血浆C-反应蛋白与肥胖者胰岛素抵抗关系的研究

目的　研究肥胖者中的胰岛素抵抗与C反应蛋白 (CRP)浓度的关系。方法　选择肥胖者及正常对照各10 4例 ,测定血中CRP、胰岛素、血糖、血脂水平 ,肥胖者分为胰岛素抵抗 (IR)组及胰岛素敏感 (IS)组 ,测定两组减轻体重后的上述指标。结果　肥胖组的CRP、胰岛素、甘油三酯、总胆固醇、胰岛素、低密度脂蛋白水平高于对照组 (P <0 .0 1)。肥胖者中 ,IR组CRP、胰岛素水平高于IS组 (P <0 .0 1)。减轻体重后CRP、胰岛素下降 (P <0 .0 1)仅见于IR组。肥胖组 ,仅胰岛素水平与CRP浓度的相关系数有统计学意义 (r =0 .5 6 ,P <0 .0 1)。结论　胰岛素抵抗与CRP浓度有关 ,CRP升高仅见于IR的肥胖者 ,且与随体重下降胰岛素抵抗的改善相平行。     

Early age at menarche is associated with insulin resistance: a systemic review and meta-analysis

Objectives: We aimed to conduct a systemic review and meta-analysis of the relevant studies to further investigate the association between age at menarche and insulin resistance.

Methods: PubMed, EMBASE, and Web of Science (SCI) databases were systemically searched until December 2017. Observational studies comparing the incidences of insulin resistance in patients with early, average, and late menarchal ages were identified. Weighted mean difference (WMD) for HOMA-IR scores and fasting serum insulin levels in early vs late, early vs average. and average vs late comparisons were calculated with a random- or fixed-effects model.

Results: A total of eight articles involving 5504 subjects were finally included. In the analysis of HOMA-IR, the pooled WMDs in five studies were 0.45 (95% confidence interval [CI] 0.31–0.60, p < 0.001), 0.40 (95% CI 0.28–0.52, p < 0.001), and ?0.01 (95% CI ?0.09 to 0.07, p = 0.854) for early vs late, early vs average, and average vs late comparisons, respectively. The fasting serum insulin levels in eight studies were analyzed, and it was significantly higher in subjects with earlier age at menarche (WMD 1.28, 95% CI 0.92–1.63, p < 0.001 for early vs late comparison, WMD 1.28, 95% CI 1.13–1.43, p < 0.001 for early vs average comparison) with mild and acceptable heterogeneity (I² = 42.5% and 7.4%, respectively). Publication bias was not detected via funnel plots and Egger’s tests.

Conclusions: Our study revealed that earlier age at menarche was significantly associated with insulin resistance.

Trial Registration Number: CRD42018083874     

Inflammatory markers in relation to insulin resistance and the metabolic syndrome

Background Inflammation has repeatedly been demonstrated to be associated with the metabolic syndrome (MetS) and insulin resistance, but the relative importance of different aspects of the inflammatory process is largely unexplored. Design We measured circulating interleukins (IL‐1α, IL‐1β, IL‐2, IL‐4, IL‐6, IL‐8, IL‐10); other cytokines (tumour necrosis factor‐α, interferon gamma and monocyte chemotactic protein‐1), cell adhesion molecules [vascular cell adhesion molecule‐1 (VCAM‐1), intercellular adhesion molecule‐1, E‐selectin, P‐selectin, l ‐selectin], and systemic inflammation markers [C‐reactive protein (CRP) and leukocyte count] in 943 70 year old participants (50% women) of the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study. We related these biomarkers to MetS and the homeostasis model assessment insulin resistance index (HOMA‐IR). Results In a multivariable model including all inflammatory markers conjointly together with sex, log VCAM‐1 [odds ratio (OR), 1·45; 95% confidence interval (CI), 1·22–1·72 per 1 SD increase; P < 0·0001], log E‐selectin (OR, 1·33; 95% CI, 1·12–1·57 per 1SD increase; P = 0·001), and log CRP (OR, 1·41; 95% CI, 1·20–1·66 per 1‐SD increase; P < 0·0001) were independently associated with MetS. These biomarkers were also independently associated with HOMA‐IR. Conclusions Among 17 inflammatory biomarkers, most of them previously not examined in relation to MetS and insulin resistance, VCAM‐1, E‐selectin and CRP demonstrated the strongest associations with MetS and insulin resistance in our community based sample of the elderly. The relative importance of these biomarkers in predicting the development of MetS, insulin resistance and cardiovascular disease needs to be further examined in a longitudinal setting.     

