腹膜透析患者大动脉僵硬度与代谢综合征组分密切相关

目的探讨腹膜透析患者中大动脉僵硬度与代谢综合征成分之间的关系。方法纳入148例持续非卧床腹膜透析患者,根据其存在代谢综合征成分的个数分为非代谢综合征组、代谢综合征高危组和代谢综合征组;采用颈-股动脉脉搏波传导速度评估大动脉僵硬度。结果颈-股动脉脉搏波传导速度与年龄(r=0.427,P<0.01)、收缩压(r=0.444,P<0.01)、脉压(r=0.498,P<0.01)和血糖(r=0.366,P<0.01)呈正相关,与血清白蛋白(r=-0.216,P<0.05)呈负相关;多元回归分析显示年龄及代谢综合征评分是脉搏波传导速度的独立影响因素,在校正R2的模型里,相关系数为0.24。结论腹膜透析患者代谢综合征组分增加与大动脉僵硬度升高有密切关系,提示代谢综合征的诊断标准对预测腹膜透析患者心血管疾病仍然适用。     

腹部内脏脂肪沉积的老年非代谢综合征患者脂联素瘦素比值的变化

目的 观察体质指数正常、腹部内脏脂肪沉积的非代谢综合征老年男性患者血清脂联素、瘦素水平及脂联素瘦素比值的变化.方法 将入选的老年非代谢综合征男性患者109例分为2组,内脏无脂肪沉积组67例,内脏脂肪沉积组42例.采用CT方法测定内脏脂肪面积,当腹部内脏脂肪面积≥100cm2,为内脏脂肪沉积;采用LINCO公司提供的放射免疫试剂盒测定空腹血脂联素、瘦素水平;代谢综合征的诊断采用2004年中国糖尿病学会制定的标准.结果 (1)脂肪沉积组与无脂肪沉积组比较,体质指数、内脏脂肪面积均显著升高,体质指数分别为(22.94±1.35)kg/m2对(21.38±2.55)kg/m2(P＜O.001),内脏脂肪面积(135.6±31.7)cm2对(68.6±22.6)cm2(P＜O.001);脂联素瘦素比值降低.分别为2.17±1.77对4.54±7.00(P=0.031);而脂联素、瘦素水平在两者间差异无统计学意义;(2)脂联素瘦素比值与体质指数(r=-0.552,P＜0.001)、腰围(r=-0.390,P＜0.001)、腹部内脏脂肪面积(r=-0.311,P＜0.001)呈负相关.结论 体质指数正常有内脏脂肪沉积与无内脏脂肪沉积的老年男性比较.脂联素瘦素比值明显下降.并与腹部脂肪面积显著负相关.提示血清脂联素瘦素比值可能可用于筛选体质指数正常有腹部内脏脂肪肪沉积的患者.     

不同诊断标准下腹膜透析患者代谢综合征与大动脉僵硬度的关系

目的 对腹膜透析患者在不同诊断标准下诊断的代谢综合征与大动脉僵硬度的关系进行研究,从而确定一个最适合腹膜透析患者的标准,同时对影响大动脉僵硬度的因素进行分析.方法 选取稳定透析的持续不卧床腹膜透析患者155例,测量颈股动脉脉搏波速度作为大动脉僵硬度的评价指标,用WHO 1999、IDF 2007和ATPⅢ2001三个标准分别诊断代谢综合征,比较不同标准下代谢综合征组与非代谢综合征组脉搏波速度有无差别,并对脉搏波速度的相关因素进行分析.结果 用WHO 1999、IDF 2007和ATPⅢ2001标准诊断的合并代谢综合征的持续不卧床腹膜透析患者均比无代谢综合征患者有较高的脉搏波速度(P<0.05).脉搏波速度与持续不卧床腹膜透析患者的年龄、腰围、收缩压及血糖呈正相关(P<0.05或P<0.01),与血高密度脂蛋白胆固醇呈负相关(P<0.05),它们都是脉搏波速度的独立影响因素.结论 无论用WHO 1999、IDF 2007和ATPⅢ2001中任何一个代谢综合征标准,合并代谢综合征的持续不卧床腹膜透析患者大动脉僵硬度均较非代谢综合征患者增加.年龄和代谢综合征中多数因子均是脉搏波速度的独立影响因素.经多方考虑,我们推荐在持续不卧床腹膜透析患者用ATPⅢ标准诊断代谢综合征.     

