肥胖人群抵抗素表达与血清游离脂肪酸、肿瘤坏死因子α、脂联素水平的研究

目的了解3种脂肪细胞因子(游离脂肪酸、肿瘤坏死因子α和脂联素)与肥胖人群抵抗素表达的关系。方法选取19例肥胖和29例非肥胖受试者,采用逆转录聚合酶链反应(RT-PCR)方法,检测腹部皮下与大网膜脂肪组织中抵抗素mRNA的表达,同时测定血清抵抗素、肿瘤坏死因子α(TNF-α)、游离脂肪酸(FFA)和脂联素等指标,计算胰岛素敏感性指数及胰岛素抵抗指数(HOMA-IR)。结果肥胖组的血清FFA、TNF-α和抵抗素水平高于非肥胖组(均P<0.05);而血清脂联素水平却低于非肥胖组(P<0.05);抵抗素在各组皮下及网膜脂肪组织中的表达差异均无统计学意义;以血清抵抗素为因变量进行多元逐步回归分析,显示脂联素、TNF-α、皮下脂肪组织中抵抗素表达、FFA进入回归方程;相关分析显示,血清抵抗素与体质量指数、FFA、TNF-α、HOMA-IR呈正相关(分别r=0.457,P=0.008;r=0.708,P=0.000;r=0.520,P=0.006;r=0.703,P=0.000),与血清脂联素水平呈负相关(r=-0.928,P=0.000);皮下脂肪中抵抗素表达与TNF-α呈负相关(r=-0.352,P=0.039),与网膜脂肪中抵抗素的表达呈正相关(r=0.285,P=0.05),与血清FFA和脂联素水平无相关性。结论提示TNF-α、皮下脂肪组织中抵抗素表达和FFA对血清抵抗素水平具有正性影响,而脂联素对抵抗素水平产生负性作用;TNF-α可能下调皮下脂肪中抵抗素的表达。     

急性冠脉综合征患者血清抵抗素和脂联素水平的研究

【目的】研究急性冠脉综合征（ACS）患者血清抵抗素和脂联素水平的变化及其病理生理意义。【方法】酶联免疫法测定76例ACS患者的血清抵抗素、脂联素及超敏C反应蛋白水平,其中急性心肌梗死组46例,不稳定性心绞痛组30例,并选取24例健康体检者为正常对照组。【结果】与正常对照组相比,ACS患者血清抵抗素、超敏C反应蛋白水平升高（均P〈0．01）,脂联素水平降低（P〈0．01）;另外与不稳定性心绞痛组相比较,急性心肌梗死组血清抵抗素（P〈0．05）、超敏C反应蛋白（P〈0．01）和脂联素（P〈0．01）水平差异均有统计学意义。在各指标之间的相关性分析中,血清抵抗素与超敏C反应蛋白（r=0．536,P〈0．01）呈正相关,脂联素与超敏C反应蛋白（r=-0．446,P〈0．01）呈负相关。[结论]ACS患者血清抵抗素水平升高,脂联素水平降低,与超敏C反应蛋白具有相关性,提示了脂肪细胞分泌的血清抵抗素和脂联素与动脉粥样硬化的形成和ACS的发病有关。     

血清脂联素和抵抗素与初诊2型糖尿病的相关性研究

目的：探讨脂联素和抵抗素与2型糖尿病（T2DM）的关系。方法：对39例初诊T2DM患者做研究对象，选37例健康人做对照。采用酶联免疫测定法测定空腹血清脂联素和抵抗素浓度，并测定各组的空腹血糖、胰岛素、尿酸和血脂水平等；用HOMA—IR评价胰岛素抵抗，分析各指标间的相关性。结果：DM组血清脂联素浓度（3．66±0．91）ng／ml低于正常对照组（5．26±0．78）ng／ml，差异有显著性（P〈0．01）。DM组血清抵抗素浓度（6．10±0．43）μg／ml与正常对照组（6．09±0．47）μg／ml差异无显著性。在DM组，采用相关分析发现，血清脂联素浓度与患者收缩压、舒张压、年龄、病程、空腹胰岛素、体重指数、胆固醇、低密度脂蛋白胆固醇、HOMAIR呈负相关，与脂蛋白A1正相关；血清抵抗素与年龄、病程、收缩压、舒张压、甘油三酯呈正相关；与脂蛋白A1呈负相关，与体重指数、HOMAIR等不相关。结论：脂联素水平的下降与DM发病有关，而抵抗素与之无关。     

