急性脑梗死患者血清脂联素及抵抗素检测分析

目的探讨血清脂联素与抵抗素检测在急性脑梗死中的应用价值。方法选取郑州市第三人民医院神经内科及郑州大学第二附属医院ICU 2010-10—2012-06收治的急性脑梗死患者137例作为观察组,按照梗死体积分为小、中、大3个梗死组别,按照神经功能缺损程度分为轻、中、重3个组别,使用ELISA法检测患者的血清脂联素和抵抗素水平,并以50例健康人为对照组进行比较。结果观察组血清脂联素均明显低于对照组,观察组抵抗素均明显高于对照组。梗死体积越大、神经功能缺损程度越严重,血清脂联素越低,抵抗素越高(P<0.05)。血清脂联素与抵抗素呈明显负相关(r=-0.782,P<0.01)。结论血清脂联素和抵抗素与急性脑梗死病变程度密切相关。血清脂联素与抵抗素检测对改善患者预后有重要的指导意义。     

急性脑梗死患者颈动脉内-中膜与炎症因子IL-18和脂联素的关系分析

目的 通过研究颈动脉内-中膜厚度(IMT)与血清细胞因子白介素(IL-18)、脂联素的水平的关系,探讨IMT增厚的机制.方法 选择64例急性脑梗死(ACI)患者和30名健康志愿者作为研究对象,并分为IMT＜1.0 mm亚组和IMT ＞1.0 mm亚组.酶联免疫吸附法(ELISA法)测定血清IL-18、脂联素水平,分析IMT与IL-18、脂联素的相关性.结果 脑梗死组IMT≥1.0 mm者IMT与IL-18水平呈正相关(r=0.543,P＜0.01),与脂联素呈负相关(r=-0.594,P＜0.01).IMT＜1.0 mm者IMT与血清脂联素、IL-18水平无明显相关性(r=0.241、0.191,P均＞0.05).结论 脑梗死颈动脉IMT＞1.0 mm者血清IL-18水平升高,脂联素水平降低,动脉内膜增厚可能与IL-18和脂联素的比例失调有关.     

非典型抗精神病药致糖脂代谢紊乱与血抵抗素和脂联素水平的相关研究

目的观测非典型抗精神病药物对精神分裂症患者血糖、血脂及血清抵抗素和脂联素水平的影响。方法纳入76例精神分裂症患者和30名正常对照,患者组分为奥氮平组(20例)、喹硫平组(31例)和利培酮组(25例),给予相应药物治疗6周,治疗前后测量体重,并检测空腹血糖、血清甘油三酯、总胆固醇、高密度脂蛋白及血清抵抗素和脂联素水平。结果①总的患者组体重、胆固醇、甘油三脂、脂联素、抵抗素水平在治疗后显著升高(P<0.05);②奥氮平组治疗前后体重变化较利培酮组明显,差异具有统计学意义(P<0.05),而与喹硫平组差异无统计学意义(P>0.05)。空腹血糖、血脂、血抵抗素和脂联素变化值在3组间均无明显差异(P>0.05);③治疗后体重增加>7%和<7%的两组患者比较,组间治疗前甘油三酯及抵抗素变化值的差异有统计学意义(P<0.05)。④治疗后甘油三酯异常组和正常组间治疗后体重、治疗前胆固醇和治疗后脂联素水平的差异具有统计学意义(P<0.05);⑤治疗后甘油三酯与胆固醇(r=0.39,P=0.01)和抵抗素(r=0.42,P=0.02)正相关,而与脂联素负相关(r=-0.51,P=0.002)。抵抗素和脂联素水平呈负相关(r=-0.35,P=0.03)。结论非典型抗精神病药治疗可导致体重增加和脂代谢紊乱,而脂联素和抵抗素的升高可能参与药源性体重增加和脂代谢紊乱。     