代谢综合征患者血浆生长素水平降低

背景 生长素(Ghrelin)是一种主要由胃黏膜分泌的,作用于内源性生长激素促分泌剂受体,通过加快胃排空调节食欲,抑制体质量.目的 检测代谢综合征病人血浆生长素水平,分析其与糖、脂代谢紊乱和高血压的关系.方法 测定正常对照30例及代谢综合征病人54例清晨空腹血浆生长素水平.结果 代谢综合征病人生长素[(69.7±43.6)ng/L]低于正常对照组[(96.8±28.8)ng/L](P＜0.01),生长素水平与胰岛素水平呈负相关(r=-0.554,P＜0.01),亦与收缩压和舒张压呈负相关(r=-0.77,P＜0.01和r=-0.849,P＜0.01),其中超重组病人生长素显著低于正常对照组(P＜0.01);而体质量指数正常的代谢综合征病人血浆生长素水平也低于正常对照组(P＜0.05).高血脂亚组病人生长素低于正常对照组(P＜0.01);而血脂正常亚组与正常对照组差异无统计学意义(P＞0.05).多元回归分析显示:影响生长素的因素有年龄、收缩压和三酰甘油,以三酰甘油影响最大.结论 代谢综合征病人清晨空腹血浆生长素水平明显降低,且与胰岛素水平、高血压、年龄和高血脂相关,与三酰甘油的关系最为明显.     

T2DM患者血浆内脏脂肪素、瘦素与胰岛素抵抗的相关性研究

目的 探讨2型糖尿病(T2DM)患者血浆内脏脂肪素、瘦素水平与胰岛素抵抗(IR)的相关性.方法 102例T2DM患者和64例正常糖耐量(NGT)对照者,根据BMl分为肥胖组(Ob)和非肥胖(Non-Ob)组,均测定空腹血浆内脏脂肪素、瘦素和相关临床指标,计算胰岛素抵抗指数(HOMA-IR)和腰臀比(WHR).结果 T2DM组与NGT组比较空腹血浆内脏脂肪素和瘦素水平明显升高(t=3.922,P=0.00;t=2.128,P=0.038).相关分析显示T2DM患者空腹血浆内脏脂肪紊与HOMA-IR、WHR、瘦素、HbA<,1> c和TG正相关(r=0.543,P=0.001;r=0.442,P=0.008;r=0.385,P=0.013,r=0.345,P=0.025;r=0.427,P=0.005),瘦素与HOMA-IR、性别、BMI正相关(r=0.578,P<0.01;r=0.547,P<0.01;r=0.607,P<0.01).结论 T2DM患者空腹血浆内脏脂肪素和瘦素水平显著升高,且与IR关系密切.     

高血压合并代谢综合征患者血清脂联素与游离脂肪酸谱等代谢参数关系研究

目的 研究原发性高血压合并代谢综合征和未合并代谢综合征患者血清脂联素水平、游离脂肪酸谱特征及与其他糖脂代谢参数间关系.方法 用放射免疫分析法测定128例高血压合并或未合并代谢综合征患者与43例正常对照组血清脂联素,同时用气相色谱/质谱测定其游离脂肪酸成分.结果 高血压合并代谢综合征患者血清脂联素低于未合并代谢综合征组和正常对照组(P＜0.05或P＜0.01),总脂肪酸、不饱和脂肪酸(亚油酸、油酸、花生四烯酸、二十二碳六烯酸、花生三烯酸)、多不饱和脂肪酸(PUFA)和n6PUFA高于未合并代谢综合征组和正常组,差异有统计学意义(P＜0.05或P＜0.01).在研究对象中,脂联素与体重指数、腰围、腰臀比、甘油三酯呈负相关(r=-0.222,-0.235,-0.179,-0.194,P＜0.01或P＜0.05),与高密度脂蛋白胆固醇呈正相关(r=0.336,P＜0.01).总脂肪酸、多不饱和脂肪酸与体重指数、腰围、空腹血糖、平均血压呈正相关(r=0.241和0.280,0.198和0.188,0.226和0.298,0.274和0.334,P＜0.01或P＜0.05).结论 脂联素与游离脂肪酸代谢紊乱、n6系多不饱和脂肪酸升高,可能在原发性高血压合并代谢综合征的发病中起重要作用.     

