality is much higher than in patients free of diabetes. In type 2 diabetes mellitus a high risk of an unfavourable course and outcome of myocardial infarction was registered both within 30 postinfarction days and 1-3 years of follow-up. Poor prognosis persists despite adequate and early treatment. The results of the attempts to correct MI prognosis in diabetics by means of carbohydrate metabolism correction (multicenter trials DIGAMI-1, DIGAMI-2) are reviewed.     

Withdrawal of pioglitazone in patients with type 2 diabetes mellitus

Background and objective: The remodelling of the adipose tissue by pioglitazone may be associated with the sustained therapeutic effects. We studied the effects of withdrawal of pioglitazone after 3‐month treatment on glucose, lipid and high‐molecular weight (HMW) adiponectin levels as well as liver function in patients with type 2 diabetes mellitus. Methods: Forty‐nine Japanese patients with type 2 diabetes mellitus were randomly assigned into the withdrawal group after 3‐month treatment with pioglitazone (15 or 30 mg daily) and the non‐withdrawal group. Results and discussion: Three‐month treatment with pioglitazone improved glycaemic control, homeostasis model assessment for insulin resistance (HOMA), dyslipidaemia and liver function tests in association with a marked increase in serum HMW adiponectin level. Three months later after the withdrawal of pioglitazone, however, fasting plasma glucose and HOMA increased, whereas serum HMW adiponectin decreased to the pretreatment levels. Dyslipidaemia also returned to the pretreatment level. On the other hand, liver enzymes at 3 months after the withdrawal remained lower after a mild rebound. In addition, the bone formation marker, serum bone‐specific alkaline phosphatase, was significantly reduced by pioglitazone treatment in post‐menopausal women. Conclusions: The present study suggests that 3‐month treatment with pioglitazone has no sustained beneficial effects except in liver function tests in patients with type 2 diabetes mellitus.     

2型糖尿病患者的心率变时性功能不全及其意义

目的:检测2型糖尿病患者运动时心率变时性功能不全情况。方法:2型糖尿病患者进行运动平板试验,计算其心率变时性反应指数,并与非糖尿病患者进行比较。结果:69例2型糖尿病患者心率变时性反应指数为0.74±0.16,明显低于对照组0.90±0.17(P<0.0001),提示2型糖尿病患者存在心率变时性功能不全,并且与有无心血管并发症及有无缺血性ST改变无关。结论:2型糖尿病患者较普遍存在运动心率变时性功能不全情况,可能与心脏自主神经损害有关。     

2型糖尿病患者血清抵抗素水平的变化研究

目的探讨人血清抵抗素水平与2型糖尿病的关系.方法 2型糖尿病患者48例和正常对照组47例,采用酶联免疫分析法检测空腹血清抵抗素、胰岛素水平;同时测血糖、血压、血脂、身高、体重,计算腰围、臀围、体重指数、腰臀比值和胰岛素敏感指数、胰岛素抵抗性、胰岛B细胞功能.结果 2型糖尿病组的体重指数、甘油三酯、血清抵抗素水平显著高于正常对照组（P＜0.05）;相关分析显示血清抵抗素水平与体重指数、腰围、空腹胰岛素、血压呈正相关.在正常对照组,血清抵抗素水平与胰岛素敏感指数、胰岛素抵抗性、胰岛B细胞功能相关.而且血清抵抗素水平在糖尿病肥胖组显著高于糖尿病非肥胖组和正常对照组（P＜0.05）.结论 2型糖尿病患者血清抵抗素水平升高,与肥胖相关,血清抵抗素可能是联系肥胖和2型糖尿病的重要因素.     

2型糖尿病病人抑郁情况分析

糖尿病是一种严重影响人们心身健康的疾病 ,其患病率呈逐年上升的趋势 ,1994年— 1995年全国 2 5万人口 (>2 5岁 )调查发现 ,糖尿病和葡萄糖耐量降低 (IGT)病人各占 2 .5 % ,患病数较 15年前增长 3倍多 ,其后北京调查糖尿病患病率约 4% ,上海某社区约 5 % [1] 。然而糖尿病病因至今并不十分清楚 ,普遍认为与遗传、自身免疫和环境因素有关[1] 。流行病学表明 ,糖尿病与肥胖及负性生活事件有关[2 ] ,但糖尿病本身也可致抑郁症状的发生或加重[3 ] ,本文对 86例新诊断糖尿病病人的心理状况作了调查 ,现报告如下。1　对象与方法1.1　对象　随机…     

Regulation of phosphatidylinositol 3-kinase activity in liver and muscle of animal models of insulin-resistant and insulin-deficient diabetes mellitus.

