2型糖尿病患者腹部脂肪分布与糖尿病并发症的相关性研究

目的探讨2型糖尿病患者腹部脂肪分布与糖脂代谢及糖尿病并发症的关系。方法选本院内分泌科住院的2型糖尿病患者357例,定量CT测量内脏脂肪(VAT)和皮下脂肪(SAT)面积,同时检查患者糖尿病肾病、视网膜病变、周围神经病变、外周动脉粥样硬化、心脑血管疾病的患病情况。根据VAT的值以三分位数法分为3组:T1组(VAT<162.0 cm^2)、T2组(162.0≤VAT<221.1 cm^2)、T3组(VAT≥221.1 cm^2)。结果T1组HbA1C水平高于T3组(P<0.05);T1组高密度脂蛋白胆固醇(HDL-C)、肾小球滤过率(eGFR)高于T2、T3组(P<0.05);T2、T3组男性比例、年龄、体重指数(BMI)、收缩压、舒张压、三酰甘油(TG)、24h尿白蛋白、糖尿病肾病和外周动脉粥样硬化的比例高于T1组(P<0.05);T3组空腹C肽(FCP)、改良稳态模型评估的胰岛素抵抗指数(HOMA-IR)高于T1、T2组(P<0.01)。Spearman相关分析显示,VAT、SAT与BMI、FCP、HOMA-IR呈正相关(P<0.01),VAT与年龄、收缩压、舒张压、TG、24h尿白蛋白、糖尿病肾病、外周动脉粥样硬化、心脑血管疾病呈正相关(P<0.05),与HbA1C、HDL-C、eGFR呈负相关(P<0.05),SAT与总胆固醇、低密度脂蛋白胆固醇呈正相关(P<0.01),与外周动脉粥样硬化呈负相关(P<0.01)。多因素相关分析显示,校正年龄、BMI、收缩压、空腹血糖等因素后,VAT仍是发生糖尿病肾病的危险因素(P=0.013)。结论VAT、SAT均与血脂和胰岛素抵抗相关,VAT可能是2型糖尿病患者发生糖尿病肾病的危险因素。     

Tumor necrosis factor-alpha promoter -308 A/G polymorphism and rheumatoid arthritis susceptibility: a metaanalysis

OBJECTIVE: Tumor necrosis factor-alpha (TNF-alpha) promoter -308 A/G polymorphism has been reported to be associated with rheumatoid arthritis (RA) with inconsistent results. We investigated whether TNF-alpha -308 A/G polymorphism confers susceptibility to RA. METHODS: We conducted a random effect metaanalysis on the association of genotypes A/A (recessive effect), A/A + A/G (dominant effect), A allele, and A/A vs G/G genotypes of the TNF-alpha -308 polymorphisms with RA overall and within different ethnic populations. RESULTS: Fourteen studies, 10 of Europeans, 3 of Latin Americans, and one Asian, were included in this metaanalysis. An association between RA and the TNF-alpha -308 A allele was not found in the overall population (OR 1.005, 95% CI 0.715-1.412, p = 0.976). However, stratification by ethnicity indicated that the TNF-alpha A allele was significantly associated with RA in Latin Americans (OR 2.004, 95% CI 1.158-3.467, p = 0.013). Conversely, there was no association detected for the TNF-alpha A allele with RA patients from the European samples (OR 0.911, 95% CI 0.684-1.212, p = 0.520). The OR for the A/A + A/G genotype, the A/A genotypes, and the A/A vs G/G genotypes in samples overall and in each ethnic group showed a similar trend to those for the TNF-alpha A allele. CONCLUSION: This metaanalysis demonstrates that the TNF-alpha -308 A/G polymorphism may represent a significant risk factor for RA in Latin Americans, but not in Europeans.     

