Duggan Catherine, de Dieu Tapsoba Jean, Mason Caitlin, Imayama Ikuyo, Korde Larissa, Wang Ching-Yun, McTiernan Anne
Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington.
Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington. University of Washington, Seattle, Washington.
Cancer Prev Res (Phila). 2015 Jul;8(7):628-35. doi: 10.1158/1940-6207.CAPR-14-0449. Epub 2015 Apr 23.
Obesity and vitamin D deficiency are associated with risk for several cancers, possibly through inflammation and adipokine-related pathways. Two hundred and eighteen postmenopausal women with BMI > 25 kg/m(2) and low serum 25-hydroxyvitamin D (25(OH)D; ≥10-<32 ng/mL), were randomized to 12 months of either (i) weight-loss intervention + 2000 IU/day oral vitamin D3 or (ii) weight-loss intervention + daily placebo. Serum adiponectin, leptin, TNFα, IL6, IL1β, IL8, and IL10, were measured by immunoassay, and a composite inflammatory biomarker score calculated. Using generalized estimating equations, mean changes in outcomes were compared between arms (intent-to-treat), adjusted for possible confounders. Analyses were also stratified by weight-loss (gained/no weight-loss; <5%; 5% to 10%; ≥10%). At 12 months, there were no significant differences in analyte changes between arms. In stratified analyses, participants randomized to vitamin D3 who lost 5% to 10% of baseline weight, versus participants who gained weight/had no weight-loss, had significantly greater decreases in levels of IL6 compared with those randomized to placebo: absolute change -0.75 pg/mL (-17.2%), placebo versus -1.77 pg/mL (-37.3%), vitamin D, P = 0.004. Similar but attenuated results were observed for participants who lost ≥10% of baseline weight: -0.41 pg/mL (-13.6%), placebo versus -0.67 pg/mL (-17.3%), vitamin D, P = 0.02. Effects of vitamin D3 supplementation on levels of IL1β were inconsistent when stratified by weight loss. There were no intervention effects on IL10, TNFα, IL8, the composite score, adiponectin, or leptin, when stratified by weight-loss. In conclusion, vitamin D3 supplementation in combination with weight-loss of at least 5% of baseline weight was associated with significant reductions in levels of IL6.
肥胖和维生素D缺乏与多种癌症风险相关,可能是通过炎症和脂肪因子相关途径。218名体重指数(BMI)>25kg/m²且血清25-羟维生素D(25(OH)D;≥10 - <32ng/mL)水平低的绝经后女性,被随机分为两组,进行为期12个月的干预:(i)减肥干预 + 每日口服2000IU维生素D3或(ii)减肥干预 + 每日安慰剂。采用免疫测定法测量血清脂联素、瘦素、肿瘤坏死因子α(TNFα)、白细胞介素6(IL6)、白细胞介素1β(IL1β)、白细胞介素8(IL8)和白细胞介素10(IL10),并计算复合炎症生物标志物评分。使用广义估计方程,比较两组(意向性治疗)结局的平均变化,并对可能的混杂因素进行调整。分析还按体重减轻情况分层(体重增加/未减重;<5%;5%至10%;≥10%)。12个月时,两组间分析物变化无显著差异。在分层分析中,与体重增加/未减重的参与者相比,随机接受维生素D3且体重减轻了基线体重5%至10%的参与者,其IL6水平的下降幅度明显大于随机接受安慰剂的参与者:绝对变化为 -0.75pg/mL(-17.2%),安慰剂组对比维生素D组为 -1.77pg/mL(-37.3%),P = 0.004。对于体重减轻≥基线体重10%的参与者,观察到类似但减弱的结果:-0.41pg/mL(-13.6%),安慰剂组对比维生素D组为 -0.67pg/mL(-17.3%),P = 0.02。按体重减轻情况分层时,补充维生素D3对IL1β水平的影响不一致。按体重减轻情况分层时,对IL10、TNFα、IL8、复合评分、脂联素或瘦素均无干预作用。总之,补充维生素D3并结合至少减轻基线体重5%与IL6水平显著降低相关。