单纯性肥胖患者血清抵抗素和脂联素水平的研究

目的探讨单纯性肥胖患者血清抵抗素和脂联素水平的变化及意义。方法分别测定单纯性肥胖组（40例）和正常对照组（42例）的体质量指数（BMI）、腰围（WC）、腰臀比（WHR）、抵抗素、脂联素、空腹血糖（FBG）、空腹胰岛素（FINS）、胰岛素抵抗指数（HOMA-IR）、总胆固醇（TC）、甘油三酯（TG）高密度脂蛋白胆固醇（HDL-C）和低密度脂蛋白胆固醇（LDL-C）的水平。结果单纯性肥胖组的抵抗素和脂联素水平与对照组相比差异有统计学意义（均P〈0．01）,抵抗素分别为（25．79±6．14）μg／Lvs（15．76±4．39）μg／L（P〈0．01）;脂联素分别为（2．58±1．03）mg／Lvs（7．29±2．14）mg／L（P〈0．01）。抵抗素水平与BMI、WC、WHR、FINS和HOMA-IR、WHR、LDL-C呈正相关（r=0．523,P〈0．01;r=0．608,P〈0．01;r=0．350,P〈0．05;r=0．501,P〈0．01;r=0．317,P〈0．05）;脂联素则仅与HDL—C呈正相关（r=0．331,P〈0．05）,与BMI、WC、WHR、FBG、FINS、HOMA—IR、TG、LDL—C呈负相关（r=0．649,P〈0．01;r=-0．744,P〈0．01;r=-0．712,P〈0．01;r=-0．357,P〈0．05;r=-0．631,P〈0．01;r=-0．685,P〈0．01;r=-0．384,P〈0．05;r=-0．364,P〈0．05）;抵抗素与脂联素两者呈负相关（r=-0．517,P〈0．01）。抵抗素和脂联素是BMI和WC的预测因素。结论抵抗素升高、脂联素降低易导致单纯性肥胖和胰岛素抵抗。抵抗素、脂联素水平可能是肥胖发生的预测指标。     

首发抑郁症患者血清脂肪因子水平的研究

目的:探讨首发抑郁症患者瘦素、脂联素及抵抗素等血清脂肪因子的水平。方法:首发抑郁症患者60例纳入抑郁组,健康体检者40例纳入对照组,进行体脂参数及瘦素、脂联素和抵抗素水平的测定。结果:2组体脂参数差异无统计学意义(P0.05)。抑郁组血浆瘦素、脂联素浓度显著低于对照组(P0.01),抵抗素浓度差异无统计学意义(P0.05);2组内女性的瘦素水平均明显高于同组男性(P0.01),不同性别患者脂联素和抵抗素差异无统计学意义(P0.05)。结论:首发抑郁症患者存在一定水平的瘦素和脂联素浓度异常。     

老年男性高尿酸血症与血清脂联素、瘦素水平及其比值的相关性研究

目的研究老年男性血清脂联素、瘦素水平及其比值与血尿酸水平的相关性。方法选择122名年龄≥65岁的老年男性，以血清尿酸≥420μmol／l诊断为高尿酸血症，高尿酸组52人，尿酸正常组70人。采用放免法测定血清脂联素、瘦素水平，计算脂联素／瘦素比值（A/L）。结果老年男性高尿酸血症表现为高瘦素低脂联素，脂联素／瘦素比值下降；老年男性血尿酸水平与空腹血瘦素水平显著负相关，与空腹血脂联素水平及A／L比值显著负相关。结论血瘦素水平升高，脂联素水平下降是老年男性发生高尿酸血症的机制之一，可能与其他代谢异常指标共同参与了代谢综合征的代谢紊乱状态。     