A polymorphism in the promoter of the tumor necrosis factor-alpha gene (-308) is associated with coronary heart disease in type 2 diabetic patients

BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) is a key cytokine in the inflammation process of atherosclerosis. Through its effects on lipid metabolism, insulin resistance and endothelial function, it might be involved in coronary heart disease (CHD). A biallelic polymorphism within the promoter of TNF-alpha locus at the position -308 has been reported to be associated with TNF production. We have studied the association of this polymorphism with CHD in a Mediterranean non-diabetic and type 2 diabetic population. METHODS: Three hundred and forty one CHD patients (106 with type 2 diabetes), 207 healthy matched control subjects and 135 type 2 diabetic patients without CHD were evaluated. A single nucleotide polymorphism at the promoter TNF-alpha (-308) was analyzed by RFLP-PCR. RESULTS: TNF-alpha (-308) genotype and allele frequencies for A carriers were higher in CHD patients than those observed in the control group (32.3 vs. 23.2%, P=0.03; and 18.8 vs. 12.1%, P=0.0047; respectively) independently of other risk factors. Genotypic analysis revealed that CHD patients with type 2 DM displayed a greater prevalence of the -308 TNF-alpha A allele (40.6%) than controls (23.2%) or CHD patients without type 2 DM (28.5%) (P=0.0056). The odds ratio for CHD in type 2 diabetic patients in presence of -308 TNF-alpha A allele was 2.86 (CI 95%: 1.55-5.32). This difference was observed mainly in diabetic women for the A allele carriers (OR: 4.29; CI 95%: 1.6-11.76). CONCLUSIONS: These results suggest that -308 TNF-alpha gene polymorphism may contribute to CHD risk in patients with type 2 diabetes and it could constitute an useful predictive marker for CHD in type 2 diabetic women.     

Relationship between polymorphisms 804C/A and 252A/G of lymphotoxin-alpha gene and -308G/A of tumor necrosis factor alpha gene and diabetic retinopathy in Japanese patients with type 2 diabetes mellitus

To clarify whether polymorphisms of the lymphotoxin-alpha (LTA) gene and tumor necrosis factor alpha (TNF-alpha) gene were related to diabetic retinopathy (DR), we performed a case-control study in 251 Japanese patients with type 2 diabetes mellitus participating in a multicenter research protocol. Genetic analyses were performed by using a fluorescent allele-specific DNA primer assay system. Diabetic retinopathy was diagnosed in a masked manner by an independent ophthalmologist using fundus photographs and was classified as nondiabetic retinopathy (NDR), nonproliferative retinopathy (NPDR), and proliferative retinopathy (PDR). The results showed that the genotype frequencies of 804C/A in exon 3 and 252A/G in intron 1 of the LTA gene were not significantly different among patients with NDR, NPDR, and PDR. A allelic frequency of the TNF-alpha gene (-302A/G in promoter) was also identical among NDR, NPDR, and PDR groups. Multivariate logistic regression analyses showed that significant associations with DR were glycosylated hemoglobin level and diabetes duration, but not polymorphisms of the LTA gene or TNF-alpha gene. In conclusion, the present study showed no association between polymorphisms 804C/A and 252A/G of the LTA gene and -302A/G of the TNF-alpha gene and DR in Japanese type 2 diabetic patients.     

Tumor necrosis factor-alpha -308 promoter gene polymorphism and increased tumor necrosis factor serum bioactivity in farmer's lung patients

Hypersensitivity pneumonitis (HP) represents an immunologic reaction of the pulmonary parenchyma to an inhaled agent. Since tumor necrosis factor (TNF)-alpha is thought to be involved in the pathogenesis of HP, and polymorphisms in the TNF genes have been associated with variations in the production of TNF-alpha, we investigated the serum bioactivity and genotype of TNF in HP. TNF bioactivity was measured after hay dust challenge in eight patients with farmer's lung (Group A) and in 12 healthy, sensitized (antibody-positive) controls (Group B). Genotyping for the -308 TNF-alpha promoter polymorphism and the TNF-beta intron 1 gene polymorphism was performed in 20 patients with farmer's lung, 25 patients with pigeon breeder's lung, and 216 controls. TNF bioactivity increased in Group A at 4 to 10 h after hay dust challenge, but not in Group B (p < 0.05). The frequency for the TNFA2 allele, a genotype associated with high TNF-alpha production in vitro, was significantly higher in farmer's lung patients (frequency [f] = 0.43, p = 0.0012) than in controls (f = 0.19) or patients with pigeon breeder's lung (f = 0.16). Genotyping for TNF-beta revealed no significant abnormalities. Thus, increased production of TNF-alpha after hay contact, and a genetic predisposition to TNF-alpha production, are implicated in the pathogenesis of alveolitis in farmer's lung.     

