血浆脂联素与2型糖尿病胰岛素抵抗关系的研究

目的　测定 2型糖尿病患者血浆脂联素的水平 ,并分析它与体重指数、血糖、胰岛素、血脂和胰岛素抵抗的关系 ,从而探讨脂联素在糖尿病发病中的作用。方法　健康对照组 2 8例 ,2型糖尿病组 60例 ,根据体重指数又将糖尿病组分为非肥胖糖尿病组 3 0例 (BMI <2 5kg/m2 )和肥胖糖尿病组 3 0例 (BMI >2 5kg/m2 )。用ELISA方法检测空腹血浆脂联素浓度 ,同时测定各组的空腹血糖、胰岛素、血脂的水平 ;根据HOMA模型提出的公式 ,计算分析胰岛素抵抗指数 ,并分析各指标间的相关性。结果　 (1)糖尿病各组血浆脂联素的水平明显低于正常对照组 ,且肥胖糖尿病组脂联素的水平低于非肥胖组 ,差异均有显著性 (P 0 .0 1) ;(2 )血浆脂联素浓度与体重指数、空腹胰岛素、胰岛素抵抗指数 (IR)、甘油三酯呈显著负相关。结论　脂联素参与了胰岛素抵抗的发生过程 ,与糖尿病的发生发展密切相关 ;脂联素可作为评价胰岛素抵抗程度的一种新的敏感指标     

2型糖尿病患者血清脂联素浓度的变化

目的 探讨2型糖尿病患者血清脂联素水平的变化。方法 2型糖尿病患者60例,根据BM I水平分为肥胖2型糖尿病组（BM I≥25kg/m＆2）,正常体重2型糖尿病组;将30名正常体重健康人设为对照组;检测血清脂联素、空腹胰岛素、空腹血糖、血脂等指标。结果 糖尿病各组血清脂联素水平明显低于对照组,并且肥胖糖尿病各组低于非肥胖组,差异有显著性（P〈0.01）。相关分析发现,脂联素水平与体重指数、空腹血糖、甘油三酯含量呈负相关,与胰岛素敏感性呈正相关。结论 2型糖尿病患者血清脂联素水平是降低的。提示血清脂联素水平升高可能对肥胖及糖代谢紊乱的治疗有益。     

初发2型糖尿病患者血脂联素和瘦素与胰岛素抵抗的关系

目的 研究初发2型糖尿病患者血脂联素和瘦素水平的变化及其与胰岛素抵抗的关系.方法 选择46例初发2型糖尿病患者,及与其体脂含量相匹配的糖耐量正常者43名,计算体重指数(BMI)和腰臀围比(WHR),并空腹采血,测定血糖(FPG)、血脂、真胰岛素(FTI)、胰岛素原(FPI)、脂联素和瘦素浓度,分析血清脂联素和瘦素水平的变化及其与胰岛素抵抗的关系.用胰岛素抵抗指数(HOMA-IR)评估胰岛素抵抗程度.结果 2型糖尿病组与正常对照组比较,年龄、BMI无统计学意义(P>0.05),三酰甘油、FPG及FPI和HOMA-IR明显升高(P<0.05或P<0.01),舒张压、脂联素水平明显降低(P<0.05或P<0.01);相关分析显示,脂联素与FPG、FTI、HOMA-IR、BMI、WHR呈负相关(P<0.05或P<0.01);瘦素与BMI、FTI、HOMA-IR、FPG呈正相关(P<0.05或P<0.01),与WHR无关.人血清脂联素和瘦素间无相关性.结论 人血清脂联素和瘦素与胰岛素抵抗密切相关,体脂含量相同的初发2型糖尿病患者血脂联素水平低于正常人.     