血透与腹透患者血清脂蛋白(a)的变化及意义

目的观察血透(HD)与腹透(PD)患者之间脂蛋白(a)[lipoprotein(a),Lp(a)]及脂质水平影响的差别及其临床意义.方法对68例HD患者及50例PD患者的临床及实验室资料作研究,比较两种透析方式对血Lp(a)及脂质水平影响的差别,分析血Lp(a)与其他相关因素特别是与心脑血管事件的关系.结果HD与PD患者血Lp(a)水平均较对照组呈显著性升高(P＜0.05),其中PD组较HD组更高(P＜0.01);HD组血Tch较对照组及PD组均呈显著性下降(P＜0.05)、血HDL-C较对照组呈显著性下降(P＜0.01);PD组血TG较对照组及HD组均呈显著性升高(P＜0.05);血ApoA、ApoB100与对照组间无统计学差异.HD与PD患者血Lp(a)水平与超声心动图异常(P＜0.05)、ECG异常(P＜0.001)及心脑血管事件的发生(P＜0.01)、24h腹水蛋白质浓度(P＜0.01)、血Tch及LDL-C浓度(P＜0.05)、纤维蛋白原(P＜0.05)呈正相关;而与血浆白蛋白浓度(P＜0.05)、24h腹水Lp(a)浓度(P＜0.05)呈负相关.结论HD与PD患者普遍存在严重的脂质代谢变化,其中以血Lp(a)、TG、HDL-C变化尤为显著,PD组由于长期吸收大量葡萄糖,因此脂质代谢紊乱更为明显.Lp(a)有可能是HD、PD患者并发心脑血管事件的危险因素之一.     

多囊卵巢综合征患者血浆酰化刺激蛋白和瘦素与胰岛素抵抗的关系

目的 探讨多囊卵巢综合征(PCOS)患者血浆酰化刺激蛋白(ASP)和瘦素水平的变化及其与胰岛素抵抗(IR)的关系.方法 将39例PCOS患者分为肥胖PCOS组和非肥胖PCOS组,42名健康孕龄妇女分为单纯肥胖组和正常体重对照组.测定血浆ASP、瘦素、空腹血糖(FPG)、空腹胰岛素(Fins)水平,并计算胰岛素抵抗指数(HOMA-IR).结果 ①与正常体重对照组相比,其余三组ASP水平显著升高(P＜0.01);单纯肥胖组和肥胖PCOS组的血浆瘦素水平显著高于正常体重对照组(P＜0.05;P＜0.01),而非肥胖PCOS组与正常体重对照组无显著性差异(P＞0.05);与正常体重对照组相比,非肥胖PCOS组和肥胖PCOS组的HOMA-IR显著升高(P＜0.05;P＜0.01 ).②在PCOS患者中,ASP与Fins、HOMA-IR成正相关(r=0.284,P=0.04;r=0.297,P=0.03);瘦素与BMI、Fins、HOMA-IR成正相关(r=0.677,P＜0.01;r=0.609,P＜0.01;r=0.588,P＜0.01);ASP与瘦素不相关(r=-0.043).结论 PCOS患者存在胰岛素抵抗,其血浆ASP水平显著升高;ASP、瘦素可能与PCOS的胰岛素抵抗有关.     

