Gary D Miller1, Scott Isom2, Timothy M Morgan2, Mara Z Vitolins2, Caroline Blackwell2, K Bridget Brosnihan3, Debra I Diz3, Jeff Katula4, David Goff5. 1. Department of Health and Exercise Science, and Translational Science Center, Wake Forest University, United States. Electronic address: millergd@wfu.edu. 2. Department of Public Health Sciences, Wake Forest School of Medicine, United States. 3. Department of General Surgery and The Hypertension and Vascular Research Center, Wake Forest School of Medicine, United States. 4. Department of Health and Exercise Science, and Translational Science Center, Wake Forest University, United States. 5. Colorado School of Public Health, United States.
Abstract
AIMS: 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. MATERIALS AND METHODS: 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). RESULTS: 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. CONCLUSION: 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.
RCT Entities:
AIMS: 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. MATERIALS AND METHODS: 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). RESULTS: 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. CONCLUSION: 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.
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