2型糖尿病合并肥胖患者脂联素水平与胰岛素抵抗的相关性

目的 研究2型糖尿病合并肥胖患者脂联素水平和胰岛素抵抗之间的相关性,探讨脂联素在2型糖尿病合并肥胖患者发生胰岛素抵抗中的作用.方法 选择30例2型糖尿病合并肥胖患者、25例2型糖尿病患者及25例非糖尿病对照人员(其中13例为肥胖者),检测体质指数、腰/臀比值、空腹血糖、糖化血红蛋白、血清空腹胰岛素、血脂、脂联素水平,计算胰岛素抵抗指数和胰岛素敏感指数.分析血清脂联素与胰岛素抵抗的相关性.结果 (1)糖尿病肥胖组的检测体质指数、糖化血红蛋白、空腹血糖、胰岛素抵抗指数、血清空腹胰岛素、腰/臀比值均高于对照肥胖组,脂联素、胰岛素敏感指数低于对照肥胖组(P<0.05).(2)糖尿病非肥胖组甘油三酯、糖化血红蛋白、空腹血糖、胰岛素抵抗指数、血清空腹胰岛素均高于对照非肥胖组,胰岛素敏感指数、脂联素低于对照非肥胖组(P<0.05).(3)糖尿病肥胖组甘油三酯、胆固醇、体质指数、糖化血红蛋白、空腹血糖、胰岛素抵抗指数、血清空腹胰岛素、腰/臀比值均高于糖尿病非肥胖组,胰岛素敏感指数、脂联素低于糖尿病非肥胖组(P<0.05).结论 脂联素与2型糖尿病肥胖患者的胰岛素抵抗发生有关,脂联素降低易导致胰岛素抵抗,脂联素水平可作为2型糖尿病合并肥胖患者发生胰岛素抵抗的监测标准.     

老年2型糖尿病血浆脂联素与瘦素和胰岛素的关系

目的 :探讨血浆脂联素、瘦素和胰岛素在老年 2型糖尿病和 2型糖尿病伴高血压患者的水平及其相互关系。方法 :对 75例居住在武汉的被检者同时采集病史、进行体格检查并留取血浆 ,测定其血糖、胰岛素、瘦素、血脂和脂联素的水平。结果 :①老年糖尿病组与糖尿病合并高血压组之间的血浆脂联素水平无显著性差异 ,但二者均低于对照组 ;老年与非老年对照组之间的血浆脂联素水平无显著性差异。②简单相关分析提示脂联素与体重指数、空腹和餐后 1h和 2h血糖、胰岛素抵抗指数、高血压、瘦素、载脂蛋白A负相关 ,与高密度脂蛋白正相关 ;采用逐步回归法分析 ,校正其它参数 ,体重指数、瘦素和空腹血糖为影响脂联素水平的独立因素。结论 :老年糖尿病患者的血浆脂联素水平降低 ,在肥胖、2型糖尿病、瘦素、胰岛素和脂联素之间可能存在互动的相关性     

不同血糖水平老年人脂联素、瘦素水平及其比值与胰岛素抵抗的相关性

目的研究不同血糖水平老年人脂联素、瘦素水平的变化,脂联素瘦素比值与胰岛素抵抗的相关性。方法选取不同血糖水平老年人146例,包括对照组:糖耐量正常的健康人群52例,研究组:糖耐量异常(IGT)患者39例,新近诊断糖尿病(T2DM)患者55例。研究脂联素、瘦素水平以及其比值和胰岛素抵抗指数、体重指数、腰臀比、血脂等指标的相关性。结果 IGT组和T2DM组的腰臀比、体重指数、甘油三酯、瘦素、胰岛素抵抗指数较正常对照组显著增加,脂联素水平较正常组明显下降;脂联素/瘦素与腰围、腰臀比、体重指数、空腹胰岛素、甘油三酯、低密度脂蛋白、HO-MA-IR负相关,与高密度脂蛋白正相关。Logistic回归结果显示脂联素/瘦素是胰岛素抵抗指数的独立危险因素。结论不同血糖水平老年人中,脂联素/瘦素比值与胰岛素抵抗密切相关。     