Relationship between serum tumor necrosis factor-alpha and insulin resistance in obese men with Type 2 diabetes mellitus

We analyzed serum concentrations of tumor necrosis factor-alpha (TNF-alpha) for their role in insulin resistance in 12 obese men with untreated Type 2 diabetes mellitus and in 6 age-and BMI-matched obese controls. Insulin resistance was expressed using the homeostasis model assessment (HOMA-R). Six of the patients were insulin-resistant (HOMA-R>5.0), while six were not (HOMA-R相似文献   

Effects of rosiglitazone on body fat distribution and insulin sensitivity in Korean type 2 diabetes mellitus patients

The objective of the study was to investigate the effects of rosiglitazone (RSG), a thiazolidinedione derivative, on body fat distribution and insulin sensitivity in Korean subjects with type 2 diabetes mellitus. This study was a phase IV, multicenter, single-blind, positive-controlled parallel group study. Eighty-nine patients with type 2 diabetes mellitus, aged 30 to 75 years, were enrolled in this study. Their fasting plasma glucose levels ranged from 126 to 270 mg/dL, and subjects had hemoglobin A1c levels of greater than 7.0%. We compared the effect of the treatment with glibenclamide plus RSG 4 mg/d (increased to 8 mg/d after 6 months) with glibenclamide plus placebo on body fat distributions, which were determined by computed tomography scanning and glycemic and insulinemic responses to oral glucose load. During the 12-month treatment period, the difference between the changes in the ratio of the intraabdominal adipose tissue (IAAT) to abdominal subcutaneous adipose tissue areas (SAT) between treatment groups was significant (from 1.13 +/- 0.53 to 1.00 +/- 0.40 in the RSG group and from 0.92 +/- 0.54 to 0.96 +/- 0.62 in the placebo group, P = .0351). The glycemic responses to oral glucose load (area under the curve, millimoles per liter per hour) were improved in the RSG group with 12 months of treatment (from 4.88 +/- 1.10 to 4.38 +/- 1.35 in 1 hour and from 13.78 +/- 2.83 to 12.16 +/- 2.52 in 2 hours), and the difference between the changes of the glycemic response showed statistical significance between groups (RSG group vs placebo group: -0.53 +/- 1.42 vs 0.38 +/- 1.31, difference in 1 hour; -0.76 +/- 2.98 vs 1.43 +/- 2.58, difference in 2 hours). However, there was no difference between insulin responses from baseline to follow-up and no differences in the change in insulin response between groups. In Korean subjects with type 2 diabetes mellitus, 12 months of treatment with RSG may increase SAT, but may have a neutral effect on IAAT, resulting in a decrease in the IAAT:SAT ratio. The RSG treatment improved the glucose control in type 2 diabetes mellitus. However, it is important to determine whether the glucose-lowering effect of RSG occurs mainly through direct enhancement of insulin sensitivity.     

TNF-α与2型糖尿病合并非酒精性脂肪肝胰岛素抵抗及动脉粥样硬化的关系

目的探讨2型糖尿病（T2DM）合并非酒精性脂肪肝（NAFL）患者肿瘤坏死因子-α（TNF-α）与胰岛素抵抗（IR）及颈动脉内膜-中层厚度（CIMT）的相关性。方法将192例T2DM患者根据是否合并NAFL进行分组并与正常对照组比较。采用多因素相关分析和回归分析评价TNF-α对IR及CIMT的影响。结果与正常对照组及T2DM无NAFL组相比,T2DM合并NAFL患者TNF-α显著升高（P〈0．01）;多因素相关分析和回归分析显示,TNF-α与IR（r=0．525,P〈0．01）及CIMT（r=0．548,P〈0．01）呈显著正相关。结论T2DM合并NAFL患者TNF-α与IR及CIMT密切相关,参与了动脉粥样硬化的形成。     