男性吸烟与骨密度及骨生化指标关系

目的:探讨男性吸烟与骨密度及骨生化指标关系.方法:用DXA仪测定腰椎及髋部BMD,用ELISA测定389例20～80岁健康男性血清骨特异性碱性磷酸酶(sBAP)和Ⅰ型胶原氨基末端肽(sNTX).结果:(1)腰椎正位总体、腰椎侧位、髋部总体、股骨颈及Ward's区BMD均与年龄呈显著负相关(均P＜0.05).各部位BMD均在20～29岁年龄组最高,29岁之后随增龄而缓慢下降;40～60岁各年龄组之间的BMD无显著差异.(2)除腰椎侧位BMD外,吸烟组其他各部位BMD显著低于非吸烟组;吸烟组的BAP显著高于非吸烟组,两组之间的sNTX无显著差异.(3)校正年龄与BMI后,烟龄与腰椎正位,髋部总体,股骨颈及Ward's区BMD均呈显著负相关(P＜0.05).每日吸烟量与腰椎正位及Ward's区BMD呈显著负相关(P＜0.05).结论:男性随年龄增长骨量丢失.男性吸烟者骨生化指标与骨转换水平增高,骨量丢失加速.吸烟等生活方式增高骨转换水平,影响骨转换的增龄性变化并加速骨量的丢失.吸烟是骨质疏松的一个危险因素.预防骨质疏松症(OP)应提倡戒烟.     

绝经后妇女血清基质金属蛋白酶与骨转换生化指标及骨密度的关系

目的探讨绝经后妇女血清基质金属蛋白酶(MMP)-1和MMP-2与骨密度及骨转换生化指标之间的关系。方法采用酶联免疫吸附法测定297名48~80岁女性志愿者的血清MMP-1、MMP-2和血清骨碱性磷酸酶(BAP)、血清骨钙素(OC)及血清Ⅰ型胶原氨基末端肽(NTX),用双能X线吸收法测定腰椎正位1~4总体、股骨颈、华氏区、髋部总体的骨密度。结果MMP-1与骨密度及骨转换生化指标无明显相关性;MMP-2与骨密度呈较弱的负相关,校正年龄与体重指数后,MMP-2与股骨颈、髋部骨密度的相关性消失;MMP-2与BAP、OC、NTX正相关(P<0.01);绝经后骨质疏松症患者血清MMP-2水平高于年龄匹配的正常对照组和骨量减少组(P<0.01)。结论绝经后妇女血清MMP-2与骨转换生化指标相关联,血清MMP-2水平升高可能为高骨代谢转换过程(如绝经后骨质疏松症)中的一种伴随表现。     

乳腺癌患者血清抵抗素、脂联素和瘦素水平及其临床意义

目的了解乳腺癌患者血清中抵抗素、脂联素、瘦素及血脂变化及临床意义。方法测定90例乳腺癌患者(48例未绝经,42例已绝经)及50名健康对照者血清抵抗素、脂联素、瘦素、空腹血糖(FBG)及血脂。结果乳腺癌患者脂联素及高密度脂蛋白胆固醇(HDL-C)显著低于对照组(P<0.01或P<0.05),抵抗素、瘦素、FBG及三酰甘油(TG)均明显增加(P<0.01或P<0.05)。但抵抗素、脂联素及瘦素在未绝经乳腺癌患者与健康对照组之间差异无统计学意义(P>0.05)。有淋巴结转移的乳腺癌患者抵抗素、脂联素及瘦素水平与无淋巴结转移乳腺癌患者间差异有统计学意义(P<0.01)。逐步回归分析,脂联素及HDL-C的降低,瘦素和抵抗素的升高将会增加罹患乳腺癌的风险。血清脂联素降低和瘦素的增加与乳腺癌患者淋巴结的转移呈现相关性。结论血清脂联素水平的降低和抵抗素及瘦素水平的升高是患乳腺癌的危险因素。血清中较低的脂联素和较高的瘦素水平是乳腺癌转移的危险因素。     