血清脂联素水平在磺脲类药物继发性失效的2型糖尿病患者中的变化及临床意义

目的观察磺脲类降糖药（SU）继发性失效2型糖尿病患者血清脂联素水平与血糖控制良好2型糖尿病患者及正常人之间的差异。方法采用ELISA法检测所有受试者血清脂联素水平,同时检测血糖和血脂,计算体重指数,进行相关性分析。结果血糖控制良好的患者脂联素明显低于正常人（P〈0．05）,SU继发性失效的患者明显低于血糖控制良好的患者（P〈0．05）;两组2型糖尿病患者胰岛素抵抗水平均明显高于正常人（P均〈0．05）,而两组患者比较无明显差异（P〉0．05）。SU继发性失效患者脂联素水平与空腹血糖、餐后2小时血糖、糖化血红蛋白、体重指数、空腹胰岛素、胰岛素抵抗指数、胆固醇、总甘油三酯及低密度脂蛋白胆固醇呈明显负相关（P均〈0．05）,与高密度脂蛋白胆固醇呈明显正相关（P〈0．05）。结论脂联素水平下降和胰岛素抵抗相互影响,可能参与了2型糖尿病SU继发性失效的发生发展。     

2型糖尿病患者皮下、大网膜脂肪组织脂联素mRNA表达的定量研究

目的　探讨 2型糖尿病患者皮下及大网膜脂肪组织脂联素 (adiponectin)表达水平及与血脂联素、体重指数、腰臀比 (WHR)、胰岛素敏感性的相关关系。方法　用实时荧光定量RT PCR检测 2型糖尿病患者和非糖尿病患者皮下及大网膜脂肪组织脂联素mRNA的表达水平 ,用ELISA方法测定血浆脂联素水平。结果　 2型糖尿病患者大网膜脂肪组织脂联素mRNA表达水平较非糖尿病组显著下降 (P <0 .0 5 ) ;糖尿病组与非糖尿病组的血浆脂联素水平差异无显著性 ;糖尿病组大网膜脂肪组织脂联素mRNA表达与WHR成负相关 (r=- 0 .5 1,P <0 .0 5 )。糖尿病组血浆脂联素水平与大网膜脂肪组织脂联素mRNA的表达成正相关 (r=0 .5 7,P <0 .0 1)。结论　 2型糖尿病患者大网膜脂肪组织脂联素mRNA表达显著降低。内脏脂肪组织脂联素mRNA的表达水平可以作为胰岛素抵抗的重要参数。     

血浆脂联素水平与糖尿病患者冠状动脉粥样硬化的相关性研究

目的探讨脂联素水平与糖尿病患者冠状动脉粥样硬化病变程度的相关性。方法根据冠状动脉造影结果将临床诊断为急性冠脉综合征的283例患者进行分组,应用放射免疫法检测血浆脂联素水平,同时监测血压、血糖、血浆胰岛素、血脂等相关指标。结果⑴脂联素水平与HDL-C、空腹血糖、胰岛素抵抗指数显著相关。⑵糖尿病组血浆脂联素水平明显高于非糖尿病组。⑶糖尿病患者冠状动脉粥样硬化程度随血浆脂联素水平进行性降低。结论低血浆脂联素水平是糖尿病患者冠状动脉粥样硬化发生发展的独立危险因素。     