Subcutaneous adipose tissue expression of tumour necrosis factor-alpha is not associated with whole body insulin resistance in obese nondiabetic or in type-2 diabetic subjects

BACKGROUND: An association with subcutaneous adipose tissue TNFalpha expression and insulin resistance has been suggested in obesity/type-2 diabetes, but this has not been examined directly. In the first part of the study we investigated whether this association is present in 7 lean, 10 obese nondiabetic and 9 type-2 diabetic men. In the second part of the study we examined the relationship between adipose tissue TNFalpha mRNA levels and BMI in 81 nondiabetic subjects spanning a wide range of BMIs. METHODS: Subcutaneous adipose tissue TNFalpha mRNA levels and insulin sensitivity were determined with quantitative RT-competitive PCR and hyperinsulinaemic clamp, respectively. RESULTS: Subcutaneous adipose tissue TNFalpha mRNA levels were similar in 7 lean and 10 obese nondiabetic and 9 type-2 diabetic men (P = 0.68), and did not change in response to 240-min hyperinsulinaemia. TNFalpha mRNA levels and insulin sensitivity were not correlated. Unexpectedly, no correlation between TNFalpha mRNA and BMI was found. The relationship between adipose tissue TNFalpha mRNA and BMI was examined further in 31 male and 50 female nondiabetic subjects. The subcutaneous adipose tissue TNFalpha mRNA level correlated with BMI in all subjects (rS = 0.32, P < 0.01), and in a subgroup analysis in men (rS = 0.55, P < 0.01) but not in women (rS = - 0.08). The correlation in men was dependent on a fourfold higher TNFalpha mRNA level in 5 morbidly obese men while there was no difference in TNFalpha mRNA levels in lean or obese men. CONCLUSIONS: Subcutaneous adipose tissue TNFalpha expression does not correlate with insulin sensitivity in nondiabetic or type-2 diabetic men; is not regulated by acute hyperinsulinaemia; and is increased only in morbidly obese men.     

脂肪肝与体重、血脂、血糖、胰岛素抵抗的关系

目的　探讨脂肪肝患者糖脂代谢紊乱及脂肪肝与胰岛素抵抗、肿瘤坏死因子 α(TNF α)水平之间的关系。方法　采用对照研究 ,脂肪肝组 3 5例 ,正常对照组 18例 ,检测两组患者血脂、血糖 (空腹和 2小时 )、胰岛素 (空腹和 2小时 )、肿瘤坏死因子 α(TNF α) ,采用稳态模式 (HOMA)评价胰岛素抵抗 ,并根据体重指数 (BMI)将脂肪肝患者分为非肥胖组 (BMI<2 5kg/m2 )和肥胖组 (BMI≥ 2 5kg/m2 ) ,进行分层分析。结果　肥胖与非肥胖脂肪肝组的空腹血糖 (FBG)和餐后 2小时血糖 (BG2h)、2小时胰岛素 (INS2h)、总胆固醇 (TC)、甘油三酯 (TG)、低密度脂蛋白胆固醇(LDL C)、TNF α和胰岛素抵抗指数 (HOMA IR)均高于正常对照组 (均P <0 .0 5 )。脂肪肝肥胖组TG、HOMA IR水平高于非肥胖组 (均P <0 .0 5 )。Logistic回归分析显示 ,BG2h、TC、腰臀比 (WHR)是脂肪肝形成主要的危险因素。多元逐步回归分析结果显示 ,FBG、TG是脂肪肝患者胰岛素抵抗独立的危险因素。结论　脂肪肝患者无论是否肥胖都存在糖脂代谢紊乱、胰岛素抵抗 ,肥胖型脂肪肝患者更严重。降低血脂、减轻体重、减少腹内脂肪堆积对于减少脂肪肝的形成有重要的意义     