乳腺癌患者血清抵抗素、脂联素和瘦素水平及其临床意义

目的了解乳腺癌患者血清中抵抗素、脂联素、瘦素及血脂变化及临床意义。方法测定90例乳腺癌患者（48例未绝经,42例已绝经）及50名健康对照者血清抵抗素、脂联素、瘦素、空腹血糖（FBG）及血脂。结果乳腺癌患者脂联素及高密度脂蛋白胆固醇（HDL-C）显著低于对照组（P〈0.01或P〈0.05）,抵抗素、瘦素、FBG及三酰甘油（TG）均明显增加（P〈0.01或P〈0.05）。但抵抗素、脂联素及瘦素在未绝经乳腺癌患者与健康对照组之间差异无统计学意义（P〉0.05）。有淋巴结转移的乳腺癌患者抵抗素、脂联素及瘦素水平与无淋巴结转移乳腺癌患者间差异有统计学意义（P〈0.01）。逐步回归分析,脂联素及HDL-C的降低,瘦素和抵抗素的升高将会增加罹患乳腺癌的风险。血清脂联素降低和瘦素的增加与乳腺癌患者淋巴结的转移呈现相关性。结论血清脂联素水平的降低和抵抗素及瘦素水平的升高是患乳腺癌的危险因素。血清中较低的脂联素和较高的瘦素水平是乳腺癌转移的危险因素。     

Relationships between serum adiponectin, leptin, resistin, visfatin levels and bone mineral density, and bone biochemical markers in Chinese men

BACKGROUND: Adiponectin, leptin, resistin, and visfatin, as the main circulating peptides secreted by adipose tissue, are potential contributors to bone metabolism. We investigated whether these serum adipocytokines levels are associated with BMD and bone turnover biochemical markers in 232 Chinese men (20-80 y). METHODS: Serum adiponectin, leptin, resistin, and visfatin levels were determined by ELISA. RESULTS: Leptin had a positively correlation with fat mass, and remained significant after adjustment for age and BMI. There was a significant negative weak correlation between adiponectin and fat mass, and disappear after adjustment for age and BMI. Resistin and visfatin were not significantly correlated with fat mass. In the multiple linear stepwise regression analysis, lean mass and adiponectin, but not leptin, resistin and visfatin, were independent predictors of BMD. The significant positive correlations between adiponectin and bone-specific alkaline phosphatase (BAP), bone cross-linked N-telopeptides of type collagen (NTX) were found, and remained significant after adjustment for age and fat mass. CONCLUSIONS: Adiponectin was an independent predictor of BMD in Chinese men, and positively correlated with bone turnover biochemical markers. It suggested that adiponectin exert a negative effect on bone mass in men.     

Relationships between serum adiponectin,leptin concentrations and bone mineral density,and bone biochemical markers in Chinese women

