Markers of Inflammation and Fat Distribution Following Weight Loss in African‐American and White Women

Department of Nutrition Sciences, University of Alabama-Birmingham, Birmingham, Alabama, USA.
Obesity (Impact Factor: 3.73). 04/2011; 20(4):715-20. DOI: 10.1038/oby.2011.85
Source: PubMed


Changes in markers of inflammation (MOI) and fat distribution with weight loss between African-American (AA) and white (W) women have yet to be characterized. The purpose of this study was to examine potential ethnic differences in MOI and regional fat distribution with weight loss, and identify the associations between these markers and changes in regional fat distribution with weight loss among AA and W women. Subjects were 126 healthy, premenopausal women, BMI 27-30 kg/m(2). They were placed on a weight-loss intervention consisting of diet and/or exercise until a BMI <25 was achieved. Fat distribution was measured with computed tomography, and body composition with dual-energy X-ray absorptiometry. Serum concentrations of tumor necrosis factor-α (TNF-α), soluble TNF receptor-I (sTNFR-I), sTNFR-II, C-reactive protein (CRP), and interleukin-6 (IL-6) were assessed. All MOI and adiposity measures significantly decreased with weight loss. Significant ethnic differences with weight loss were observed for fat mass, body fat, intra-abdominal adipose tissue (IAAT), sTNFR-I, and sTNFR-II. Mixed-model analysis indicated that adjusting for change in IAAT explained ethnic differences in change in TNF-α and the decrease in TNF-α with weight loss, while total fat mass only explained the decrease in sTNFR-I and sTNFR-II with weight loss. In conclusion, all MOI decreased following weight loss among W, whereas only IL-6 and CRP decreased following weight loss in AA. The most distinct phenotypic difference observed was a greater impact of weight loss on TNF-α in W compared to AA, which was directly associated with IAAT in W.

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Available from: Gordon Fisher, Oct 21, 2014
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    • "In mice, a reduction in abdominal adiposity obtained by bariatric surgery was accompanied by an improvement in adipose tissue inflammation [24]. In white women Fisher et al. found that caloric restriction induced weight loss resulted in a greater TNF-α decrease as compared to Afro American women and that this could be explained by a greater loss of intra abdominal adipose tissue as measured by dual-energy X-ray absorptiometry [25]. Our study is the first in which visceral and subcutaneous fat loss are directly compared in terms of association with changes in adipokynes profile. "
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    ABSTRACT: Obesity is characterized by a low grade chronic inflammation state. Indeed circulating pro-inflammatory cytokines, such as TNF-α and IL-6, are elevated in obese subjects, while anti-inflammatory cytokines, such as IL-10, appear to be reduced. Cytokines profile improves after weight loss, but how visceral or subcutaneous fat loss respectively affect pro- or anti-inflammatory cytokines plasma levels has not been precisely assessed. Therefore in the present study we correlated changes in circulating cytokine profile with quantitative changes in visceral and subcutaneous adipose tissue depots measured by an ad hoc Magnetic Resonance Imaging (MRI) protocol before and after weight loss. In 14 obese subjects, MRI determination of visceral and subcutaneous fat and plasma glucose, insulin, TNF-α IL-6, and IL-10 measurements were performed before and after a caloric restriction induced weight loss of at least 5% of the original body weight. WEIGHT LOSS IMPROVED INSULIN SENSITIVITY (QUICKI INDEX: 0.35±0.03 vs 0.37±0.04; P<0.05), increased IL-10 (3.4±1.9 vs 4.6±1.0 pg/mL; P<0.03), and reduced TNF-α and IL-6 plasma levels (2.5±1.3 vs 1.6±1.5 pg/mL, P<0.0015, 2.3±0.4 vs 1.6±0.6 pg/mL, P<0.02 respectively). A significant correlation was observed between the amount of visceral fat loss and the percentage reduction in both TNF-α (r = 0.56, p<0.05) and IL-6 (r = 0.19 p<0.05) plasma levels. In a multiple regression analysis, the amount of visceral fat loss independently correlated with the increase in IL-10 plasma levels. The reduction in visceral adipose tissue is the main driver of the improved inflammatory profile induced by weight loss.
    Full-text · Article · Dec 2012 · PLoS ONE
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    • "However to date, results vary as to whether or not inflammation differs between AA and EA. Khera et al. found higher hs-CRP concentrations among AA men and women between ages 30–65 years as compared to EA [12], whereas we have previously shown no differences in hs-CRP concentrations between AA and EA premenopausal women [13]. Additionally, AA have been shown to have greater arterial stiffness and endothelial dysfunction compared to EA [14] [15] [16]. "
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    ABSTRACT: Elevated serum high-sensitivity C-reactive protein (hs-CRP) and low serum 25-hydroxyvitamin D [25(OH)D] are associated with increased cardiovascular disease (CVD) risk. Ethnic differences in serum hs-CRP and 25(OH)D concentrations and CVD are known. to investigate the ethnic differences in hs-CRP concentrations, to assess the influence of 25(OH)D on these ethnic differences and to examine the influence of 25(OH)D on association between hs-CRP and cardiovascular health indices. 62 healthy adults [26 African Americans (AA), 26 European Americans (EA), and 10 Hispanic Americans (HA)], ages 18-55 years. Serum hs-CRP and 25(OH)D as well as pulse wave velocity (PWV), augmentation index (AIx), and flow-mediated dilatation (FMD) were measured. hs-CRP was inversely associated with 25(OH)D (r = -0.25, P = 0.049), and hs-CRP was positively associated with PWV (r = 0.29, P = 0.04). The association of hs-CRP with PWV attenuated after adjustment for 25(OH)D (P = 0.15). hs-CRP was higher in AA compared to EA (P = 0.05); this differences was reduced by 32% after adjusting for serum 25(OH)D. eventhough the inverse association between serum 25(OH)D and CRP does not infer causality, lower serum 25(OH)D may increase risk for inflammation and endothelial dysfunction. The lower 25(OH)D in AA may predispose to greater inflammation and associated vascular dysfunction.
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    No preview · Article · Mar 2012 · The Journal of Clinical Endocrinology and Metabolism
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