On the paradox insulin resistance/insulin hypersensitivity and obesity: two tales of the same history

Insulin resistance (IR) associated with obesity represents a well-known risk factor for chronic disease. IR development may occur to hinder stressful conditions to provide an appropriate energetic supply to non-insulin-sensitive tissues. However, conditions of stress turn out to be ‘maladaptive’ in the long term, leading to chronic diseases. Paradoxically, insulin hypersensitivity and/or hypersecretion causing post-prandial hypoglycemia resulting in increased food intake and weight gain, can represent an event preceding obesity and IR. By performing an OGTT in obese or obese-prone individuals we observed that tardive post-prandial hypoglycemia (3h from glucose load) is not a rare event (32%); in 12% of cases it paralleled with low insulin levels, resulting in the ‘true insulin hypersensitivity’. By using Matsuda-method, we confirmed the presence of insulin hypersensitivity in this group. Therefore the early recognition of this phenomenon could be useful as a predictive biomarker to identify patients prone to develop obesity and obesity related-disorders.     

Increased insulin resistance and fat cell lipolysis in obese but not lean women with a high waist/hip ratio

Increased lipolysis in abdominal adipocytes has been suggested to be of importance for the insulin resistance typical for abdominal obesity. In order to differentiate between fat distribution, measured as waist/hip ratio (WHR), and amount of body fat, glucose disposal during a euglycaemic clamp as well as lipolysis in isolated cells from abdominal and gluteo-femoral regions were studied in 20 obese and 20 lean postmenopausal women with a high (n = 10) and low (n = 10) WHR, respectively. The lipolytic response was increased in cells from obese women irrespective of region. Furthermore, lipolysis was enhanced in abdominal compared with the gluteo-femoral cells in obese women with a high WHR. Fasting blood glucose and insulin were increased in both groups of obese women while the degree of insulin resistance was most pronounced in the obese women with a high WHR. It is concluded that increased body fat is associated with both insulin resistance and increased lipolysis, and that this relationship is stronger in the presence of a high WHR. A high WHR may increase the expression of obesity as a risk for insulin resistance and this may be mediated through an increased lipolytic rate.     

Effect of an acute hyperinsulinaemic clamp on post-prandial lipaemia in subjects with insulin resistance

BACKGROUND: Obese, insulin-resistant individuals have raised levels of intestinal and hepatic lipoproteins. Insulin decreases the production of hepatic lipoproteins in vivo and so this study aimed to investigate whether an acute hyperinsulinaemic, euglycaemic clamp could correct fasting and post-prandial dyslipidaemia. SUBJECTS AND METHODS: In a randomized, cross-over design, post-prandial lipaemia was compared in subjects infused either with insulin to achieve a steady-state concentration of 100 mU L(-1) or with saline. Nine obese (Body Mass Index > 26 kg m(-2); waist : hip > 1.0) insulin-resistant (Homeostatic Model Assessment score > 2.0) male subjects were given an oral fat load 3 h after the infusions began, and sampling continued for 6 h. Plasma apoB-48, triglyceride and nonesterified fatty acid (NEFA) were measured hourly. RESULTS: Average steady-state serum insulin levels during the hyperinsulinaemic clamp were 123 +/- 4.4 mU L(-1). A paired analysis showed no net effect of insulin on post-prandial chylomicron metabolism when calculated as the (apoB-48) incremental area under the curve (IAUC). However, there was a trend towards a delay in the apoB-48 peak, consistent with possible changes in the rates of chylomicron biogenesis, lipolysis and/or clearance. Similarly, post-prandial lipaemia (depicted as triglyceride IAUC) was similar for subjects infused with insulin or saline, but the peak post-prandial response was delayed during insulin infusion. The NEFA were rapidly decreased by 83% after 3 h of insulin infusion. CONCLUSIONS: In obesity and insulin resistance, short-term changes in plasma insulin do not appreciably exert a regulatory effect on exogenously-derived post-prandial lipoproteins. The data suggest that hyperchylomicronaemia in insulin-resistant subjects is a result of chronic aberrations in insulin-mediated regulation of post-prandial lipid metabolism.     