BackgroundAdiponectin and leptin, as the main circulating peptides secreted by adipose tissue, are potential contributors to bone metabolism. However, their association with bone mineral density (BMD) is unknown. We investigated whether these serum adipocytokines concentrations are associated with BMD and bone turnover markers.MethodsSerum adiponectin, leptin concentrations, bone turnover biochemical markers, and BMD were determined in 265 premenopausal and 336 postmenopausal Chinese women.ResultsIn postmenopausal Chinese women, the multiple linear stepwise regression analysis showed that year since menopause, lean mass, estradiol, and adiponectin, but not fat mass, leptin, were independent predictors of BMD in postmenopausal Chinese women. However, in premenopausal Chinese women, adiponectin was not the predictor of BMD. The significant positive correlations between adiponectin and bone-specific alkaline phosphatase (BAP), bone cross-linked N-telopeptides of type I collagen (NTX) were found only in postmenopausal women. Serum BAP, and NTX, but not adiponectin, decreased in response to alendronate therapy.ConclusionsAdiponectin was an independent predictor of BMD, and positively correlated with bone turnover biochemical markers in postmenopausal Chinese women, but not premenopausal women. It suggested that adiponectin may exert a negative effect on bone mass by promoting excessive bone resorption associated with bone loss. However, these effects may be mediated by menopausal status.     

肥胖人群脂联素、抵抗素和胰岛素抵抗水平的研究

目的 探讨肥胖患者血清脂联素、抵抗素和胰岛素抵抗水平的变化及意义.方法 分别测定106例肥胖者和107名健康对照者的体重指数(BMI)、腰围、臀围、空腹胰岛素、空腹血糖、血脂、脂联素和抵抗素水平,计算胰岛素抵抗指数(HOMA-IRI). 结果 肥胖者的体重指数(BMI)、体脂分布百分比(BF)、HOMA-IRI、抵抗素...     

Plasma adiponectin and hyperglycaemia in diabetic patients.

The insulin-sensitising adipose hormone adiponectin is reduced in type 2 diabetic patients. We assessed the relationships between plasma adiponectin and chronic hyperglycaemia. Adiponectin levels and glycated haemoglobin (HbA1c) were measured at enrolment and after 90 days in 16 patients with type 2 diabetes aged (mean +/- SEM) 63.0 +/- 0.6 years, with body mass index (BMI) 30.2 +/- 0.5 kg/m2 and HbA1c concentration 7.4 +/- 0.1%, who did not modify their hypoglycaemic treatment during the observation period. Furthermore, plasma adiponectin was measured in 29 adult patients with type 1 diabetes and compared with 29 control subjects matched for sex, age, BMI, waist circumference and bioimpedance-estimated fat mass. In type 2 diabetic patients at enrolment, adiponectin concentration correlated with BMI (r = -0.46; p < 0.05), but not with HbA1c. During the prospective observation, variations of adiponectin showed a significant correlation with variations of BMI (r = -0.47; p < 0.01), but not with variations of HbA1c concentration. These results were confirmed by multivariate analysis after adjustment for sex and age. Adiponectin levels in type 1 diabetic patients (380.8 +/- 13.7 ng/ml in women, 192.5 +/- 13.9 ng/ml in men) were significantly (p < 0.05) higher than in control subjects (277.6 +/- 11.0 ng/ml in women, 102.7 +/- 5.1 ng/ml in men); plasma adiponectin correlated significantly with BMI and waist circumference, but not with HbA1c. In conclusion, the reduction of plasma adiponectin levels in type 2 diabetic patients does not appear to be determined by chronic hyperglycaemia. Adiponectin levels are increased in type 1 diabetes, but this phenomenon is not attributable to differences in nutritional status or body composition.     

Adiponectin in a native Canadian population experiencing rapid epidemiological transition

