Snijder M B, Flyvbjerg A, Stehouwer C D A, Frystyk J, Henry R M A, Seidell J C, Heine R J, Dekker J M
Department of Health Sciences, VU University Amsterdam, Amsterdam, The Netherlands.
Eur J Endocrinol. 2009 Mar;160(3):387-95. doi: 10.1530/EJE-08-0817. Epub 2008 Dec 18.
To investigate whether adiponectin is associated with arterial stiffness, and whether adiponectin explains the association between body composition and arterial stiffness.
Cross-sectional cohort study.
Subjects were participants (n=456, mean age 68.9+/-6.1 years; age range 60-86 years) of the third follow-up examination of the Hoorn Study. Trunk fat, leg fat, trunk lean, and leg lean mass were measured by dual-energy X-ray absorptiometry. Ultrasound was used to measure distensibility and compliance of the carotid, femoral, and brachial arteries, and carotid Young's elastic modulus (as estimates of peripheral arterial stiffness). Results Trunk fat mass was negatively associated with (ln-transformed) adiponectin (standardized beta=-0.49, P<0.001), while leg fat mass was positively associated with adiponectin (beta=0.44, P<0.001), after adjustment for each other, age, and lean mass. After adjustment for age, sex, mean arterial pressure, and estimated glomerular filtration rate, higher adiponectin was associated with decreased peripheral arterial stiffness (beta of mean Z-scores of all three arteries=0.14, P=0.001). However, the associations of trunk fat (beta=-0.26, P<0.001) and leg fat (beta=0.16, P=0.006) with peripheral arterial stiffness were only minimally explained by adiponectin levels.
Trunk fat and leg fat are oppositely associated with adiponectin. Although low adiponectin was a determinant of increased peripheral arterial stiffness, it only explained a small part of the association between body fat and peripheral arterial stiffness. This indicated that factors other than adiponectin may be more important in the pathophysiological mechanisms by which abdominal obesity leads to arterial stiffness.
研究脂联素是否与动脉僵硬度相关,以及脂联素是否能解释身体成分与动脉僵硬度之间的关联。
横断面队列研究。
研究对象为霍恩研究第三次随访检查的参与者(n = 456,平均年龄68.9±6.1岁;年龄范围60 - 86岁)。采用双能X线吸收法测量躯干脂肪、腿部脂肪、躯干瘦体重和腿部瘦体重。使用超声测量颈动脉、股动脉和肱动脉的扩张性和顺应性,以及颈动脉杨氏弹性模量(作为外周动脉僵硬度的估计值)。结果在相互调整、年龄和瘦体重后,躯干脂肪量与(经自然对数转换的)脂联素呈负相关(标准化β=-0.49,P<0.001),而腿部脂肪量与脂联素呈正相关(β=0.44,P<0.001)。在调整年龄、性别、平均动脉压和估计肾小球滤过率后,较高的脂联素与外周动脉僵硬度降低相关(所有三条动脉平均Z分数的β=0.14,P = 0.001)。然而,脂联素水平仅略微解释了躯干脂肪(β=-0.26,P<0.001)和腿部脂肪(β=0.16,P = 0.006)与外周动脉僵硬度之间的关联。
躯干脂肪和腿部脂肪与脂联素的关联相反。虽然低脂联素是外周动脉僵硬度增加的一个决定因素,但它仅解释了身体脂肪与外周动脉僵硬度之间关联的一小部分。这表明在腹部肥胖导致动脉僵硬度的病理生理机制中,脂联素以外的因素可能更重要。