拉莫三嗪对成年癫患者血清中瘦素、抵抗素和脂联素水平的影响

目的探讨抗癫新药拉莫三嗪对成年癫患者血清瘦素、抵抗素、脂联素水平的影响。方法对30名女性健康查体人员和60例首发癫全面性强直-阵挛发作女性患者随机分为拉莫三嗪组和丙戊酸钠组,在治疗前和治疗后分别进行血清瘦素、抵抗素和脂联素水平测定,并测量腰臀比(帆)、体重指数(BMI)。结果拉莫三嗪治疗后、对照组BMI、WHR及血清瘦素、抵抗素、脂联素水平间均无明显差异,而丙戊酸钠治疗后血清瘦素、抵抗素水平明显升高,脂联素水平明显降低(P<0.01)。结论拉莫三嗪治疗不引起癫患者体重增加,瘦素、脂联素、抵抗素水平可能是肥胖发生的预测指标。     

原发性高血压与血清抵抗素、脂联素水平的关系

目的 探讨原发性高血压患者中抵抗素和脂联素水平.方法 正常对照组38例和原发性高血压患者46例常规抽取空腹静脉血检测其血糖、血脂、空腹胰岛素、脂联素、抵抗素.结果 与正常对照组相比,原发性高血压患者,抵抗素水平升高(P<0. 05),脂联素水平下降(P<0. 01).结论 在原发性高血压患者中,抵抗素水平升高,而脂联素水平下降.     

多种脂肪细胞因子与脑梗死患者颈动脉粥样硬化斑块稳定性的关系

目的探讨多种脂肪细胞因子与急性脑梗死(ACI)患者颈动脉粥样硬化斑块稳定性的关系。方法根据颈动脉彩色多普勒超声仪检查结果,将113例ACI患者分为无斑块组、稳定斑块组和不稳定斑块组;采取酶联免疫法检测ACI患者发病<48h和14d时以及31名健康对照者的血清脂联素、抵抗素、内脏脂肪素、白介素-6(LI-6)和白介素-8(LI-8)的水平。结果 (1)ACI患者发病<48h和14d时血清内脏脂肪素、抵抗素、LI-6、LI-8水平明显高于对照组,脂联素水平明显低于对照组。与发病<48h相比,ACI患者发病14d时血清内脏脂肪素、抵抗素、LI-6、LI-8水平明显升高,脂联素水平明显降低。(2)不稳定斑块组血清内脏脂肪素、抵抗素、LI-6、LI-8水平高于稳定斑块组和无斑块组,脂联素水平明显低于稳定斑块组和无斑块组。(3)血清内脏脂肪素、抵抗素、LI-6、LI-8水平与颈动脉斑块不稳定性呈正相关,而血清脂联素水平与颈动脉斑块不稳定性呈负相关。结论血清脂肪细胞因子内脏脂肪素、抵抗素、LI-6、LI-8水平升高和脂联素水平降低与脑梗死患者颈动脉粥样硬化斑块的不稳定显著相关,有望成为评价斑块稳定性及预测脑梗死发生的理想生化指标。     

转化生长因子β1与骨生化指标和骨密度的关系

背景： 转化生长因子β1是一种重要的调节骨构塑的细胞因子,其是否能作为反应骨转换的敏感因子尚不清楚。 目的：探讨转化生长因子β1与骨形成、骨吸收指标,以及腰椎正位骨密度间的关系。 方法：实验共纳入来自长沙的健康妇女663名,年龄20~80岁。采用ELISA法测定空腹血清转化生长因子β1、骨特异性碱性磷酸酶和Ⅰ型胶原羧基末端肽的水平,同时应用双能X射线骨密度仪测定腰椎正位的骨密度。并分析转化生长因子β1与其他各指标的相关性。 结果与结论：检测结果显示30~39岁,40~49岁年龄段妇女的血清转化生长因子β1水平最高,转化生长因子β1水平与年龄呈负相关,与体质量指数无相关。校正体质量指数后发现,转化生长因子β1与骨特异性碱性磷酸酶和Ⅰ型胶原羧基末端肽负相关,校正体质量指数和年龄后血清转化生长因子β1水平与腰椎正位骨密度正相关。说明转化生长因子β1能动态地反映骨转换情况。     