Serum resistin level is associated with insulin sensitivity in Japanese patients with type 2 diabetes mellitus

Impaired insulin secretion and decreased insulin sensitivity are the main pathophysiologic features responsible for development of hyperglycemia in type 2 diabetes mellitus. Insulin resistance is often associated with increased adipose tissue mass. To examine which variables influence insulin sensitivity, we compared metabolic parameters, serum resistin, leptin, and adiponectin concentrations to the insulin sensitivity, obtained by frequently sampled intravenous glucose tolerance test using the minimal model analysis, in 113 Japanese patients with type 2 diabetes mellitus. Duration of diabetes, fasting plasma glucose, fasting insulin, homeostasis model assessment of insulin resistance index, and serum resistin concentration were significantly higher in the insulin-resistant subgroup compared with the insulin-sensitive subgroup and correlated with insulin sensitivity. Stepwise regression analysis also identified these parameters as independent regulators of insulin sensitivity. The present study reconfirmed that fasting insulin level or homeostasis model assessment of insulin resistance would be a surrogate measure of insulin resistance and demonstrated that insulin resistance increases progressively after the onset of overt diabetes and that the serum resistin level is associated with insulin sensitivity, suggesting that resistin plays an important role in the development of insulin resistance in Japanese patients with type 2 diabetes mellitus.     

肿瘤坏死因子α基因多态性与2型糖尿病胰岛素抵抗的相关性

目的　探讨肿瘤坏死因子α(TNF α)水平及其基因第 3 0 8位G→A变异与 2型糖尿病 (DM )胰岛素抵抗 (IR)的相关情况。方法　 ( 1)放射免疫法检测 70例 2型DM患者和 60例健康对照者空腹血清胰岛素 (FINS)、TNF α水平。 ( 2 )以PCR RFLP检测TNF α基因型。 ( 3 )用自我平衡模型分析法(HOMA)评价IR。结果　 ( 1) 2型DM组及对照组血清TNF α水平分别为 ( 1.2 6± 0 .2 8) μg/L和 ( 1.15±0 .2 4) μg/L(P <0 .0 5 ) ;FINS分别为 ( 11.3 1± 4.3 1)mIU/L和 ( 14 .67± 4.96)mIU /L(P <0 .0 1) ;HOMA IR分别为 5 .5 4± 2 .2 5和 3 .3 9± 1.48(P <0 .0 1)。 ( 2 ) 2型DM组和对照组GA +AA基因型频率分别为0 .3 0和 0 .13 ,A等位基因频率分别为 0 .16和 0 .0 7(P <0 .0 5 )。 ( 3 ) 2型DMGA +AA基因型组及GG基因型组TNF α分别为 ( 1.3 5± 0 .2 5 ) μg/L和 ( 1.2 2± 0 .16) μg/L(P <0 .0 5 ) ;FINS分别为 ( 13 .42± 4.73 )mIU /L和 ( 10 .40± 3 .63 )mIU/L(P <0 .0 1) ;HOMA IR分别为 7.42± 1.93和 4.11± 1.3 1(P <0 .0 1)。( 4 )多元逐步回归分析显示 :HOMA IR与TNF α及TNF α基因型呈显著正相关。结论　TNF α第 3 0 8位G→A变异与中国闽南人 2型DM的发生有关 ,A等位基因可能通过增加TNF α的释放     

Effect of pioglitazone on abdominal fat distribution and insulin sensitivity in type 2 diabetic patients