Insulin stimulates tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1), which in turn binds to and activates phosphatidylinositol 3-kinase (PI 3-kinase). In the present study, we have examined these processes in animal models of insulin-resistant and insulin-deficient diabetes mellitus. After in vivo insulin stimulation, there was a 60-80% decrease in IRS-1 phosphorylation in liver and muscle of the ob/ob mouse. There was no insulin stimulation of PI 3-kinase (85 kD subunit) association with IRS-1, and IRS-1-associated PI 3-kinase activity was reduced 90%. Insulin-stimulated total PI 3-kinase activity was also absent in both tissues of the ob/ob mouse. By contrast, in the streptozotocin diabetic rat, IRS-1 phosphorylation increased 50% in muscle, IRS-1-associated PI 3-kinase activity was increased two- to threefold in liver and muscle, and there was a 50% increase in the p85 associated with IRS-1 after insulin stimulation in muscle. In conclusion, (a) IRS-1-associated PI 3-kinase activity is differentially regulated in hyperinsulinemic and hypoinsulinemic diabetic states; (b) PI 3-kinase activation closely correlates with IRS-1 phosphorylation; and (c) reduced PI 3-kinase activity may play a role in the pathophysiology of insulin resistant diabetic states, such as that seen in the ob/ob mouse.     

2型糖尿病并冠心病患者血浆同型半胱氨酸水平与单纯糖尿病患者及健康者比较

目的了解糖尿病合并冠心病与单纯糖尿病患者糖尿病病程、血糖、血脂、血压、同型半胱氨酸、纤维蛋白原及超敏C反应蛋白水平的差异.方法收集北京大学第一医院心内科2002-01/2004-12行冠状动脉造影者378例.根据冠状动脉造影显示,将糖尿病患者分为2组冠状动脉直径减少≥50%为糖尿病合并冠心病组70例,男55例,女15例;冠状动脉直径减少＜50%为单纯糖尿病组34例,男26例,女8例.选择同期本院健康体检者20人为对照组,均知情同意.①病例纳入时,询问其病程、年龄、吸烟情况、是否有冠心病家族史、高血压患病情况.②造影前空腹取血10 mL,采用全自动生化仪测定血肌酐、空腹血糖、血脂和尿酸,乳胶增强免疫浊度法检测超敏C反应蛋白,Claus法检测纤维蛋白原,电化学发光法检测同型半胱氨酸.③分析糖尿病患者冠状动脉造影特点.④多组计量资料的显著性检验采用单因素方差分析和两两比较LSD法.变量间采用单因素直线相关分析.以病程、收缩压、空腹血糖、血脂、纤维蛋白原、同型半胱氨酸、超敏C反应蛋白为自变量,冠心病为因变量,进行多因素Logistic逐步回归分析.结果按意向处理分析,进入结果分析2型糖尿病患者104例,健康者20例.①病程＞5年例数糖尿病合并冠心病组明显多于单纯糖尿病组[74%(52/70),29%(10/34),x2=78.52,P＜0.05].②血超敏C反应蛋白、同型半胱氨酸、空腹血糖、三酰甘油、总胆固醇、纤维蛋白原及水平糖尿病合并冠心病组明显高于单纯糖尿病组和对照组(P＜0.05),而高密度脂蛋白胆固醇水平明显低于单纯糖尿病组和对照组(P＜0.05).血同型半胱氨酸、总胆固醇水平单纯糖尿病组明显高于对照组(P＜0.05).③2型糖尿病患者同型半胱氨酸与空腹血糖、三酰甘油、总胆固醇均呈显著正相关(r=0.178,0.238,0.258,P＜0.05),与高密度脂蛋白呈显著负相关(r=-0.283,P＜0.05).④多元Logistic回归分析显示糖尿病病程(OR=1.038,95%CI1.000～1.067)、收缩压(OR=1.064,95%CI1.007～1.045)和血浆同型半胱氨酸水平(OR=1.896,95%CI1.165～2.743)是2型糖尿病患者冠心病危险的独立预测因素.⑤70例糖尿病合并冠心病患者冠状动脉造影显示,冠状动脉双支和三支病变比例显著高于单支病变[36%(25/70),44%(31/70),19%(13/70),x2=56.84,P＜0.05];弥漫性病变发生高于局限病变和管状病变[56%(39/70),26%(18/70),14%(10/70),x2=45.86,P＜0.05].34例单纯糖尿病组冠状动脉造影显示冠状动脉硬化27例(79%),正常7例(21%).结论①糖尿病合并冠心病患者较单纯糖尿病患者糖尿病病程长,血糖、血脂、血压、同型半胱氨酸、纤维蛋白原及超敏C反应蛋白水平更高.②2型糖尿病患者血浆同型半胱氨酸水平与血糖、血脂变化有关,且其变化与血糖、血脂变化可能存在共同的病理基础.③多因素分析结果显示病程、收缩压和血浆同型半胱氨酸水平是2型糖尿病患者冠心病的独立危险因素.④糖尿病合并冠心病患者冠状动脉多支弥漫性病变发生率较高.     