慢性酒精中毒患者血清脂联素、叶酸、维生素B12含量测定及其临床意义

目的:探讨慢性酒精中毒患者血清脂联素( APN)、叶酸(FA)、维生素B12水平的变化及其与甘油三酯、胆固醇、HDL-C、LDL-C、空腹血糖、谷草转氨酶、谷丙转氨酶等指标的相关性,进一步探讨慢性酒精中毒与脑血管疾病及其高危因素的关系,为临床预防和治疗慢性酒精中毒患者、观察其预后均有重要的临床价值。方法:慢性酒精中毒患者54例,年龄37 ～68岁,平均48.42±6.39岁。饮酒年限为5～42年,纳入标准符合《中国精神障碍分类与诊断标准-CCMD3》;正常对照组43例,年龄24 ～ 59岁,平均32.60±7.00岁。采用ELISA法测定血清中脂联素水平;用化学发光法测定叶酸和B12水平,同时测定空腹血糖、甘油三酯、胆固醇、HDL-C、LDL-C、谷草转氨酶、谷丙转氨酶等相关指标的水平,研究它们与血清脂联素、叶酸、B12的关系。结果:(1)脂联素(mg/L)：对照组平均水平为2.05±1.10(mg/L);酒精组脂联素平均水平为1.5±0.57(mg/L)。Pearson相关分析表明：脂联素与空腹血糖呈负相关;与叶酸、B12、甘油三酯、胆固醇、HDL-C、LDL-C无明显相关性。(2)叶酸(ng/ml)：对照组为7.33±2.4;酒精组为3.63±1.97。Pearson相关分析表明：叶酸与B12、甘油三酯、HDL-C呈负相关;与脂联素、胆固醇、空腹血糖、LDL-C无明显相关性。(3) B12(pg/ml)：对照组403.4±116. 17;酒精组497.57±289.57。Pearson相关分析表明：与叶酸呈负相关;与HDL-C呈正相关;与脂联索、胆固醇、LDL-C、空腹血糖无明显相关性。结论:(1)长期饮酒可降低血清APN水平,且血清APN水平与血糖呈负相关。随着饮酒年限的增加,未发现血清APN随之降低的规律性。(2)长期饮酒可引起血清FA水平降低,并且随着饮酒年限的逐年增加,叶酸FA降低越明显。     

药源性肥胖患者血清瘦素和脂联素水平检测

目的:探讨抗精神病药药源性肥胖患者血清瘦素和脂联素的水平及相关性.方法:选择21例药源性肥胖的住院患者(A组),20例首发精神分裂症患者(B组),20名健康体检人员作为对照组(C组),采用放射免疫法检测各组血清瘦素和脂联素水平,并分析各组血清瘦素及脂联素与体质量指数(BMI)相关性.结果:A组血清瘦素水平(13.3±8...     

重度子痫前期合并脑出血患者血清瘦素脂联素和抵抗素变化特点

目的：探索分析重度子痫前期合并脑出血患者血清瘦素、脂联素和抵抗素变化特点。方法选择48例重度子痫前期患者为研究对象,依据是否合并脑出血进行分组,分为重度子痫前期合并脑出血组（n＝16）和单纯重度子痫前期组（n＝32）,同期选择32例健康孕妇作为阴性对照。留取空腹静脉血,检测血清瘦素、脂联素及抵抗素水平变化。结果子痫前期合并脑出血组患者收缩压、舒张压、24h尿蛋白水平显著高于单纯子痫前期组患者,分别为170.03±12.03vs164.87±11.96mmHg、113.52±10.03vs108.79±9.23mmHg、4.08±1.46vs2.37±1.03g,均有P＜0.001;而血小板计数显著低于单纯子痫前期组（P＜0.001）。子痫前期合并脑出血组孕妇血清瘦素和抵抗素水平分别为90.26±7.34ng/L、28.10±4.89ug/L,显著高于对照组和单纯子痫前期组,而血清脂联素水平显著低于单纯子痫前期组（4.57±2.03vs7.42±2.68;P＜0.001）。结论重度子痫前期患者血清瘦素和抵抗素水平降低,脂联素升高,合并脑出血后这种变化更显著。     