2型糖尿病患者血清抵抗素、脂联素与下肢动脉病变的关系

目的 探讨初诊2型糖尿病患者空腹血清抵抗素、脂联素水平与下肢动脉病变(PAD)的关系.方法 根据踝肱指数(ABI)将96例初诊2型糖尿病患者分为PAD组和非PAD组,另选取52例健康体检者作为正常对照组,测定患者空腹血清抵抗素、脂联素、血糖、血脂及胰岛素,测量身高、体重、血压;计算体重指数(BMI)、胰岛素抵抗指数(HOMA-IR).结果 1.与正常对照组相比,2型糖尿病患者血清抵抗素水平明显升高(P＜0.01),脂联素水平明显降低(P＜0.01).2.与非PAD组相比,PAD组患者年龄明显偏高(P＜0.01),血清总胆固醇(TC)、低密度脂蛋白(LDL)水平升高(P＜0.05)、HOMA-IR、血清抵抗素明显升高(P＜0.01),脂联素水平降低(P＜0.01).3.相关分析表明,2型糖尿病患者血清脂联素与ABI呈正相关(r=0.367,P＜0.05),血清抵抗素与ABI负相关(r=-0.421,P＜0.05).结论 2型糖尿病合并PAD患者血清抵抗素、脂联素水平明显改变且与ABI相关,抵抗素、脂联素可能在2型糖尿病下肢动脉病变的发生发展中起重要作用.     

高血压病患者血清脂联素浓度的变化及其意义

目的探讨原发性高血压病患者血清脂联素浓度的变化及其与血压之间的关系。方法本研究选取原发性高血压病患者50例及健康人50例(正常对照组),常规测量血压、体质量、身高,计算体质量指数,检测血清脂联素、空腹血糖、血清胰岛素、总胆固醇、高密度脂蛋白胆固醇、甘油三酯等指标。再将50例高血压病患者分成两组,每组25例,分别用血管紧张素转换酶抑制剂西拉普利及血管紧张素Ⅱ受体拮抗剂替米沙坦治疗2周,治疗前后均检测上述指标。结果①原发性高血压病患者与健康对照者比较,血清脂联素水平下降犤(4.13±1.89)μg/mlvs(7.09±2.85)μg/ml,P<0.05犦,健康对照组脂联素浓度与体质量指数、总胆固醇呈负相关(r=-0.28,-0.26,P<0.05);②原发性高血压组血清脂联素浓度与收缩压、舒张压、甘油三酯呈显著负相关(r=-0.36、-0.32、-0.37,P<0.05),高血压组与健康对照组两组合并比较,脂联素浓度与BMI体质量指数、收缩压、舒张压呈显著负相关(r=-0.29、-0.28、-0.31,P<0.01);③高血压患者分别用西拉普利及替米沙坦治疗两周后,血压显著下降(P<0.05),血清脂联素浓度明显升高(P<0.05)。结论在原发性高血压病患者中,血清脂联素水平下降并与血压之间存在一定的相关性,与脂代谢紊乱亦相关。     

Adiponectin is independently associated with insulin sensitivity in women with polycystic ovary syndrome