腹膜透析患者心胸比例的变化及相关因素分析

目的:探讨腹膜透析(PD)患者心胸比例变化情况及相关影响因素. 方法:选取2010年6月至2011年12月于南京军区南京总医院全军肾脏病研究所行PD置管术的123例终末期肾病(ESRD)患者,观察PD治疗后心脏形态相关指标的变化.患者每3月随访一次,全面评估透析状况,包括血清白蛋白、血红蛋白(Hb)、收缩压、舒张压、体重、体质量指数(BMI)、尿量、超滤量、液体清除量、血钠、每周尿素氮总清除率(Kt/V total)、每周肌酐总清除率(Ccr)、残余肾肾小球滤过率(rGFR)水平,并通过心脏超声和胸部平片检查,每6月对PD患者的心脏形态学指标及功能进行评估,观察其动态变化. 结果:(1)随PD时间延长患者心胸比例逐渐增加,透析前、透析后6月、12月时分别为0.465±0.041、0.474±0.045、0.492±0.060(P＜0.01),射血分数呈下降趋势(P＞0.05).(2)20例(16.3％)患者出现胸闷、夜间不能平卧等心功能不全表现,分析这些患者临床特点发现,糖尿病肾病7例(35％),难治性高血压16例(80％),持续不卧床腹膜透析8例(40％)且rGFR下降快,贫血重.(3)相关回归分析发现,PD患者心胸比例与BMI(r=0.375,β =0.442)、收缩压(r=0.281,β=0.217)、血红蛋白(r=-0.283,β=-0.199)、液体清除量(r=-0.231,β=-0.851)独立相关.(4)不同rGFR状态下心胸比例不同,rGFR水平为＜3 ml/(min·1.73m2)、3～6 ml/(min· 1.73m2)、＞6 ml/(min·1.73m2),心胸比分别为0.493±0.062、0.468±0.043、0.456±0.042(P ＜0.05). 结论:随着透析时间的延长,PD患者心脏结构及功能发生改变,除与透析本身导致机体容量负荷持续增高外,与残余肾功能、BMI、Hb、液体清除量及血压状态亦密切相关.     

透与腹透患者血清脂蛋白（a）的变化及意义

目的：观察血透（HD）与腹透（PD）患者之间脂蛋白（a)[lipoprotein(a),Lp(a)]及脂质水平影响的差别及其临床意义。方法：对68例HD患者及50例PD患者的临床及实验室资料作研究，比较两种透析方式对血Lp(a)及脂质水平影响的差别，分析血Lp(a）与其他相关因素特别是与心脑血管事件的关系。结果：HD与PD患者血Lp(a）水平均较对照组呈显著性升高（P＜0.05），其中PD组较HD组更高（P＜0.01）；HD组血Tch较对照组及PD组无呈显著性下降（P＜0.05）、血HDL－C较对照组呈显著性下降（P＜0.01）；PD组血TG较对照组及HD组均呈显生升高（P＜0.05）；血ApoA、ApoB100与对照组间无统计学差异。HD与PD患者血Lp(a)水平与超声心动图异常(（P＜0.05）、EG异常（P＜0.001）及心脑血管事件的发生（P＜0.01）、24h腹水蛋白质浓度（P＜0.01）、血Tch及LDL-C浓度（P＜0.05）、纤维蛋白原（P＜0.05）呈正相关；而与血浆白蛋白浓度（P＜0.05）、24h腹水Lp(a)浓度（P＜0.05）呈负相关。结论：HD与PD患者普遍存在严重的脂质代谢变化，其中以血Lp(a)、TG、HDL－C变化尤为显著，PD组由于长期吸收大量葡萄糖，因此脂质代谢紊乱更为明显。Lp(a）有可能是HD、PD患者并发心脑血管事件的危险因素之一。     

The association between abdominal visceral fat and carotid stiffness is mediated by circulating inflammatory markers in uncomplicated type 2 diabetes