OBJECTIVE: Adiponectin is emerging as an important protein in the etiology of obesity and related metabolic disorders. The objectives of this study were to determine cross-sectional and prospective associations of adiponectin concentration with adiposity, type 2 diabetes, and cardiovascular disease (CVD) risk factors in a population-based study of Native Canadians, a group experiencing dramatic increases in diabetes and CVD. RESEARCH DESIGN AND METHODS: During the 1993-1995 baseline survey, samples for glucose, insulin, adiponectin, and lipids were collected after an overnight fast. Waist circumference and percent body fat were measured, and a 75-g oral glucose tolerance test was administered: n = 505 with normal glucose tolerance (NGT), 74 with impaired glucose tolerance (IGT), and 149 with diabetes. In 1998, 95 high-risk subjects, defined as those who, at baseline, had either IGT or NGT with an elevated 2-h glucose concentration (>/==" BORDER="0">7.0 mmol/l), participated in a follow-up examination using the protocol used at baseline. RESULTS: After adjustment for covariates including percent body fat and homeostasis model assessment of insulin resistance (HOMA-IR), adiponectin concentrations were significantly lower among men versus women (10.8 vs. 15.0 micro g/ml, P < 0.0001) and among diabetic versus NGT subjects (11.1 vs. 13.1 micro g/ml, P < 0.05). Adiponectin was inversely correlated with percent body fat, waist circumference, HOMA-IR, and triglyceride and positively correlated with HDL (r = |0.30|-|0.44|, all P < 0.0001). In multivariate linear regression analysis in nondiabetic subjects, HDL and percent body fat were significantly related to adiponectin variation among both men and women (R(2) = 28-29%). Factor analysis returned three underlying factors among these variables, with adiponectin loading on the second factor along with insulin, waist circumference, triglyceride, and HDL. In the follow-up study, higher adiponectin at baseline was significantly associated with increases in HDL (r = 0.24, P = 0.03) and decreases in HOMA-IR (r = -0.29, P = 0.009) after adjustment for covariates, including age, adiposity, and diabetes status at baseline and follow-up. CONCLUSIONS: These population-based findings support the hypothesis that low circulating levels of adiponectin are an important determinant of risk of CVD.     

Plasma adiponectin and leptin levels,body composition,and glucose utilization in adult women with wide ranges of age and obesity

OBJECTIVE: The purpose of this study was to determine the relationships between plasma adiponectin and leptin levels, total and central obesity, and glucose utilization across the adult age span. RESEARCH DESIGN AND METHODS: We studied 148 women aged 18-81 years with a BMI range of 17.2-44.3 kg/m(2). Total percent body fat was determined by dual-energy X-ray absorptiometry and abdominal fat by computed tomography. Glucose tolerance in non-type 2 diabetic volunteers was determined with an oral glucose tolerance test. Glucose utilization (M) was measured during the last 60 min of hyperinsulinemic-euglycemic clamps (240 pmol x m(-2) x min(-1)). Plasma adiponectin levels were measured by radioimmunoassay. The women were separated into three age-groups: young, middle, and old (<40, 40-59, and >or=60 years, respectively), as well as by glucose tolerance status. RESULTS: Adiponectin concentrations did not differ by age-groups. There were significant age effects for BMI, percent body fat, visceral fat, subcutaneous abdominal fat, VO(2max), and M. Adiponectin levels were lower in the prediabetic women (n = 18) than in the normal glucose-tolerant women (n = 108) and the women with type 2 diabetes (n = 22) (both P < 0.05). Univariate correlations revealed significant negative relationships between plasma adiponectin levels and BMI, percent body fat, visceral fat, subcutaneous abdominal fat, fasting leptin, and fasting insulin and positive relationship with M (all P < 0.05). In a multiple stepwise regression model to predict adiponectin, only M remained in the model at P < 0.001. Multivariate analyses revealed a significant relation for M as a function of adiponectin, insulin, and VO(2max). CONCLUSIONS: The data suggest that plasma adiponectin does not change with age but levels are negatively associated with percent body fat, visceral fat, subcutaneous abdominal fat, insulin, and leptin levels in women. Adiponectin is positively associated with M across the age span in women.     