OBJECTIVE: The polycystic ovary syndrome (PCOS) is associated with obesity and insulin resistance predisposing to diabetes mellitus type 2 and atherosclerosis. Adiponectin is a recently discovered adipocytokine with insulin-sensitizing and putative antiatherosclerotic properties. The aim of the study was to elucidate determinants of circulating adiponectin levels and to investigate the potential role of adiponectin in insulin resistance in PCOS women. PATIENTS AND MEASUREMENTS: Plasma adiponectin and parameters of obesity, insulin resistance and hyperandrogenism were measured In 62 women with PCOS and in 35 healthy female controls. RESULTS: Both in PCOS and controls, adiponectin levels were lower in overweight or obese women than in normal-weight women, without any difference between PCOS and controls after adjustment for body mass index (BMI). In PCOS and in controls there was a significant correlation of adiponectin with BMI (r = -0.516, P < 0.001), fasting insulin (r = -0.404, P < 0.001), homeostasis model sensitivity (HOMA %S) (r = -0.424, P < 0.001) and testosterone (r = -0.279, P < 0.01), but no correlation with androstenedione (r = -0.112, P = 0.325), 17-OH-progesterone (r =-0.031, P = 0.784) or the LH/FSH ratio (r =-0.033, P = 0.753). Multiple linear regression analysis revealed that BMI and HOMA %S but not testosterone were independently associated with adiponectin plasma levels, explaining 16% (BMI) and 13% (HOMA %S) of the variability of adiponectin, respectively. In PCOS patients insulin sensitivity, as indicated by continuous infusion of glucose with model assessment (CIGMA %S) was significantly correlated with adiponectin (r = 0.55; P < 0.001), BMI (r =-0.575; P < 0.001), waist-to-hip ratio (WHR) (r =-0.48; P = 0.001), body fat mass assessed by dual-energy X-ray-absorptiometry (DEXA) [Dexa-fat (total) (r = -0.61; P < 0.001) and Dexa-fat (trunk) (r = -0.59; P < 0.001)] and with testosterone (r = -0.42; P = 0.001). Multiple linear regression analysis demonstrated that markers of obesity such as BMI, total or truncal fat mass, age and adiponectin were independently associated with CIGMA %S, and that circulating adiponectin accounted for about 18% of the degree of insulin resistance in PCOS. By contrast, testosterone was not a significant factor, suggesting that PCOS per se did not affect insulin sensitivity independent from obesity, age and adiponectin. Metformin treatment for 6 months in insulin-resistant PCOS women (n = 9) had no effect on plasma adiponectin (P = 0.59) despite significant loss of weight and fat mass and improvement in hyperandrogenaemia. CONCLUSIONS: PCOS per se is not associated with decreased levels of plasma adiponectin. However, circulating adiponectin is independently associated with the degree of insulin resistance in PCOS women and may contribute to the development and/or maintenance of insulin resistance independent from adiposity.     

Glucose-to-insulin ratio rather than sex hormone-binding globulin and adiponectin levels is the best predictor of insulin resistance in nonobese women with polycystic ovary syndrome

Polycystic ovary syndrome (PCOS), the main androgen disorder in women, has been suggested to be associated with a high risk of developing cardiovascular disease and type 2 diabetes. In many PCOS patients, overweight or central obesity is generally associated with increases in fasting insulin levels, insulin resistance, and glucose intolerance, and has been identified as a target for new therapeutic strategy, including early change in lifestyle. Early biochemical marker(s) for identifying at-risk patients will be useful for prevention studies. The main goal of the present study was to search for such tool(s). We investigated 16 nonobese PCOS women by performing euglycemic hyperinsulinemic clamp and measuring insulin levels during fasting and oral glucose tolerance test, as well as the serum concentrations of SHBG, leptin, and adiponectin, the newly identified adipose factors. Eight of the 16 patients had a steady-state glucose disposal rate less than 8.5 mg/kg.min, the lowest normal value for nonobese control women. These insulin-resistant patients had significant higher body mass index (BMI) and waist-to-hip ratio (WHR), and lower high-density lipoprotein cholesterol and SHBG levels. As expected, glucose disposal correlated negatively with BMI (P = 0.01), WHR (P = 0.01), and fasting insulin level (P = 0.003). On stepwise regression analysis, however, the glucose-to-insulin ratio (GIR) emerged as the strongest independent parameter to appraise insulin resistance (R(2) = 0.61). SHBG level correlated positively with GIR (P < 0.001) and negatively with BMI (P = 0.003) but did not correlate with either insulin response during the glucose tolerance test or plasma leptin and/or adiponectin levels. In contrast, BMI was the only independent predictive parameter of SHBG (P = 0.003, R(2) = 0.73). Interestingly, plasma adiponectin levels were positively associated with glucose disposal rate (P = 0.043) and negatively with WHR (P = 0.024), waist circumference being the best predictor of adiponectin level (P < 0.01). Leptin level correlated only with BMI (r = 0.62, P = 0.01). This study confirmed that insulin resistance, despite the lack of obesity as such, is clearly present in many PCOS women, and demonstrated that GIR is the best predictor for insulin resistance. It was also shown that adiponectin level is a good indicator of abdominal fat mass and is associated to insulin resistance. Finally, low SHBG levels in PCOS are intimately associated with BMI, suggesting that some signal(s) from the adipose tissue, independent of adiponectin and leptin, may regulate liver production of SHBG.     