Relationships between plasma adiponectin and blood cells, hepatopancreatic enzymes in women

Adiponectin, which is secreted specifically from adipocyte, is thought to play a key role in the metabolic syndrome. We studied the associations of plasma adiponectin concentrations with blood cells and hepatopancreatic enzymes in 339 women aged 54.0 +/- 0.8 (mean +/- SE) years. Plasma adiponectin before and after adjustment for body composition or calculated insulin resistance increased in slight anemic women (372.6 +/- 2.6 x 10(4)/mm3) compared with non-anemic subjects (471.1 +/- 1.7) (all p < 0.0001), and were inversely associated with red blood cells (RBC), hemoglobin, hematocrit, white blood cells and platelet values (p < 0.0001-0.02), independent of age, diastolic blood pressure, body mass index, serum triglyceride, insulin resistance or blood urea nitrogen. Age and adiponectin/body fat mass (%) were negative, and blood pressure and insulin resistance were positive significant independent determinants of RBC in step-wise regression analysis. Moreover, adiponectin before and after adjustment were inversely associated with serum ALAT, gammaGTP and ChE, and positively with amylase levels (p < 0.0001-0.02). These results indicate the possibility that increased adiponectin may contribute to the suppressive bone marrow function in vivo. Combined with the leptin's data, adipocyte derived proteins were related to the hematopoiesis, therefore it has shown the possible existence of adipose tissue/ bone marrow function linkage more clearly. Furthermore, hepatopancreatic enzyme associations with this protein may indicate the possibility that adiponectin will regulate the hepatopancreatic function in health and disease.     

Levels of the adipocyte-derived plasma protein, adiponectin, have a close relationship with atheroma

INTRODUCTION: Inflammation is a key process in atherosclerotic formation. Structural changes in the carotid arterial wall including detection of focal plaques are measured as the intima-media thickness (IMT) providing an index of atheroma. Coronary arterial plaques may be considered as vascular structural changes. Distensibility of the arteries can be assessed by functional changes in pulse wave velocity (PWV) providing an index of sclerosis. Adiponectin has potential antiatherosclerotic properties. We hypothesized that adiponectin was associated with atherosclerotic vascular changes involved in inflammation. MATERIALS AND METHODS: We enrolled 142 patients with coronary artery disease (CAD) and 108 control patients, matched for age, sex, and body mass index (BMI) with CAD patients. We investigated the relationship between adiponectin, C-reactive protein (CRP), and atherosclerotic vascular changes. RESULTS: CRP (p=0.0009), high-density lipoprotein cholesterol (HDL-C; p=0.02), and IMTmax (p=0.02) were determinants of adiponectin independent of glucose intolerance (p=0.0001), BMI (p=0.002), and CAD (p=0.03), all of which have been significantly associated with adiponectin (r=0.38). Adiponectin was not correlated with PWV. CRP, glucose intolerance, and HDL-C that correlated with adiponectin were inversely correlated with IMTmax and CAD. CRP was negatively correlated with HDL-C (r=-0.24, p=0.0002) and positively correlated with glucose intolerance (r=0.15, p=0.01). CONCLUSIONS: Adiponectin has a close relationship with CRP, IMTmax, CAD, HDL-C, and other established risk factors. CRP, glucose intolerance, and HDL-C are common mediators between adiponectin and atheromatous vascular changes, which are contrary to each other. The exacerbation of atherogenesis may be involved in a decrease of adiponectin through abnormal glyco- and lipid-metabolism by promoting inflammation.     