Central obesity, insulin resistance, inflammation, as well as vascular changes are common in patients with type 2 diabetes. In this study we assessed the relationship among stiffness of the carotid artery, visceral fat, and circulating inflammatory markers in type 2 diabetic subjects. Carotid stiffness, quantified as the distensibility coefficient (DC), was measured by ultrasound in asymptomatic, normotensive patients with uncomplicated, well-controlled type 2 diabetes and in controls. Body fat distribution was quantified by magnetic resonance imaging. In patients, the carotid DC was inversely associated with visceral fat area (r = -0.660; P = 0.005) and plasma levels of C-reactive protein (CRP; r = -0.687; P = 0.002), but most strongly with plasma IL-6 (r = -0.766; P < 0.001). In multivariate analysis, the association between DC and visceral fat disappeared after adjustment for CRP and IL-6. Correction for age, body mass index, blood pressure, glycosylated hemoglobin, or fasting plasma glucose did not affect the association between carotid DC and inflammatory markers. Thus, carotid stiffness is associated with visceral obesity in patients with uncomplicated type 2 diabetes, but this association seems to be mediated by circulating IL-6 and CRP, of which IL-6, at least in part, originates from adipose tissue and stimulates hepatic CRP production.     

Large artery stiffening with weight gain in humans: role of visceral fat accumulation

We tested the hypothesis that weight gain would increase arterial stiffness in healthy nonobese adults. To address this, we overfed 14 nonobese men (age: 23+/-1 years) approximately 1000 kcal/d for 6 to 8 weeks until a 5-kg weight gain was achieved. Carotid diameters (high-resolution ultrasound) and pressures (applanation tonometry), body composition (dual energy x-ray absorptiometry), and abdominal fat distribution (computed tomography) were measured at baseline and following 4 weeks of weight stability at each individual's elevated body weight. Overfeeding increased body weight 5.1+/-0.1 kg and body fat 3.4+/-0.4 kg (both P<0.001) in 45+/-7 days. Total abdominal fat increased 46+/-7 cm(2) with weight gain due to increases in both subcutaneous (30+/-6 cm(2)) and visceral fat (15+/-4 cm(2); all P<0.01). As hypothesized, weight gain increased arterial stiffness 13+/-6% and decreased arterial compliance 21+/-4% (both P<0.05). Furthermore, those individuals above the median increase in abdominal visceral fat demonstrated a significantly greater increase in arterial stiffness (0.97+/-0.29 versus 0.06+/-0.36 U; P<0.05) compared with those below the median. Consistent with these observations, the only correlates of the changes in arterial stiffness with weight gain were the increases in total abdominal fat (r=0.794), abdominal visceral fat (r=0.651), and waist circumference (r=0.470; all P<0.05). Taken together, these findings suggest that modest weight gain is associated with increases arterial stiffness in nonobese men. The degree of large artery stiffening with weight gain seems to be determined, in part, by the amount of abdominal visceral fat gain. Importantly, this relation is independent of the amount of total body fat gained.     

The metabolic syndrome in obese postmenopausal women: relationship to body composition, visceral fat, and inflammation

The purpose of this study was to investigate whether aerobic fitness, body composition, body fat distribution, and inflammation are different in obese postmenopausal women with and without the metabolic syndrome (MS), and whether the severity of MS is associated with these characteristics. Fifty-eight women (age, 59 +/- 1 yr; body mass index, 33.0 +/- 0.6 kg/m2)completed testing of maximal aerobic capacity, body composition (fat mass, lean mass, and percent body fat), body fat distribution (sc and visceral fat areas, and regional adipocyte sizes), and inflammation (C-reactive protein, IL-6, and TNF-alpha,and their soluble receptors). Lean mass (44.4 +/- 0.9 vs. 41.2 +/- 0.9 kg; P < 0.05), visceral fat area (180 +/- 10 vs. 135 +/- 7 cm2; P <0.001), and plasma soluble TNF receptor 1 (sTNFR1; 860 +/- 25 vs. 765 +/- 42 pg/ml; P < 0.05) were higher in women with the MS(n = 27) than in those without the MS (n = 31). The number of MS components was directly related to weight, body mass index, fat mass, lean mass, visceral fat area, and plasma sT-NFR1. We conclude that obese older women with the MS are characterized by high lean mass, high visceral fat, and elevated sTNFR1, and the severity of the MS is associated with body composition, visceral adiposity, and inflammation.     