Associations between plasma adiponectin concentrations and liver histology in patients with nonalcoholic fatty liver disease

OBJECTIVES: To explore associations between plasma adiponectin concentrations and liver histology in patients with nonalcoholic fatty liver disease (NAFLD). DESIGN AND PATIENTS: In a cross-sectional study, we enrolled 60 consecutive NAFLD patients and 60 age-, sex- and body mass index (BMI)-matched healthy controls. MEASUREMENTS: NAFLD (by liver biopsy), plasma adiponectin concentrations, insulin resistance (by homeostasis model assessment, HOMA-IR) and metabolic syndrome (MetS) features. RESULTS: NAFLD patients had a marked decrease in plasma adiponectin concentration (6.1 +/- 2.8 vs. 13.6 +/- 3.8 microg/ml, P < 0.001) compared with matched controls. MetS, as defined by the Adult Treatment Panel III (ATP III) criteria, and its individual components were more frequent among NAFLD patients. The marked differences in adiponectin concentrations that were observed between the groups were little affected by adjustment for age, sex, BMI, HOMA-IR score and MetS components. Notably, decreased adiponectin levels were closely associated with the degree of hepatic steatosis, necroinflammation and fibrosis (P < 0.001 for all) among NAFLD patients. By logistic regression analysis, low adiponectin levels independently predicted hepatic steatosis [odds ratio (OR) 2.3, 95% confidence interval (CI) 1.5-5.8, P < 0.001] and necroinflammation (OR 3.1, 95% CI 1.9-7, P < 0.001), but not fibrosis (P = 0.07), after adjustment for age, sex, BMI, HOMA-IR and MetS components. CONCLUSIONS: NAFLD patients have markedly lower plasma adiponectin concentrations than control subjects. Low adiponectin levels are strongly associated with the severity of liver histology, thus further supporting the hypothesis that adiponectin might be involved in the development of NAFLD.     

Decreased plasma adiponectin concentrations are closely related to steatosis in hepatitis C virus-infected patients

OBJECTIVES: The mechanisms underlying steatosis during hepatitis C virus (HCV) infection are complex and multifactorial. Obesity is a well-recognized risk factor for the development of steatosis in chronic hepatitis C infection. The aim of our study was to investigate the role of adipocytokines in HCV-related steatosis. Therefore, we hypothesized that the endocrine function of adipose tissue could be, in part, responsible for HCV-related steatosis. Seventy-one consecutive untreated chronic hepatitis C patients were studied to assess the effects of adipocytokines, body mass index (BMI), age, and HCV genotype on steatosis. We used ELISA to determine serum adiponectin, leptin, and soluble TNF receptors I and II concentrations. RESULTS: Steatosis was observed in 42 (59.1%) patients. BMI was significantly associated with leptin (r = 0.64; P = 0.0001) and was border significantly associated with adiponectin concentrations (r = -0.22; P = 0.06). In univariate analyses, age, HCV genotype 3, BMI, increased leptin level, increased insulin level, and decreased adiponectin concentration were associated with steatosis. In multivariate analysis, steatosis was significantly associated with low adiponectin concentration, age, HCV genotype 3, and aspartate aminotransferase (ASAT) level, whereas steatosis was not associated with leptin, insulin, and BMI. CONCLUSION: In chronic HCV patients, hypoadiponectinemia is significantly associated with the development of liver steatosis. The fact that the plasma levels of adiponectin inversely correlate with steatosis in HCV-infected subjects suggests that hypoadiponectinemia may contribute to hepatic steatosis progression and liver injury in this population. One practical implication is that therapy to increase circulating adiponectin concentration, such as overweight reduction or thiazolidinediones, provides the potential to improve steatosis in chronic hepatitis C infection.     