Circulating adiponectin and resistin levels in relation to metabolic factors, inflammatory markers, and vascular reactivity in diabetic patients and subjects at risk for diabetes

OBJECTIVE: Adiponectin and resistin, two recently discovered adipocyte-secreted hormones, may link obesity with insulin resistance and/or metabolic and cardiovascular risk factors. We performed a cross-sectional study to investigate the association of adiponectin and resistin with inflammatory markers, hyperlipidemia, and vascular reactivity and an interventional study to investigate whether atorvastatin mediates its beneficial effects by altering adiponectin or resistin levels. RESEARCH DESIGN AND METHODS: Associations among vascular reactivity, inflammatory markers, resistin, and adiponectin were assessed cross-sectionally using fasting blood samples obtained from 77 subjects who had diabetes or were at high risk to develop diabetes. The effect of atorvastatin on adiponectin and resistin levels was investigated in a 12-week-long randomized, double-blind, placebo-controlled study. RESULTS: In the cross-sectional study, we confirm prior positive correlations of adiponectin with HDL and negative correlations with BMI, triglycerides, C-reactive protein (CRP), and plasma activator inhibitor (PAI)-1 and report a negative correlation with tissue plasminogen activator. The positive association with HDL and the negative association with PAI-1 remained significant after adjusting for sex and BMI. We also confirm prior findings of a negative correlation of resistin with HDL and report for the first time a positive correlation with CRP. All of these associations remained significant after adjusting for sex and BMI. No associations of adiponectin or resistin with any aspects of vascular reactivity were detected. In the interventional study, atorvastatin decreased lipid and CRP levels, but adiponectin and resistin were not specifically altered. CONCLUSIONS: We conclude that adiponectin is significantly associated with inflammatory markers, in part, through an underlying association with obesity, whereas resistin's associations with inflammatory markers appear to be independent of BMI. Lipid profile and inflammatory marker changes produced by atorvastatin cannot be attributed to changes of either adiponectin or resistin.     

Lipid profile, obesity and bone mineral density: the Hertfordshire Cohort Study

BACKGROUND: Body mass index (BMI) and bone mineral density (BMD) are positively correlated in several studies, but few data relate bone density, lipid profile and anthropometric measures. AIM: To investigate these relationships in a large, well-characterized cohort of men and women (The Hertfordshire Cohort Study). METHODS: Men (n = 465) and women (n = 448) from Hertfordshire, UK were recruited. Information was available on demographic and lifestyle factors, anthropometric measurements, body fat percentage, fasting triglycerides, cholesterol (total, HDL, LDL), apolipoprotein (a) and apolipoprotein (b); bone mineral density (BMD) was recorded at the lumbar spine and total femur. RESULTS: BMD at the lumbar spine (males r = 0.15, p = 0.001; females r = 0.14, p = 0.003) and total femoral region (males r = 0.18, p = 0.0001; females r = 0.16, p = 0.0008) was related to serum triglyceride level, even after adjustment for waist-hip ratio, age, social class and lifestyle factors, but not if body fat percentage was substituted for waist-hip ratio in the regression model. Fasting HDL cholesterol level was related to lumbar spine BMD in women (r = -0.15, p = 0.001) and total femoral BMD in both sexes (males r = -0.15, p = 0.002; females r = -0.23, p < 0.0001); these relationships were also attenuated by adjustment for body fat percentage but not waist-hip ratio. No relationships were seen between total or LDL cholesterol with BMD. DISCUSSION: In this cohort, relationships between lipid profile and BMD were robust to adjustment for one measure of central obesity (waist-hip ratio), but not total body fat. This broadly supports the idea that adiposity may confound the relationship between lipids and bone mass.     