Metabolic syndrome and ambulatory arterial stiffness index in non-diabetic patients with primary hypertension

Increased arterial stiffness and the presence of metabolic syndrome (MS) have been shown to predict cardiovascular events in patients with primary hypertension. We investigated the relationship between a recently proposed index of arterial stiffness derived from ambulatory blood pressure (BP) monitoring and MS in 156 untreated, non-diabetic patients with primary hypertension. Ambulatory arterial stiffness index (AASI) was defined as 1 minus the regression slope of diastolic over systolic BP readings obtained from 24-h recordings. A modified National Cholesterol Education Program definition for MS was used, with body mass index replacing waist circumference. The prevalence of MS was 23%. Patients with MS were more frequently male (0.0291) and had increased serum uric acid (P=0.0005), high-sensitivity C-reactive protein (P=0.0259), as well as total and low-density lipoprotein (LDL)-cholesterol (P=0.0374 and P=0.0350, respectively) as compared to those without MS. After adjusting for these confounders, the association between AASI and the presence of MS was statistically significant (P=0.0257). Moreover, the prevalence of increased AASI (upper tertile, that is >or=0.550) was greater in patients with MS (P=0.0156). After adjusting for age and 24-h mean BP, the presence of MS entailed a more than twofold greater risk for increased AASI (0.0280). MS is associated with increased AASI in non-diabetic patients with primary hypertension. These data support the role of this new index of arterial stiffness as a marker of risk and help to explain the high cardiovascular morbidity and mortality that is observed in hypertensive patients with MS.     

Regional body composition as a determinant of arterial stiffness in the elderly: The Hoorn Study

OBJECTIVE: To estimate the relation of precisely measured regional body composition with peripheral and central arterial stiffness in the elderly. METHODS: We investigated 648 participants (mean age 69.0 +/- 6.0 years) of the Hoorn Study, a population-based cohort study. Trunk fat, leg fat, trunk lean and leg lean mass were distinguished by dual-energy X-ray absorptiometry. We used ultrasound to measure the distensibility and compliance of the carotid, femoral and brachial arteries, and carotid Young's elastic modulus, as estimates of peripheral stiffness. As estimates of central stiffness we measured carotid-femoral transit time, aortic augmentation index and systemic arterial compliance. RESULTS: After adjustment for sex, age, height, mean arterial pressure, leg lean and leg fat mass, a larger trunk fat mass was consistently associated with higher peripheral arterial stiffness (standardized beta (beta) of mean Z-scores of all three large arteries -0.24, P < 0.001). In contrast, larger leg fat mass (beta = 0.15, P = 0.009) and leg lean mass (beta = 0.09, P = 0.20) were associated with lower peripheral arterial stiffness. Trunk or leg fat mass were not associated with central arterial stiffness. Leg lean mass, however, was consistently associated with lower central arterial stiffness (beta = 0.29, P < 0.001). CONCLUSIONS: Trunk fat mass may have adverse effects on peripheral, but not on central arterial stiffness, while leg fat was not harmful and may have a slight protective effect. Larger leg lean mass was the most important determinant of lower central arterial stiffness. These results provide a pathophysiological framework to explain not only the higher cardiovascular risk in individuals with larger trunk fat mass, but also the reduced cardiovascular risk in individuals with larger leg lean and fat mass.     