Elevated plasma adiponectin concentrations in patients with liver cirrhosis correlate with plasma insulin levels

Abstract: Background: Adiponectin is a hormone secreted by adipocytes and has anti‐diabetic and anti‐atherogenic properties. Hypoadiponectinemia is associated with insulin‐resistant diabetes and liver dysfunction. The aim of this study was to determine plasma adiponectin and insulin levels in patients with liver cirrhosis. Methods: Adiponectin and insulin levels were determined in 38 patients with cirrhosis and 30 healthy controls, and were correlated with various clinical and biochemical parameters. Patients included 21 with Child A, eight Child B, and nine with Child C liver cirrhosis. Results: Log adiponectin and insulin levels were significantly elevated in patients with cirrhosis compared with the control. In liver cirrhosis, the level of adiponectin increased proportionately with the Child's classification score. In control subjects, plasma adiponectin correlated inversely with insulin levels. In contrast, plasma adiponectin correlated positively with insulin levels in patients with liver cirrhosis. Plasma adiponectin levels did not correlate with age, sex, body mass index, total bilirubin, aspartate aminotransferase, and fasting blood sugar levels in both groups, while alanine aminotransferase correlated negatively with adiponectin in control subjects as reported previously. Conclusion: Our results of high plasma adiponectin in patients with liver cirrhosis could reflect an imbalance between its production by adipocytes and metabolism in the liver.     

High molecular weight adiponectin correlates with insulin sensitivity in patients with hepatitis C genotype 3, but not genotype 1 infection

BACKGROUND: Obesity is recognized as a cofactor in hepatitis C (HCV) liver injury. Adipokines may be the link between increasing body mass index (BMI) and disease progression in HCV. Adiponectin is an anti-inflammatory adipokine that is present in serum in a range of multimeric forms that appear to have different metabolic functions. METHODS: We studied 30 male patients with untreated chronic HCV (15 each with genotypes 1 and 3) and 12 controls. The three groups were matched for age and BMI. Total adiponectin and high (HMW) and low (LMW) molecular weight adiponectin multimers were measured. The relationships between adiponectin, BMI, insulin sensitivity, and liver histology were examined. RESULTS: Genotype 3 was associated with greater hepatic steatosis and inflammation than genotype 1. Patients with genotype 1 were less insulin sensitive than genotype 3, who had similar insulin sensitivity to controls. Insulin resistance was associated with a decrease in total and HMW adiponectin in both HCV and controls, while LMW adiponectin was unchanged. When the effect of genotype was examined, this association was present with genotype 3 but not genotype 1 infection. CONCLUSIONS: These data demonstrate that the relationship between insulin resistance and adiponectin is similar in controls and patients with genotype 3 but not genotype 1 infection. The greater degree of insulin resistance in genotype 1 appears to be a genotype-specific effect.     

Total and high molecular weight adiponectin, haemodynamics, and mortality in patients with chronic heart failure.

AIMS: To evaluate whether plasma high molecular weight (HMW) adiponectin provides prognostic information in addition to that obtained from clinical, haemodynamic, and biochemical variables previously known to be associated with a high mortality in chronic heart failure (CHF) patients. METHODS AND RESULTS: We measured the plasma levels of total and HMW adiponectin, atrial natriuretic peptide, brain natriuretic peptide (BNP), and N-terminal-proBNP (NT-proBNP), and haemodynamic parameters in 449 consecutive CHF patients. Based on body mass index (BMI), patients were classified into three groups: low (<21 kg/m(2), n = 133), normal (21-25 kg/m(2), n = 205), and high (>25 kg/m(2), n = 111). After adjustment for clinical variables associated with CHF including haemodynamics, plasma total adiponectin level was an independent prognostic predictor but HMW adiponectin was not in the overall patient group. On subgroup analyses, in patients with abnormal BMI, plasma total adiponectin level was not an independent prognostic predictor, but in patients with normal BMI, plasma levels of log NT-proBNP (P = 0.017) and log total adiponectin (P = 0.003) were independent prognostic predictors. CONCLUSION: These findings indicate that total adiponectin is more useful for assessing mortality risk than HMW adiponectin and a high plasma total adiponectin is an independent prognostic predictor especially in CHF patients with normal BMI.     