Resistin and adiponectin in major depression: the association with free cortisol and effects of antidepressant treatment

Major depression is associated with an increased risk for myocardial infarction. Adipokines have been shown to link obesity with metabolic disturbances. Based on this finding the present study was designed to investigate the effect of antidepressive treatment with either amitriptyline or paroxetine on circulating concentrations of resistin and adiponectin in depressed patients, and to establish, whether these adipokines are associated with the activation of the hypothalamic-pituitary-adrenal (HPA)-system. Thirty-seven depressed in-patients were treated in a double-blind, randomized protocol with either amitriptyline or paroxetine over a period of five weeks. After six drug free days blood was drawn on day 1 and again 36 days after antidepressive treatment for the measurement of resistin and adiponectin, fasting glucose and insulin concentrations. For quantification of free cortisol levels saliva was obtained daily at 0800 hours during weeks 1 and 5. While resistin concentrations decreased in patients remitting under amitriptyline and paroxetine (p<0.03), no changes were observed in non-remitters. At baseline, though not during treatment, circulating resistin concentrations correlated positively with free cortisol levels and with BMI (p<0.01). Adiponectin levels, however, did not change during treatment and were not associated with free cortisol concentrations but were instead positively related to QUICKI (p<0.03). In conclusion, the present data revealed resistin but not adiponectin to be related to free cortisol concentrations and to decline in remitters to antidepressive treatment.     

Gender differences in association of plasma adiponectin with obesity reflect resultant insulin resistance in non-diabetic Japanese patients with schizophrenia

Adipose tissues poorly produce adiponectin in the population with increased body fat mass and diabetes mellitus. It was investigated whether hypoadiponectinemia is associated with obesity and insulin resistance in patients with chronically medicated schizophrenia. A cross-sectional study was designed for 73 non-diabetic Japanese patients with schizophrenia. The patients aged <70 years with body mass index (BMI) > or =18.5 were selected. Anthropometrics and blood parameters including fat-derived cytokines were measured, and then the BMI and homeostasis model assessment-insulin resistance (HOMA-IR) was calculated. The variables were compared between the non-obesity (BMI, 18.5-24.9) and obesity (> or = 25.0) groups, and between genders. Plasma adiponectin negatively correlated with BMI (r = -0.554, P < 0.0003) and HOMA-IR (r = -0.380, P = 0.007) in men, but not in women. The obesity group in men, as compared with the non-obesity group, showed significantly lower plasma adiponectin (P = 0.008) and higher HOMA-IR (P < 0.05), but not in women. Plasma leptin showed a significant positive correlation with BMI (r = 0.604, P < 0.0001 in men; r = 0.763, P < 0.0001 in women) and HOMA-IR (r = 0.618, P < 0.0001 in men; r = 0.679, P < 0.0001 in women). The mean plasma leptin in the obesity group was significantly higher than that in the non-obesity group (P < 0.01 in men; P < 0.01 in women). In contrast to plasma leptin, plasma adiponectin showed gender difference in relation to BMI and HOMA-IR.     

Long-term central infusion of adiponectin improves energy and glucose homeostasis by decreasing fat storage and suppressing hepatic gluconeogenesis without changing food intake