Associação da Composição Corporal com Rigidez Arterial em Longevos

BackgroundArterial stiffness, obesity and sarcopenia correlate with each other and with cardiac outcomes in younger adults. However, there is little evidence of the association between body composition and markers of central arteries stiffness in long-lived people.ObjectiveTo evaluate the relationship between arterial stiffness and body composition in functionally independent long-lived individuals.MethodsThis is a cross-sectional analysis of the association between markers of arterial stiffness and body composition among participants in a longitudinal cohort of elderly individuals aged 80 years or older who were functionally independent and lived in the community . Body composition measurements were performed using dual energy X-ray absorptiometry (DEXA) and central circulation parameters (CCP) obtained by a non-invasive oscillometric method through the Mobil-O-Graph 24h PWA Monitor® device. The central parameters evaluated were: pulse wave velocity (PWV), augmentation Index (AIx), pulse pressure amplification index (PPAi) and central pulse pressure (cPP). These were correlated to total lean mass (LM) and appendicular lean mass (aLM), body fat percentage, and Baumgartner’s Index (BI). The level of significance was set at 5% for all tests.ResultsData from 124 elderly people with a mean age of 87.1 years (SD ± 4.3 years) were analyzed, with 74.2% of women and 57.3% of white. There was a statistically significant inverse correlation of AIx with LM (r = -0.391, p <0.001), aLM (r = -0.378, p <0.001), and BI (r = -0.258, p = 0.004). Also, cPP had an inversely proportional association with LM (r = -0.268, p = 0.003), aLM (r = -0.288, p = 0.001), and BI (r = -0.265, p = 0.003). When assessing the relationship between fat mass and CCP, a statistically significant direct relationship was observed only between AIx and body fat percentage (r = 0.197, p = 0.029).ConclusionIn long-lived people, body fat percentage is directly associated with arterial stiffness and inversely associated with the amount of LM. These findings may be associated with increased cardiovascular risk.     

Association between low thigh fat and non-alcoholic fatty liver disease

Background and Aim:  Some people have a fatty liver despite having low visceral fat and a low body mass index (BMI). We investigated whether fat distribution, especially thigh subcutaneous fat and thigh intramuscular fat, is associated with non-alcoholic fatty liver disease (NAFLD).
Methods:  The patients consisted of 408 men and women. NAFLD was defined by an ultrasound scan and excluded other liver diseases. Visceral, subcutaneous abdominal, intramuscular, and subcutaneous thigh adipose tissue was measured by computed tomography.
Results:  The frequency of NAFLD decreased over a quartile of thigh fat independently of BMI in the female patients. Additional adjustments for age and visceral fat area did not change the results. This finding was not observed in the male patients. To investigate the relationship between each fat distribution and NAFLD, we performed a logistic regression analysis. Fat distribution was divided into four groups: visceral fat, abdominal subcutaneous fat, thigh subcutaneous fat, and thigh intramuscular fat. All four fat components were chosen as variables for the regression model. Age, BMI, and the homeostasis model assessment (HOMA) index were then adjusted successively. A larger subcutaneous fat area was negatively associated with NAFLD after adjustment for visceral fat and abdominal subcutaneous fat areas in women, but not in men. It did not change even after age adjustment, BMI, and the HOMA index.
Conclusion:  Low femoral subcutaneous fat amounts were shown to be independently associated with fatty liver disease in women. These results show the importance of accurate measurements of other regional body compositions as well as visceral fat amounts when investigating NAFLD.     

Current and adolescent body fatness and fat distribution: relationships with carotid intima-media thickness and large artery stiffness at the age of 36 years