2型糖尿病患者人体成分的变化

目的 了解2型糖尿病患者与正常人体内成分的差异,进一步探讨肥胖与2型糖尿病的关系.方法 随机选取80例2型糖尿病患者(糖尿病组)及80例健康体检者(对照组),分别进行人体成分分析,包括体脂肪、内脏脂肪区域、骨骼肌、腰臀比及蛋白质、矿物质含量等指标,同时测定糖尿病患者的血糖、血脂、胰岛素抵抗指数、糖化血红蛋白.结果 糖尿病组体脂肪[(19.68 ±6.78) kg]、体脂百分比[(29.87±8.04)％]、肥胖程度[(115.93 ±15.94)％]、内脏脂肪区域[(104.48 ±36.19) cm2]、体质量指数[(24.85±3.51) kg/m2]、胸围[(94.06±7.86) cm]、腰围[(85.18 ±9.50) cm]、腰臀比(0.90±0.05)均明显高于对照组[体脂肪:(17.31 ±5.55) kg、体脂百分比:(27.38±6.47)％、肥胖程度:(108.88±13.80)％、内脏脂肪区域:(85.44±44.04) cm2、体质量指数:(23.43 ±3.10) kg/m2、胸围:(91.11 ±7.52) cm、腰围:(80.79±8.17) cm、腰臀比(0.86 ±0.05)](t值分别为2.55、2.30、3.12、2.86、2.73、2.28、3.12、4.76,P均＜0.05),而体质量控制[(-7.01 ±7.49)kg]、肥胖控制[(-8.53 ±6.66)kg]、肌肉控制[(1.52±1.43) kg]均低于对照组[体质量控制:(-4.08 ±6.79)kg、肥胖控制:(-6.39±5.78) kg、肌肉控制:(2.31 ±2.09) kg(t值分别为-2.59、-2.17、-2.15,P均＜0.05).糖尿病组尿酸与体质量控制、肥胖控制呈负相关(r值分别为-0.43、-0.42,P均＜0.01),与内脏脂肪区域、体脂百分比、腰臀比、体质量指数、肥胖程度、胸围、腰围、体脂肪呈正相关(r值分别为0.32、0.31、0.40、0.36、0.36、0.31、0.42、0.42,P均＜0.05),甘油三酯与体质量控制、肥胖控制呈负相关(r值分别为-0.44、-0.41,P均＜0.01),与体脂百分比、腰臀比、体质量指数、肥胖程度、胸围、腰围、体脂肪呈正相关(r值分别为0.27、0.35、0.46、0.46、0.35、0.42、0.42,P均＜0.05).结论 2型糖尿病患者的体脂肪含量及体脂肪分布与健康人有显著差异,中心性肥胖可能与糖尿病发生存在一定关系.