Adiponectin is known to be an anti-diabetic adipocytokine. However, the action mechanism by which it produces this effect remains controversial. In the present study, we investigated the long-term central effect of adiponectin on energy homeostasis, peripheral insulin resistance, β-cell function and mass in rats and aimed to determine the mechanism by which its effect was achieved. Intracerebroventricular infusion of adiponectin (50 ng/h) and artificial cerebrospinal fluid (CSF) was conducted by means of an osmotic pump for 4 weeks on nondiabetic rats and 90% pancreatectomised diabetic rats that were both fed 45% energy fat diets. After 4-weeks of treatment, i.c.v. adiponectin improved hypothalamic insulin/leptin signalling in nondiabetic and diabetic rats compared to i.c.v. CSF but it did not change the phosphorylation of AMP kinase (AMPK) in the hypothalamus. Adiponectin infusion decreased epididymal fats, representing visceral fat, by increasing energy expenditure and fat oxidation. During the euglycaemic hyperinsulinaemic clamp, i.c.v. adiponectin improved whole body insulin sensitivity and decreased hepatic glucose output in the hyperinsulinaemic state by attenuating hepatic insulin resistance. Central infusion of adiponectin did not modulate glucose-stimulated insulin secretion during the hyperglycaemic clamp compared to i.c.v. CSF infusion but it enhanced insulin sensitivity at a hyperglycaemic state. Although there were no changes in insulin secretion capacity, central adiponectin increased pancreatic β-cell mass in nondiabetic and diabetic rats as a result of decreasing β-cell death. In conclusion, long-term central infusion of adiponectin enhanced energy homeostasis by increasing energy expenditure via activating hypothalamic leptin and insulin signalling pathways but without potentiating AMPK signalling; it also improved glucose homeostasis by attenuating insulin resistance.     

Effects of major adipokines and the −420 C > G resistin gene polymorphism on the long-term outcome of patients with acute ischemic stroke

Abstract

Aim: The association between adiponectin, leptin, and resistin and the long-term outcome of ischemic stroke are controversial. We aimed to evaluate this relationship.

Methods: We prospectively studied 83 patients consecutively hospitalized for acute ischemic stroke (38.6% males, age 79.7?±?6.3?years). Serum adiponectin, leptin, and resistin levels and the ?420C?>?G polymorphism of the resistin gene were determined at admission. Stroke severity at admission was evaluated with the National Institutes of Health Stroke Scale (NIHSS). One year after discharge, functional status, incidence of cardiovascular events and all-cause mortality were recorded. Functional status was evaluated with the modified Rankin scale (mRS).

Results: Patients with the G allele had lower mRS (p?<?.05) and patients with adverse outcome had higher serum resistin levels (p?<?.05). The only independent predictor of adverse outcome was mRS at discharge (risk ratio (RR) 2.78, 95% confidence interval (CI) 1.54–5.00; p?<?.001). Higher adiponectin levels were an independent predictor of cardiovascular morbidity (RR 1.07, 95% CI 1.01–1.14; p?<?.05). Patients who died had higher serum adiponectin levels than those who survived (p?<?.05). The only independent predictor of all-cause mortality was NIHSS at admission (RR 1.19, 95% CI 1.04–1.35; p?<?.01).

Conclusions: In patients with acute ischemic stroke, the G allele of the ?420C?>?G polymorphism of the resistin gene promoter is more frequent in those with a more favorable functional outcome at one year after discharge. Patients with higher serum resistin levels appear to have worse long-term functional outcome, while higher serum adiponectin levels are associated with higher incidence of cardiovascular events.     

Relationship between visceral fat and PAI-1 in overweight men and women before and after weight loss

This study was aimed at evaluating the relationship between visceral fat accumulation and plasma plasminogen activator inhibitor-1 (PAI-1) levels in healthy, obese men and women undergoing weight loss therapy. The subjects, 25 men and 25 premenopausal women, aged between 26 and 49 years, with an initial body mass index between 28 and 38 kg/m2, received a controlled diet for 13 weeks providing a 4.2 MJ/day energy deficit. Magnetic resonance imaging was used to measure visceral and subcutaneous abdominal fat. Our results show that before weight loss visceral fat was significantly correlated with PAI-1 in men (r = 0.45; p<0.05), but not in women (r = -0.15; ns). The association between visceral fat and PAI-1 in men remained significant after adjustment for age and total fat mass, and multiple linear regression analysis showed a significant independent contribution of visceral fat to plasma PAI-1 levels. Both visceral fat areas and PAI-1 levels decreased significantly with weight loss in both men and women. Changes in visceral fat area were related to changes in PAI-1 in women (r = -0.43; p = 0.05) but not in men (r = -0.01; ns); however, this association in women disappeared after adjustment for total fat mass. We conclude that there is a relationship between visceral fat and PAI-1 in obese men but not in obese women, and that PAI-1 levels decrease substantially (52%) by weight loss, but this change is not related to changes in visceral fat mass per se.     