We examined the effect of pioglitazone on abdominal fat distribution to elucidate the mechanisms via which pioglitazone improves insulin resistance in patients with type 2 diabetes mellitus. Thirteen type 2 diabetic patients (nine men and four women; age, 52 +/- 3 yr; body mass index, 29.0 +/- 1.1 kg/m(2)), who were being treated with a stable dose of sulfonylurea (n = 7) or with diet alone (n = 6), received pioglitazone (45 mg/d) for 16 wk. Before and after pioglitazone treatment, subjects underwent a 75-g oral glucose tolerance test (OGTT) and two-step euglycemic insulin clamp (insulin infusion rates, 40 and 160 mU/m(2).min) with [(3)H]glucose. Abdominal fat distribution was evaluated using magnetic resonance imaging at L4-5. After 16 wk of pioglitazone treatment, fasting plasma glucose (179 +/- 10 to 140 +/- 10 mg/dl; P < 0.01), mean plasma glucose during OGTT (295 +/- 13 to 233 +/- 14 mg/dl; P < 0.01), and hemoglobin A(1c) (8.6 +/- 0.4% to 7.2 +/- 0.5%; P < 0.01) decreased without a change in fasting or post-OGTT insulin levels. Fasting plasma FFA (674 +/- 38 to 569 +/- 31 microEq/liter; P < 0.05) and mean plasma FFA (539 +/- 20 to 396 +/- 29 microEq/liter; P < 0.01) during OGTT decreased after pioglitazone. In the postabsorptive state, hepatic insulin resistance [basal endogenous glucose production (EGP) x basal plasma insulin concentration] decreased from 41 +/- 7 to 25 +/- 3 mg/kg fat-free mass (FFM).min x microU/ml; P < 0.05) and suppression of EGP during the first insulin clamp step (1.1 +/- 0.1 to 0.6 +/- 0.2 mg/kg FFM.min; P < 0.05) improved after pioglitazone treatment. The total body glucose MCR during the first and second insulin clamp steps increased after pioglitazone treatment [first MCR, 3.5 +/- 0.5 to 4.4 +/- 0.4 ml/kg FFM.min (P < 0.05); second MCR, 8.7 +/- 1.0 to 11.3 +/- 1.1 ml/kg FFM(.)min (P < 0.01)]. The improvement in hepatic and peripheral tissue insulin sensitivity occurred despite increases in body weight (82 +/- 4 to 85 +/- 4 kg; P < 0.05) and fat mass (27 +/- 2 to 30 +/- 3 kg; P < 0.05). After pioglitazone treatment, sc fat area at L4-5 (301 +/- 44 to 342 +/- 44 cm(2); P < 0.01) increased, whereas visceral fat area at L4-5 (144 +/- 13 to 131 +/- 16 cm(2); P < 0.05) and the ratio of visceral to sc fat (0.59 +/- 0.08 to 0.44 +/- 0.06; P < 0.01) decreased. In the postabsorptive state hepatic insulin resistance (basal EGP x basal immunoreactive insulin) correlated positively with visceral fat area (r = 0.55; P < 0.01). The glucose MCRs during the first (r = -0.45; P < 0.05) and second (r = -0.44; P < 0.05) insulin clamp steps were negatively correlated with the visceral fat area. These results demonstrate that a shift of fat distribution from visceral to sc adipose depots after pioglitazone treatment is associated with improvements in hepatic and peripheral tissue sensitivity to insulin.     

A combination of human leukocyte antigen DQB1*02 and the tumor necrosis factor alpha promoter G308A polymorphism predisposes to an insulin-deficient phenotype in patients with type 2 diabetes

