Diabetes and Nutritional Sciences Division, School of Medicine, King's College London, London, United Kingdom.
Am J Clin Nutr. 2011 Jul;94(1):262-9. doi: 10.3945/ajcn.111.014209. Epub 2011 May 11.
Adiponectin gene expression is modulated by peroxisome proliferator-activated receptor γ, which is a transcription factor activated by unsaturated fatty acids.
We investigated the effect of the interaction between variants at the ADIPOQ gene locus, age, sex, body mass index (BMI), ethnicity, and the replacement of dietary saturated fatty acids (SFAs) with monounsaturated fatty acids (MUFAs) or carbohydrates on serum adiponectin concentrations.
The RISCK (Reading, Imperial, Surrey, Cambridge, and Kings) study is a parallel-design, randomized controlled trial. Serum adiponectin concentrations were measured after a 4-wk high-SFA (HS) diet and a 24-wk intervention with reference (HS), high-MUFA (HM), and low-fat (LF) diets. Single nucleotide polymorphisms at the ADIPOQ locus -11391 G/A (rs17300539), -10066 G/A (rs182052), -7734 A/C (rs16861209), and +276 G/T (rs1501299) were genotyped in 448 participants.
In white Europeans, +276 T was associated with higher serum adiponectin concentrations (n = 340; P = 0.006) and -10066 A was associated with lower serum adiponectin concentrations (n = 360; P = 0.03), after adjustment for age, BMI, and sex. After the HM diet, -10066 G/G subjects showed a 3.8% increase (95% CI: -0.1%, 7.7%) and G/A+A/A subjects a 2.6% decrease (95% CI: -5.6%, 0.4%) in serum adiponectin (P = 0.006 for difference after adjustment for the change in BMI, age, and sex). In -10066 G/G homozygotes, serum adiponectin increased with age after the HM diet and decreased after the LF diet.
In white -10066 G/G homozygotes, an HM diet may help to increase adiponectin concentrations with advancing age. This trial was registered at clinicaltrials.gov as ISRCTN29111298.
脂联素基因的表达受过氧化物酶体增殖物激活受体γ调节,后者是一种被不饱和脂肪酸激活的转录因子。
我们研究了 ADIPOQ 基因座的变异与年龄、性别、体重指数(BMI)、种族以及用单不饱和脂肪酸(MUFAs)或碳水化合物替代膳食饱和脂肪酸(SFAs)之间的相互作用对血清脂联素浓度的影响。
RISCK(雷丁、帝国理工学院、萨里、剑桥和国王学院)研究是一项平行设计的随机对照试验。在 4 周高 SFA(HS)饮食和 24 周参考(HS)、高 MUFA(HM)和低脂(LF)饮食干预后,测量血清脂联素浓度。在 448 名参与者中,对 ADIPOQ 基因座的单核苷酸多态性-11391 G/A(rs17300539)、-10066 G/A(rs182052)、-7734 A/C(rs16861209)和+276 G/T(rs1501299)进行了基因分型。
在白种欧洲人中,+276 T 与较高的血清脂联素浓度相关(n = 340;P = 0.006),-10066 A 与较低的血清脂联素浓度相关(n = 360;P = 0.03),调整年龄、BMI 和性别后。在 HM 饮食后,-10066 G/G 受试者血清脂联素增加 3.8%(95%CI:-0.1%,7.7%),G/A+A/A 受试者血清脂联素减少 2.6%(95%CI:-5.6%,0.4%)(P = 0.006,调整 BMI、年龄和性别变化后的差异)。在-10066 G/G 纯合子中,HM 饮食后血清脂联素随年龄增长而增加,LF 饮食后则减少。
在白种人-10066 G/G 纯合子中,HM 饮食可能有助于随着年龄的增长增加脂联素浓度。该试验在 clinicaltrials.gov 上注册为 ISRCTN29111298。