Associations of resistin with inflammation and insulin resistance in patients with type 2 diabetes mellitus

Objective. Resistin has been linked to obesity, type 2 diabetes, inflammation and atherosclerosis but the results of animal and human studies have been at variance. The purpose of this study was to investigate the potential roles of resistin in patients with type 2 diabetes and to evaluate the correlation between resistin and markers of obesity, inflammation, insulin resistance, metabolic parameters, diabetes control and complications. Material and methods. Fasting resistin, leptin, insulin, glucose, HbA1c, full lipid profile, C‐reactive protein (CRP) (high sensitivity assay) and complete blood count were determined in 135 patients with type 2 diabetes. Univariate regression and multivariate logistic regression analyses were used to relate resistin with indices of obesity, inflammation, insulin resistance (homeostasis model, HOMA), insulin sensitivity, diabetic control, coronary heart disease (CHD) and degree of microalbuminuria. Results. Resistin showed significant (p<0.05) correlations with body mass index (BMI) "(Spearman r = 0.67), waist circumference (r = 0.54), fasting insulin (0.51), insulin sensitivity (r = ?0.29), HOMA (r = 0.30), leptin (r = 0.39), CRP (r = 0.29), white cell count (r = 0.25) and lipid parameters but showed no significant correlation with glucose and HbA1c. Partial correlation analysis, with correction for BMI, abolished the correlation of resistin with insulin sensitivity and HOMA but not with the white cell count. When confounding factors were fixed using multiple logistic regression, resistin was not independently associated with CHD (odds ratio = 1.05, p = 0.08) and degree of microalbuminuria (odds ratio = 1.06, p = 0.24). Conclusions. Resistin showed significant BMI‐dependent associations with insulin resistance and factors linked with obesity and inflammation in patients with type 2 diabetes. Resistin may represent a link between obesity and insulin resistance via pro‐inflammatory pathways.     

多囊卵巢综合征的胰岛素抵抗特征及相关因素分析

目的探讨多囊卵巢综合征与胰岛素抵抗的特点及其相关影响。方法对48名多囊卵巢综合征患者与20名健康女性进行比较研究。按体重指数分为Ⅰ组（正常非肥胖组）．Ⅱ组（正常肥胖组）,Ⅲ组（综合征非肥胖组）,Ⅳ组（综合征肥胖组）。比较体重指数、腰臀围比、OGTT试验及胰岛素释放。血脂、血压、肝功、肾功、稳态模型胰岛素抵抗指数。结果空腹胰岛紊值、稳态模型胰岛素抵抗指数Ⅲ组与Ⅰ、Ⅳ组。Ⅳ组与Ⅱ组间比较差异均有显著性（P〈0．05）;空腹血糖、收缩压、TG、TC值Ⅲ组与Ⅳ组间比较差异有显著性（P〈0．05）;LDL、HDL值各组间比较差异均无显著性（P〉0．05）。稳态模型胰岛素抵抗指数与体重指数、腰臀围比、空腹胰岛素值均呈显著正相关（P〈0．01）。结论胰岛紊抵抗是多囊卵巢综合征患者代谢异常的基本特征,肥胖是引起胰岛素抵抗、多囊卵巢综合征的危险因素之一。     

Central obesity and hyperinsulinaemia in women are associated with polymorphism in the 5'' flanking region of the human insulin gene

Obesity is a multifactorial disease with a marked genetic component. The situation is further complicated by the heterogeneity of obesity demonstrated by the topographical distribution of body fat, e.g. upper body (central) and lower body (gluteal) obesity. Furthermore, the distribution of fat shows a stronger heritable tendency compared with total body fat. Central obesity is characterized by hyperinsulinaemia and insulin resistance, a feature in common with non-insulin dependent diabetes mellitus, hypertension and atherosclerosis. In order to study the molecular genetics of central obesity we have examined 56 severely obese (mean body mass index 40), unrelated British Caucasoid young non-diabetic women for associations of restriction fragment length polymorphism of candidate genes with anthropometric measurements and indices of insulin secretion and resistance. The candidate genes examined were insulin receptor, insulin sensitive glucose transporter and insulin. An association of the class 3 allele of the hypervariable region in the 5' flanking region of the insulin gene was found with upper segment obesity (P = 0.005). Furthermore, the class 3 allele was also associated with fasting hyperinsulinaemia (P = 0.01), stimulated insulin secretion (P = 0.01) and insulin resistance as calculated from the homeostatic model of assessment (HOMA; P = 0.008). No such associations were found with the other candidate genes studied. This data suggests that polymorphisms in the 5' flanking region of the insulin gene may affect expression of the gene and thereby modulate insulin production in severely obese female subjects.     