Our previous results have suggested that genes outside the human leukocyte antigen (HLA) class II locus may affect the phenotype of type 2 diabetic patients from families with both type 1 and type 2 diabetes (mixed type 1/2). To study whether the TNF alpha gene could be such a modifying gene, we studied TNF alpha promoter polymorphisms (G-->A substitution at positions -308 and -238) in relation to HLA-DQB1 genotypes in type 2 patients from mixed type 1/2 families or common type 2 diabetes families as well as in patients with adult-onset type 1 diabetes and control subjects. The TNF alpha(308) AA/AG genotype frequency was increased in adult onset type 1 patients (55%, 69 of 126), but it was similar in type 2 patients from type 1/2 families (35%, 33/93) or common type 2 families (31%, 122 of 395), compared with controls (33%, 95/284; P < 0.0001 vs. type 1). The TNF alpha(308) A and DQB1*02 alleles were in linkage disequilibrium in type 1 patients (Ds = 0.81; P < 0.001 vs. Ds = 0.25 in controls) and type 2 patients from type 1/2 families (Ds = 0.59, P < 0.05 vs. controls) but not in common type 2 patients (Ds = 0.39). The polymorphism was associated with an insulin-deficient phenotype in the type 2 patients from type 1/2 families only together with DQB*02, whereas the common type 2 patients with AA/AG had lower waist to hip ratio [0.92 (0.12) vs. 0.94 (0.11), P = 0.008] and lower fasting C-peptide concentration [0.48 (0.47) vs. 0.62 (0.46) nmol/liter, P = 0.020] than those with GG, independently of the presence of DQB1*02. In conclusion, TNF alpha is unlikely to be the second gene in the HLA area responsible for our previous findings in type 1/2 patients. However, we could show an association between TNF alpha(308) polymorphism and the phenotype of common type 2 diabetes.     

2型糖尿病患者腹部脂肪分布与胰岛素敏感性及血清瘦素水平的关系

目的 探讨2型糖尿病患者腹部脂肪分布与瘦素和胰岛素抵抗的关系。方法 48例2型糖尿病患者均进行高胰岛素正血糖钳夹试验，根据体重指数(BMI)和葡萄糖利用率(GIR)将患者分为非肥胖型胰岛素敏感组(NIS，16例)，非肥胖型胰岛素抵抗组(NIR，15例)和肥胖型胰岛素抵抗组(OIR，17例)，同时洲定血清瘦素，胰岛素水平和腹部脂肪面积。结果 两非肥胖组(NIS和NIR)之间的BMI相似，但NIR组的GIR要明显低于NIS组，NIR组的内脏脂肪面积比NIS组明显增高，NIR组的瘦素水平在皮下脂肪校正之后与NIS组差异无显著性。OIR组的皮下脂肪，内脏脂肪和瘦素水平比非肥胖组(NIS和NIR)明显增高，OIR的GIR明显低于NIS和NIR组。多元回归分析显示，无论肥胖组还是非肥胖组，内脏脂肪是预测胰岛素抵抗的最重要变量；皮下脂肪是血清瘦素水平的最重要变量。结论 两种代谢不同的脂肪分布是胰岛素抵抗和瘦素水平的决定因素。     

Association of tumor necrosis factor alpha-308 promoter polymorphism with spondyloarthritides patients in Colombia

The pathogenesis of SpA is considered to be a complex and multi-factorial process and, similar to other autoimmune diseases, includes the activity of proinflammatory cytokines such as TNF alpha. Our study compared the -308 promoter polymorphism of TNF alpha with TNF alpha levels, HLA-B27 status, age at the onset of symptoms, SpA subtype and the clinical degree of activity in Colombian SpA patients and healthy subjects (HS). Comparisons of the TNF alpha-308A genotype among HS and SpA patients (P = 0.004), uSpA patients (P = 0.040), ReA patients (P = 0.001), were significantly different and AS patients (P = 0.110), as were alleles for SpAs (P = 0.007) between patients with SpAs and controls. Initial exploratory analyses demonstrated that the TNF alpha-308 SNP genotype frequencies were different among SpA patients and HS in the Colombian population studied. Furthermore, there was no significant correlation with activity and functional clinical index, serum TNF alpha level or HLA B27 status. Allele frequencies, on the other hand, were correlated with the activity clinical index.     

Relationship between visceral fat accumulation and anti-lipolytic action of insulin in patients with type 2 diabetes mellitus

