Miller Gary D, Isom Scott, Morgan Timothy M, Vitolins Mara Z, Blackwell Caroline, Brosnihan K Bridget, Diz Debra I, Katula Jeff, Goff David
Department of Health and Exercise Science, and Translational Science Center, Wake Forest University, United States.
Department of Public Health Sciences, Wake Forest School of Medicine, United States.
Diabetes Metab Syndr. 2014 Oct-Dec;8(4):205-11. doi: 10.1016/j.dsx.2014.09.003. Epub 2014 Oct 5.
Obesity is associated with metabolic dysfunctions, which may be mediated by changes in adipose tissue signaling factors. These molecules are denoted as Adipose Tissue Generated Mediators of CardioVascular Risk (ATGMCVR) here, and include leptin, adiponectin, C-reactive protein (CRP), interleukin 6 (IL-6), tumor necrosis factor alpha (TNFα), and plasminogen activator inhibitor 1 (PAI-1). This study examined the effect of a weight loss program on ATGMCVR in obese adults with prediabetes.
Subjects were randomized to usual care (UC; n=15) or lifestyle weight loss groups (LWL; n=15). LWL was a community-based weight loss intervention to promote physical activity and healthy eating. ATGMCVR at 1-year were compared between groups by analysis of covariance; baseline value of the mediator was the covariate. Baseline means for ATGMCVR were compared between those with (n=21) and without (n=9) metabolic syndrome (MetS).
At baseline, subjects were 58±9 (SD) years, 70% female, with a BMI of 34±4kg/m(2). One-year weight loss (%) was 7.8±6.0% for LWL and 1.7±4.5% for UC. Group differences at 1-year were noted (adjusted means [95%CI] for UC and LWL, respectively) for adiponectin (8526.3 [7397.7, 9827]; 10,870.9 [9432.0, 12,529.3]ng/ml; p=0.02), leptin (30.4 [26.1, 35.4]; 23.7 [20.3, 27.5]ng/ml; p=0.02), IL-6 (0.4 [0.3, 0.5]; 0.2 [0.1, 0.2] pg/ml; p=0.001), and PAI-1 (50 [42.7, 58.7]; 36.2 [30.8, 42.4]pg/ml; p=0.01). No differences in baseline ATGMCVR were seen between subjects with and without MetS.
These findings suggest ATGMCVR can be improved with weight loss; larger studies are needed to determine if improvements in metabolic dysfunction are related to changes in ATGMCVR.
肥胖与代谢功能障碍相关，这可能由脂肪组织信号因子的变化介导。这些分子在此被称为心血管风险的脂肪组织生成介质（ATGMCVR），包括瘦素、脂联素、C反应蛋白（CRP）、白细胞介素6（IL-6）、肿瘤坏死因子α（TNFα）和纤溶酶原激活物抑制剂1（PAI-1）。本研究调查了减肥计划对患有糖尿病前期的肥胖成年人ATGMCVR的影响。
受试者被随机分为常规护理组（UC；n = 15）或生活方式减肥组（LWL；n = 15）。LWL是一项基于社区的减肥干预措施，旨在促进体育活动和健康饮食。通过协方差分析比较两组1年时的ATGMCVR；介质的基线值作为协变量。比较了患有（n = 21）和未患有（n = 9）代谢综合征（MetS）的受试者的ATGMCVR基线均值。
基线时，受试者年龄为58±9（标准差）岁，70%为女性，体重指数为34±4kg/m²。LWL组1年的体重减轻（%）为7.8±6.0%，UC组为1.7±4.5%。两组在1年时存在差异（UC组和LWL组的调整均值[95%置信区间]），脂联素（8526.3[7397.7, 9827]；10870.9[9432.0, 12529.3]ng/ml；p = 0.02）、瘦素（30.4[26.1, 35.4]；23.7[20.3, 27.5]ng/ml；p = 0.02）、IL-6（0.4[0.3, 0.5]；0.2[0.1, 0.2]pg/ml；p = 0.001）和PAI-1（50[42.7, 58.7]；36.2[30.8, 42.4]pg/ml；p = 0.01）。患有和未患有MetS的受试者在ATGMCVR基线时未见差异。
这些发现表明减肥可改善ATGMCVR；需要更大规模的研究来确定代谢功能障碍的改善是否与ATGMCVR的变化有关。