Acute insulin administration does not affect plasma leptin levels in lean or obese subjects

Abstract. Whether leptin levels are related to insulin sensitivity or subject to acute regulation by insulin is not known. In 12 obese [body mass index (BMI) = 34.0 ±1.5 kg m^-2] and 12 lean (BMI = 22.2 ±0.6 kg m^-2) non-diabetic subjects, plasma leptin concentrations were measured in the fasting state and during 2 hours of euglycaemic hyperinsulinaemia (˜600 pmol L^-2). Fasting plasma leptin was significantly higher in obese (26.6 ±3.2) than in lean subjects (6.4 ±1.2 ng mL^-1, P = 0.0001), and in women (21.1 ±3.3) than in men (7.3 = 2.3 ng mL^-1, P = 0.01). In univariate analysis, fasting plasma leptin was strongly related to all anthropometric measures (body weight, fat mass, percent fat mass, waist and hip circumferences). In multiple regression, per cent adiposity, hip circumference and duration of obesity explained 90% of the variability in fasting leptin concentrations. Fasting and stimulated (OGTT) insulin levels, insulin sensitivity (22.6 ±1.9 vs 36.7 ±2.0 μmol min^-1 kg^-1 in lean and obese subjects, respectively, P < 0.0001), glucose area, and serum triglycerides were positively related to fasting plasma leptin concentrations; none of these associations, however, was statistically significant after adjusting for BMI. During the clamp, plasma leptin concentrations remained constant in both lean and obese subjects. We conclude that neither insulin levels nor sensitivity relate to leptin levels independently of fat mass, and that leptin is not subject to acute (2 hours) regulation by insulin in lean or obese humans.     

Effects of renal denervation on insulin resistance

Hypertension and diabetes are recognized as two major comorbidities accounting for the greatest proportion of cardiovascular morbidity and mortality. Despite the availability of safe and effective pharmacological therapies, the percentage of patients achieving optimal blood pressure and glycemic control remains unsatisfactory. The contribution of sympathetic activation to the development and maintenance of systemic hypertension and comorbidities is well recognized. Aside from several novel pharmacological approaches, catheter-based sympathetic renal denervation (RDN) has gained a significant role in treatment-resistant hypertension and has recently been introduced to clinical practice. Preliminary data indicate that aside from better blood pressure control, RDN may also be associated with a reduction in fasting glucose and insulin levels, as well as improvements in the Homeostasis Model Assessment (HOMA) index. If these observations are confirmed in larger controlled clinical trials, RDN may emerge as a preferred treatment option for patients with resistant hypertension and concomitant alterations of glucose metabolism.     

Plasma plasminogen activator inhibitor 1, insulin resistance and android obesity

Plasma plasminogen activator inhibitor 1 (PAI-1) levels are elevated in insulin-resistant subjects and are associated with increased cardiovascular risk of atherothrombosis. Strong association between PAI-1 and the metabolic components of the insulin resistance syndrome is found in clinical studies, suggesting that insulin resistance may regulate circulating PAI-1. However, the mechanisms underlying increased PAI-1 levels in such conditions are still poorly understood. Several studies have been carried out specifically in patients with central or android obesity, a major characteristic of the insulin resistance syndrome, and have suggested that visceral adipose tissue may be the major component of the relationship between android obesity and PAI-1. Accordingly, adipose tissue PAI-1 production was found to be elevated in obese human subjects, particularly in visceral adipose tissue. The genetic background for having high PAI-1 levels in several populations have been looked for and its role appeared to be weaker than that of the metabolic condition. High plasma PAI-1 levels are then clearly related to android obesity and insulin resistance, but the mechanisms whereby PAI-1 increases in plasma in these diseases remain to be determined.     