Insulin resistance is closely related to developing type 2 diabetes mellitus. Visceral fat accumulation is associated with insulin resistance, which affects the free fatty acid (FFA) metabolism. We investigated the interactions among visceral fat accumulation, FFA metabolism and insulin resistance in 20 patients with type 2 diabetes mellitus, including 11 obese and 9 non-obese subjects. Body fat distribution was estimated by measuring the areas of both subcutaneous and visceral fat mass on abdominal computed tomography at the umbilical level. Glucose infusion rate (GIR) and plasma FFA responses to insulin were determined as an index of insulin resistance and anti-lipolytic action, respectively, in a euglycemic hyperinsulinemic clamp study. There was an inverse correlation between GIR and insulin-induced decrease in plasma FFA in all diabetic patients (r = -0.652, P < 0.01). Visceral fat mass area was well correlated with GIR (r = -0.583, P < 0.01) and insulin-induced decrease in plasma FFA (r = 0.724, P < 0.001), whereas subcutaneous fat mass area was not correlated either with GIR or plasma FFA decrease. These findings suggest that visceral fat accumulation results in increasing the resistance against the anti-lipolytic action of insulin, and that FFA metabolism is closely related with glucose utilization in patients with type 2 diabetes mellitus.     

罗格列酮改善2型糖尿病患者体脂分布、脂联素水平和组织胰岛素敏感性

目的研究罗格列酮(ROS)治疗后体脂含量、分布和脂联素改变与组织胰岛素敏感性的关系。方法符合1997年美国糖尿病协会糖尿病(DM)诊断标准的2型DM患者40例。试验采用前后自身配对方法。口服ROS 4 mg每天1次,总疗程8周。测定指标包括常规临床检查项目、血糖、血脂和血浆胰岛素水平,同时测定血浆脂联素、瘦素、肿瘤坏死因子α(TNF-α)和游离脂肪酸(FFA)水平。以HOMA模型和胰岛素钳夹试验评价组织胰岛素敏感性,应用双能X线和核磁共振测定机体的体脂含量和分布。结果(1)应用ROS治疗2型DM患者,虽然体重和体脂含量均有增加趋势(均P>0.05),但组织胰岛素敏感性显著改善(P<0.05);(2)ROS治疗能导致有益的脂肪重新分布,即增加低代谢活性的腹部皮下脂肪含量而相对减少高脂溶活性的腹内脂肪含量,其结果是FFA释放减少,并增加血浆脂联素水平;(3)ROS治疗增加血浆脂联素水平并降低TNF-α和FFA水平,这些脂肪细胞因子的改变直接与组织胰岛素敏感性的改变相关。结论应用ROS治疗2型DM患者能导致有益于机体代谢的脂肪重新分布,增加脂联素并降低FFA水平,从而抵消患者体重增加对组织胰岛素敏感性的负性影响,总的结果是组织胰岛素敏感性增加。     

2型糖尿病并内脏型肥胖患者内脏脂肪面积的分析

目的探讨2型糖尿病（T2DM）并内脏型肥胖患者的临床特点及内脏脂肪面积的相关性分析。 方法本研究收集2018年5月至2018年9月在山西大同大学第一附属医院住院的共350例T2DM患者的临床资料,测量内脏脂肪面积(VFA)和皮下脂肪面积( SFA),以VFA≥100 cm²作为内脏型肥胖的诊断标准。根据VFA值分为单纯2型糖尿病对照组(VFA<100 cm²)和糖尿病合并内脏型肥胖观察组(VFA≥100 cm²),测定所有患者的身高、体重、体质量指数（BMI）、腰臀比（WHR）及血糖、血脂、肾功能等指标,比较两组间差异。 结果T2DM并内脏型肥胖组中身高、体重、BMI、头围、颈围、腰围、臀围、WHR、VFA、SFA、甘油三脂（TG）、总胆固醇（TC）、血尿酸（UA）、舒张压均高于对照组（P<0.05）,以VFA为应变量,其他各因素为自变量,进行多元线性回归分析：体重、BMI、腰围、TG、舒张压被纳入回归方程,是T2DM并内脏型肥胖的独立危险因素。 结论体重、BMI、腰围、TG、舒张压的增高是VFA的危险因素,与T2DM并腹型肥胖相关。     

TNF 308 G/A polymorphism and type 1 diabetes: A meta-analysis

We conducted a meta-analysis to examine the association between TNF 308 G/A polymorphism and risk for T1DM. Eleven reports were identified. Our study confirmed that a higher frequency of TNF 308 A allele conferred a significant risk for T1DM. Potential explanations were discussed.