Plasma concentrations of a novel, adipose-specific protein, adiponectin, in type 2 diabetic patients

Adiponectin is a novel, adipose-specific protein abundantly present in the circulation, and it has antiatherogenic properties. We analyzed the plasma adiponectin concentrations in age- and body mass index (BMI)-matched nondiabetic and type 2 diabetic subjects with and without coronary artery disease (CAD). Plasma levels of adiponectin in the diabetic subjects without CAD were lower than those in nondiabetic subjects (6.6+/-0.4 versus 7.9+/-0.5 microg/mL in men, 7.6+/-0.7 versus 11.7+/-1.0 microg/mL in women; P<0.001). The plasma adiponectin concentrations of diabetic patients with CAD were lower than those of diabetic patients without CAD (4.0+/-0.4 versus 6.6+/-0.4 microg/mL, P<0.001 in men; 6.3+/-0.8 versus 7.6+/-0. 7 microg/mL in women). In contrast, plasma levels of leptin did not differ between diabetic patients with and without CAD. The presence of microangiopathy did not affect the plasma adiponectin levels in diabetic patients. Significant, univariate, inverse correlations were observed between adiponectin levels and fasting plasma insulin (r=-0.18, P<0.01) and glucose (r=-0.26, P<0.001) levels. In multivariate analysis, plasma insulin did not independently affect the plasma adiponectin levels. BMI, serum triglyceride concentration, and the presence of diabetes or CAD remained significantly related to plasma adiponectin concentrations. Weight reduction significantly elevated plasma adiponectin levels in the diabetic subjects as well as the nondiabetic subjects. These results suggest that the decreased plasma adiponectin concentrations in diabetes may be an indicator of macroangiopathy.     

Three measures of tumor necrosis factor alpha activity and insulin resistance in nonobese Japanese type 2 diabetic patients

The aim of the present study was to investigate the relationship between insulin resistance and tumor necrosis factor alpha (TNF-alpha) as well as soluble TNF receptors (sTNF-R), body mass index (BMI), leptin, adiponectin, and serum lipid profile including triglycerides in nonobese Japanese patients with type 2 diabetes. A total of 88 nonobese Japanese type 2 diabetic patients were studied. The duration of diabetes was 11.0 +/- 0.8 years. In conjunction with BMI, glycosylated hemoglobin (HbA1c), fasting concentrations of plasma glucose, serum lipids (triglycerides, high-density lipoprotein cholesterol, and total cholesterol), serum leptin, serum adiponectin, serum TNF-alpha, and soluble TNF receptors (sTNF-R1 and sTNF-R2) were also measured. Insulin resistance was estimated by the insulin resistance index of homeostasis model assessment. Insulin resistance was positively correlated with BMI, triglycerides, leptin, and total cholesterol and negatively correlated with adiponectin and high-density lipoprotein cholesterol. In contrast, insulin resistance was not associated with TNF-alpha, nor sTNF-R (sTNF-R1 and sTNF-R2) in our diabetic patients. There was no significant relationship between the 3 measures of TNF-alpha system (TNF-alpha, sTNF-R1, and sTNF-R2) and BMI, serum triglycerides, leptin, or adiponectin in these patients. From these results, it can be concluded that peripheral levels of TNF-alpha system activity are not a major factor responsible for insulin resistance in nonobese Japanese type 2 diabetic patients.