单纯性肥胖成人血清高敏C反应蛋白、血脂水平与胰岛素抵抗的相关性研究

目的 探讨单纯性肥胖成人血清高敏C反应蛋白(hs-CRP)、血脂水平与胰岛素抵抗(IR)的关系.方法 选择单纯性肥胖成人99例[按体质量指数(BMI)分为i度肥胖组46例,ii度肥胖组38例,iii度肥胖组15例],单纯性超重成人56例及健康成人80例.测定所有入选对象的身高、体质量、腰围、臀围、空腹血糖(FBG)、空腹胰岛素(FIN)、血脂、hs-CRP水平,并计算胰岛素抵抗指数(HOMA-IR)、BMI及腰臀比(WHR).结果 hs-CRP、HOMA-IR、FBG、FIN、TG、TC、LDL-C、脂肪肝发生率随着BMI的升高呈逐渐升高趋势,HDL-C则呈现逐渐降低趋势.血清hs-CRP与BMI、WHR、FIN、HOMA-IR、TG呈显著正相关(P＜0.05～P<0.01),与HDL-C呈显著负相关(P<0.01),多元逐步回归分析提示,BMI、HOMA-IR、HDL-C是影响hs-CRP的独立危险因素.结论 单纯性肥胖成人存在IR,炎性因子hs-CRP的过量表达参与并加重单纯性肥胖成人IR、血脂紊乱的发生和发展.     

胰岛素抵抗病人的健康教育指导

探讨了胰岛素抵抗的机制、胰岛素抵抗的临床意义。从饮食、运动、体重控制等方面阐述了胰岛素抵抗病人的健康教育内容。     

Gene polymorphisms of insulin secretion signaling pathway associated with clopidogrel resistance in Han Chinese population

BackgroundDue to the loss of responsiveness to insulin, diabetes mellitus (DM) patients develop increased platelet reactivity and reduced response to antiplatelet agents. Nevertheless, the relationship between the single‐nucleotide polymorphisms (SNP) of the signal pathway gene of insulin secretion and the effect of clopidogrel is elusive.MethodsBlood samples were collected from patients administered with dual‐antiplatelet therapy (clopidogrel, 75 mg, once daily and aspirin, 100 mg, once daily) after 5 days and completed test within 4 h. The VerifyNow P2Y12 assay was used to measure the platelet functions, and the results were expressed as a P2Y12 reaction unit (PRU). Notably, the selected SNPs were analyzed to demonstrate the functionality of genetic variants.ResultsAnalysis of the study population showed that old age, lower plasma albumin (ALB) level, higher creatinine (CREA) level, higher uric acid (UA) level, lower platelet (PLT) count, and lower plateletcrit (PCT) potentially increased the risk of clopidogrel resistance. In a single‐nucleotide polymorphism rs6056209 of the PCLB1 gene, the AG genotype was a risk factor for clopidogrel resistance (p < 0.05, OR = 1.574). Similarly, the CC and AG genotype in GNAS rs7121 and CCKAR rs1800857 were protective factors (p < 0.05, OR = 0.094; p <0.05, OR = 0.491). TT was a protective factor in rs10814274 of the CREB3 gene (p < 0.05, OR = 0.444). In the RAPGEF4 gene polymorphism rs17746510, TG was the protective genotype, and the TT genotype was a risk factor for clopidogrel resistance. GCG rs5645 was confirmed; there was a relationship between genotypes containing A or G and clopidogrel resistance.ConclusionSingle‐nucleotide polymorphisms of insulin secretion signaling pathway genes trigger clopidogrel resistance.     