OBJECTIVE: Body fat and its distribution are determinants of cardiovascular disease but the underlying mechanisms of these adverse effects are poorly understood. We therefore investigated (1) the cross-sectional relationship between estimates of body fatness and its distribution on the one hand and carotid atherosclerosis and stiffness of the carotid, femoral and brachial arteries and the carotido-femoral segment on the other (336 subjects, 175 women); (2) the relationship between estimates of body fatness and its distribution during adolescence (13-16 years) and the same arterial properties at age 36- prospective analyses (subpopulation of 159 subjects, 84 girls). DESIGN: Cross-sectional and prospective analyses within an ongoing observational longitudinal study: The Amsterdam Growth and Health Longitudinal Study. METHODS: Body fatness and its distribution were assessed by anthropometry and dual-energy X-ray absorptiometry (DXA); arterial properties were assessed non-invasively by ultrasound imaging. RESULTS: Total adiposity and, in men, truncal subcutaneous fat accumulation during adolescence, were positively and independently associated with carotid intima-media thickness at age 36, a pre-clinical indicator of atherosclerosis. Adolescent truncal subcutaneous fat accumulation but not total adiposity was associated with increased arterial stiffness at age 36. At age 36, both abdominal and truncal subcutaneous fat were independently associated with arterial stiffness, while the associations between total adiposity and arterial stiffness appeared to be mediated by other cardiovascular risk factors. CONCLUSIONS: Body fatness and body fat distribution are associated with large artery structural and functional properties at age 36 and the roots of these associations may already be present in adolescence.     

2型糖尿病患者血清脂联素与肝脏脂肪含量的相关性研究

目的 探讨2型糖尿病患者血清脂联素水平与肝脏脂肪含量及相关临床指标的相关性.方法 选取天津市第三中心医院收治的初发2型糖尿病患者108例,以患者肝脏脂肪含量测定结果的平均数为切点将其分为2型糖尿病伴低肝脏脂肪含量组(T2DM+ LFC组)50例和2型糖尿病伴高肝脏脂肪含量组(T2DM+ HFC组)58例.应用高效液相层析法、葡萄糖氧化酶法、放射免疫法以及ELISA等分别对两组患者的相关临床指标及血清脂联素水平进行检测.采用t检验或X2检验进行组间对比,采用Spearman相关分析和多元逐步回归分析进行指标间关系判定,采用Logistic回归分析影响肝脏脂肪含量的危险因素.结果 T2DM+ HFC组血清脂联素水平显著低于T2DM+ LFC组(t=3.947,P=0.006).2型糖尿病患者血清脂联素水平与体重、体重指数、体脂含量、内脏脂肪面积、肝脏脂肪含量、甘油三酯水平呈显著负相关(r=-0.680 ～-0.225,P＜0.05或0.01).多元逐步回归分析显示,体重、体重指数和体脂含量是血清脂联素水平的独立相关因素.Logistic回归分析显示,体重(OR=1.288,95％ CI:1.009 ～ 1.644)、脂联素(OR=0.169,95％ CI:0.053 ～0.542)、γ-谷氨酰胺转肽酶(OR=1.155,95％ CI:1.032～ 1.293)及甘油三酯(OR=0.323,95％ CI:0.172～0.609)为2型糖尿病患者肝脏脂肪含量的影响因素.结论 血清脂联素水平与体重、体重指数和体脂含量密切相关,并可能在2型糖尿病患者肝脏脂质沉积过程中发挥重要调节作用.     

女性内脏脂肪指数与代谢综合征的关系

目的探讨北京沙河镇女性内脏脂肪指数与代谢综合征的关系。方法 2009年9月～10月纳入北京市昌平区（25～70）岁妇女2228名,采用生物电阻抗分析方法测量内脏脂肪指数,并调查其代谢综合征发病情况及体重、血压、血脂、血糖指标与内脏脂肪指数的关系。结果入组调查对象平均年龄（45.1±7.1）岁,内脏脂肪指数中位数为8（1～30）,代谢综合征患病率为33.3%;内脏脂肪指数与代谢综合征及体重、血压、血脂、血糖都存在相关性（P〈0.001）。将内脏脂肪指数用三分位数法划分为低、中、高指数组（分别对应1～7分,7～10分,10～30分）。各组间代谢综合征患病率和代谢指标发生风险均有统计学差异（P〈0.001）;Logistic回归分析显示内脏脂肪指数与代谢综合征具有相关性,经年龄调整后,中、高指数组的OR值分别为7.47（5.25～10.62）和32.34（22.74～45.98）。结论内脏脂肪指数检测方法且与代谢综合征具有显著相关性,可作为代谢综合征的筛查手段。