Jain Shilpa H, Massaro Joseph M, Hoffmann Udo, Rosito Guido A, Vasan Ramachandran S, Raji Annaswamy, O'Donnell Christopher J, Meigs James B, Fox Caroline S
Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Diabetes Care. 2009 May;32(5):903-8. doi: 10.2337/dc08-1733. Epub 2009 Feb 17.
To test the association of regional fat depots with circulating adiponectin and resistin concentrations and to assess the potential mediating effect of adipokines on associations between abdominal fat depots and cardiometabolic risk factors.
Participants from the Framingham Heart Study offspring cohort (n = 916, 55% women; mean age 59 years) free of cardiovascular disease underwent computed tomography measurement of visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), pericardial fat, and intrathoracic fat volumes and assays of circulating adiponectin and resistin.
VAT, SAT, pericardial fat, and intrathoracic fat were negatively correlated with adiponectin (r = -0.19 to -0.34, P < 0.001 [women]; r = -0.15 to -0.26, P < 0.01 [men] except SAT) and positively correlated with resistin (r = 0.16-0.21, P < 0.001 [women]; r = 0.11-0.14, P < 0.05 [men] except VAT). VAT increased the multivariable model R(2) for adiponectin from 2-4% to 10-13% and for resistin from 3-4% to 3-6%. Adjustment for adipokines did not fully attenuate associations between VAT, SAT, and cardiometabolic risk factors.
Adiponectin and resistin are correlated with fat depots cross-sectionally, but none of the adipokines can serve as surrogates for the fat depots. Relations between VAT, SAT, and cardiometabolic risk factors were not fully explained by adiponectin or resistin concentrations.
检验局部脂肪储存与循环脂联素和抵抗素浓度之间的关联,并评估脂肪因子在腹部脂肪储存与心脏代谢危险因素之间的关联中所起的潜在中介作用。
来自弗雷明汉心脏研究后代队列的参与者(n = 916,55%为女性;平均年龄59岁),无心血管疾病,接受了内脏脂肪组织(VAT)、皮下脂肪组织(SAT)、心包脂肪和胸腔内脂肪体积的计算机断层扫描测量,以及循环脂联素和抵抗素的检测。
VAT、SAT、心包脂肪和胸腔内脂肪与脂联素呈负相关(r = -0.19至-0.34,P < 0.001[女性];r = -0.15至-0.26,P < 0.01[男性],SAT除外),与抵抗素呈正相关(r = 0.16 - 0.21,P < 0.001[女性];r = 0.11 - 0.14,P < 0.05[男性],VAT除外)。VAT使脂联素的多变量模型R²从2 - 4%增加到10 - 13%,使抵抗素的多变量模型R²从3 - 4%增加到3 - 6%。对脂肪因子进行调整并未完全减弱VAT、SAT与心脏代谢危险因素之间的关联。
脂联素和抵抗素与脂肪储存在横断面水平上相关,但没有一种脂肪因子可以作为脂肪储存的替代指标。VAT、SAT与心脏代谢危险因素之间的关系不能完全由脂联素或抵抗素浓度来解释。