Smoking is associated with insulin resistance and cardiovascular autonomic dysfunction in type 2 diabetic patients

BACKGROUND: Smoking and cardiovascular autonomic dysfunction are associated with high mortality in type 2 diabetic patients. This study tested the hypothesis that smoking is associated with insulin resistance/hyperinsulinaemia and cardiovascular autonomic dysfunction in type 2 diabetic patients who are not treated with insulin. MATERIALS AND METHODS: The study patients were 22 current smokers with type 2 diabetes mellitus (age: 57 +/- 5 years, mean +/- SD) and 30 age-matched never-smoked patients with type 2 diabetes mellitus (control group, 57 +/- 8 years). The quality of blood glucose was assessed by fasting plasma glucose (FPG), fasting immunoreactive insulin (F-IRI), homeostasis model assessment (HOMA) index and haemoglobin A1c (HbA1c). The severity of smoking status was expressed by the Brinkman index, which is calculated as number of cigarettes per day multiplied by years of smoking. Cardiovascular autonomic function was assessed by baroreflex sensitivity (BRS), heart-rate variability, plasma norepinephrine concentration and cardiac (123)I-metaiodobenzylguanidine (MIBG) scintigraphic findings. RESULTS: Baroreflex sensitivity was lower in the current smokers group than in the never-smoked group (P < 0.05). Early and delayed (123)I-MIBG myocardial uptake values were lower (P < 0.05, and P < 0.01, respectively) and the percentage washout-rate of (123)I-MIBG was higher (P < 0.0001) in the current smokers group than in the never-smoked group. Fasting immunoreactive insulin (F-IRI) concentration (P < 0.0001) and the homeostasis model assessment (HOMA) index (P < 0.0001) were higher in the current smokers group than the never-smoked group. Multiple logistic regression analysis revealed that smoking was independently predicted by F-IRI and the percentage washout-rate of (123)I-MIBG. CONCLUSIONS: The results of the study suggested that smoking was associated with cardiovascular autonomic dysfunction and hyperinsulinaemia and that F-IRI and the percentage washout-rate of (123)I-MIBG were independent predictors of smoking in these Japanese patients with type 2 diabetes mellitus.     

严重脓毒症患者胰岛素抵抗和胰岛素分泌功能的观察

目的探讨严重脓毒症患者入ICU后血糖、胰岛素浓度、胰岛素抵抗（IR）及胰岛素分泌功能的动态变化．与疾病的严重程度和预后的关系。方法选取严重脓毒症患者36例和正常对照20例,根据脓毒症后28d后的存活情况,分为生存组（n=20例）和死亡组（n=16）。回顾分析各组第1天、第28天空腹血糖（FBG）、胰岛素（FINS）浓度,使用稳态模式法（HOMA）计算胰岛素抵抗指数（HOMA—IR）及胰岛素分泌指数（HOMA-8）。结果严重脓毒症患者入组后第1天FBG、FINS浓度及HOMA—IR均明显高于对照组,HOMA—β明显低于对照组,差异均有统计学意义（t分别=7．46、5．64、7．07、6．73,P均〈0．05）。生存组与死亡组入组后第1天FBG、FINS浓度及HOMA—IR均高于对照组,而HOMA—β低于对照组,差异有统计学意义（t分别=5．13、4．43、5．49、4．70、6．85、3．60、5．02、8．96,P均〈0．05）;生存组第28天FBG、FINS浓度及HOMA—IR较第1天下降,而HOMA-β回升,差异均有统计学意义（t分别=3．71、2．72、4．06、2．47,P均〈0．05）;死亡组FBG和HOMA-IR高于生存组,HOMA—β低于生存组,差异有统计学意义（t分别=3．46、2．82、2．97,P均〈0．05）;而FINS浓度与生存组间差异无统计学意义（t=0．32,P〉0．05）。单个脏器功能不全患者FBG浓度、HOMA-β与对照组间比较,差异均无统计学意义（q分别=1．95、1．66,P均〉0．05）;多个脏器功能不全患者FBG、FINS浓度及HOMA—IR均高于对照组;而HOMA—β低于对照组,差异均有统计学意义（q分别=10．18、5．19、7．58、14．96,P均〈0．05）。APACHEⅡ评分与FBG、HOMA—IR呈正相关,与HOMA—β呈负相关,差异均有统计学意义（r分别=0．68、0．50、-0．66,P均〈0．05）。结论严重脓毒症患者存在IR,其中多脏器功能不全患者存在胰岛β细胞功能不全,FBG浓度、HOMA—IR及HOMA—β可作为判断严重脓毒症患者病情转归,预后的预警指标。