A pilot study on the impact of body composition on bone and mineral metabolism in Parkinson's disease

The impact of body composition on bone and mineral metabolism in Parkinson's disease (PD) was evaluated. Body fat mass, lean mass, bone mineral content, and bone mineral density (BMD) were measured by DXA in 22 PD patients and 104 controls. Female patients exhibited reduced body mass index, fat mass, and BMD compared to controls (p<0.05). Significant positive correlation was found between 25 OHD levels and BMC. Diminished bone mass in women with PD was found to be associated with alterations in body composition and low 25 OHD levels.     

广西百色地区壮族男性人群骨密度与脂联素基因单核苷酸多态性的关系***

背景：脂联素可在骨代谢中发挥重要作用。 目的：观察脂联素基因单核苷酸多态性与广西百色地区壮族男性骨密度的关系。 方法：选取广西百色地区壮族男性跟骨骨量减少患者,采用单碱基延伸的单核苷酸多态性分型技术对广西百色地区302例壮族男性的脂联素基因的5个单核苷酸多态性位点(rs1063539、rs12495941、rs266729和rs3774261)进行了基因分型。 结果与结论：以5个多态性位点作为自变量的多元 Logistic回归检测结果显示,仅rs3774261多态性与跟骨超声振幅衰减显著相关(OR=1.948,95%CI：1.184~3.203,P < 0.01),并独立于骨量减少的传统危险因素。对基因型进行纯合子与杂合子合并后的协方差分析显示,仅rs3774261的AG+GG与AA基因型的跟骨超声振幅衰减值差异有显著性意义(P < 0.05),AG+GG型对骨密度具有一定的保护作用,AA型是骨密度降低的危险因素。结果证实,脂联素基因第2内含子rs3774261位点多态性与中国百色地区壮族男性骨密度有一定关联。     

Lower levels of plasma adiponectin and endothelial progenitor cells are associated with large artery atherosclerotic stroke

Background: Both adiponectin and endothelial progenitor cells (EPCs) have been proposed recently with anti-atherosclerosis effects. However, their impacts on vascular outcomes in patients with large artery atherosclerosis (LAA) are unclear. This study aimed to investigate the relationship between adiponectin, EPCs and stroke with a case-control design. Methods: The study cohort included 127 patients (61.3 ± 11.0 years; 73.2% men) with LAA stroke and 58 control subjects (60.9 ± 9.2 years; 70.7% men) referred for adiponectin and EPCs levels testing. We collected demographic, clinical, angiographical features, and laboratory data. Influence of adiponectin and EPCs levels on cerebral atherosclerosis and LAA stroke was analyzed with regression models. Results: The levels of adiponectin and EPCs in atherosclerotic stroke patients were significantly lower compared with matched controls (p < 0.05). Logistic regression analysis identified that reduced levels of adiponectin and EPCs were closely correlated with cerebral atherosclerosis and LAA stroke. The associations remained significant after adjustment for age, sex and other confounders. Additionally, partial correlation analysis revealed a significant positive association between adiponectin and three subpopulations of EPCs levels (CD34⁺CD133⁺CD309⁺cells: r = 0.510, p = 0.001; CD34⁺ CD133^?CD309⁺cells: r = 0.262, p = 0.004; CD34^?CD133⁺CD309⁺cells: r = 0.348, p < 0.001). Conclusions: Adiponectin is positively correlated with EPCs levels, and both of them are independently associated with LAA stroke.