阻塞性睡眠呼吸暂停低通气综合征患者血浆抵抗素和脂联素水平与胰岛素抵抗的相关研究

目的 探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆抵抗素和脂联素水平与胰岛素抵抗程度的相关性.方法 根据整夜多导睡眠监测(PSG)和既往病史将68例OSAHS患者分为轻度(24例)、中度(13例)、重度(31例)OSAHS组,并设正常对照组(20例).检测各组空腹血糖、胰岛素、血脂、抵抗素、脂联素水平,计算稳态模型胰岛素抵抗指数(HOMA-IR),并分析HOMA-IR与抵抗素、脂联素、血脂、体重指数、腰臀比、睡眠呼吸暂停低通气指数(AHI)、最低血氧饱和度(LSaO2)、夜间血氧饱和度低于90%的时间占总睡眠时间的百分比(T90)等指标的相关性.结果 轻、中、重度OSAHS组的抵抗素水平[分别为(8.04±2.14)、(10.85±4.89)、(13.34±3.52)mg/L]均明显高于正常对照组[(5.14±1.94)mg/L]差异均有统计学意义(P均<0.05),且OSAHS重度组明显高于轻度组(P<0.05).脂联素在OSAHS轻度[(6.21±1.74)mg/L]、中度[(4.19±1.80)mg/L]、重度[(2.26±1.17)mg/L]组的水平均明显低于正常对照组[(9.49±2.40)mg/L],且OSAHS各组间差异均有统计学意义(P均<0.05).OSAHS中、重度组的HO-MA-IR(4.07±0.97、5.61±2.26)明显高于OSAHS轻度组(1.57±0.58)和正常对照组(2.47±1.52),且OS-AHS中、重度组间差异也有统计学意义(P均<0.05).Spearman相关分析显示HOMA-IR与抵抗素、总胆固醇、甘油三酯、体重指数、腰臀比、AHI、190有显著正相关(r值分别为0.794、0.438、0.430、0.351、0.456、0.775、0.624,P均<0.01),与脂联素、LSaO2有显著负相关(r值为-0.563、-0.623,P均<0.01).偏相关分析显示控制脂联素和抵抗素影响后,HOMA-IR与190、AHI有显著正相关(r值分别为0.231、0.358,P均<0.05).多元逐步回归分析显示AHI和抵抗素为影响HOMA-IR的最显著因素(R2=0.613,F=69.810,P<0.01).结论 OSAHS患者的HOMA-IR与OSAHS严重程度具有显著正相关,且独立于血脂、体重指数、腰臀比、抵抗素和脂联素等因素的影响;血脂、体重指数、腰臀比等因素可能通过对抵抗素和脂联素的作用影响HOMA-IR;AHI和血浆抵抗素水平可能成为判断OSAHS患者胰岛素抵抗水平的重要生物学标志.     

肥胖患者脂联素与胰岛素抵抗、内皮依赖性舒张功能相关性研究

目的：探讨肥胖患者脂联素变化及与胰岛素抵抗、内皮依赖性舒张功能之间的关系。方法：采用彩色多普勒超声检测仪检测肥胖组（O）53例和正常对照组（C）24例右肱动脉内皮依赖性舒张功能、颈总动脉内膜-中层厚度（IMT），并测定血脂、血糖、空腹胰岛素（HNS）、血管性血友病因子（vWF）、纤溶酶原激活剂抑制物-1（PAI-1）和脂联素（adiponectin）。采用稳态模式（HOMA-IR）评价胰岛素抵抗。结果：O组腰臀比（WHR）、体重指数（BMI）、体内脂肪含量（BF）、收缩压（SBP）、舒张压（DBP）、载脂蛋白B（ApoB）、空腹血糖（FBG）、FINS和HOMA-IR高于C组（P〈0．05），脂联素明显低于C组（P〈0．05）。脂联素与性别（男=1，女=2）、高密度脂蛋白-胆固醇（HDL-C）呈正相关（r分别为0．354、0．438，P值分别为0．027、0．005）；与体重、腰围（W）、甘油三酯（TG）、WHR、F1NS和HOMA-IR呈负相关（r分别为-0．358、-0．359、-0．449、-0．375、-0．363、-0．319，P值分别为0．025、0．025、0．004、0、019、0．027、0．054）。多元逐步回归分析显示，BMI和BF是影响脂联素独立的危险因素。结论：肥胖患者脂联素降低，并且与胰岛素抵抗密切相关。