Strandberg Louise, Mellström Dan, Ljunggren Osten, Grundberg Elin, Karlsson Magnus K, Holmberg Anna H, Orwoll Eric S, Eriksson Anna L, Svedberg Johan, Bengtsson Magnus, Ohlsson Claes, Jansson John-Olov
Institute of Neuroscience and Physiology/Endocrinology, Sahlgrenska Academy, Göteborg University, Göteborg, Sweden.
Obesity (Silver Spring). 2008 Mar;16(3):710-3. doi: 10.1038/oby.2007.95. Epub 2008 Jan 17.
There is growing evidence that immune functions are linked to the regulation of body fat. Our studies of knockout mice indicate that both endogenous interleukin (IL)-6 and IL-1 can suppress mature-onset obesity. We now investigated whether four common polymorphisms of the IL6 and IL1 systems are associated with the fat mass measured with dual-energy X-ray absorptiometry (DXA) in elderly men (n = 3,014). The study subjects were from the Swedish part of the MrOS multicenter population study and 69-81 years of age. The IL6 -174 G>C (Minor allele frequency (MAF) = 48%) gene promoter polymorphism was associated with the primary outcome total fat mass (P = 0.006) and regional fat masses, but not with lean body mass. The IL1B -31T>C (MAF = 34%) polymorphism was also associated with total fat (P = 0.007) and regional fat masses, but not lean body mass. The IL-1 receptor antagonist (IL-1ra) gene (IL1RN) +2018 T>C (MAF = 27%) polymorphism (in linkage disequilibrium (LD) with a well-studied variable number tandem repeat of 86 base pair (bp)) and IL1B +3953 C>T (MAF = 26%) polymorphism were not associated with total fat mass. In conclusion, the IL-1 and IL-6 systems, shown to suppress mature-onset obesity in experimental animals, contain gene polymorphisms that are associated with fat, but not lean, mass in elderly men.
越来越多的证据表明，免疫功能与身体脂肪的调节有关。我们对基因敲除小鼠的研究表明，内源性白细胞介素（IL）-6和IL-1均可抑制成年期肥胖。我们现在研究了IL6和IL1系统的四种常见多态性是否与老年男性（n = 3014）通过双能X线吸收法（DXA）测量的脂肪量相关。研究对象来自MrOS多中心人群研究的瑞典部分，年龄在69至81岁之间。IL6 -174 G>C（次要等位基因频率（MAF）= 48%）基因启动子多态性与主要结局总脂肪量（P = 0.006）和局部脂肪量相关，但与瘦体重无关。IL1B -31T>C（MAF = 34%）多态性也与总脂肪（P = 0.007）和局部脂肪量相关，但与瘦体重无关。IL-1受体拮抗剂（IL-1ra）基因（IL1RN）+2018 T>C（MAF = 27%）多态性（与一个研究充分的86碱基对（bp）可变数目串联重复处于连锁不平衡（LD）状态）和IL1B +3953 C>T（MAF = 26%）多态性与总脂肪量无关。总之，在实验动物中显示可抑制成年期肥胖的IL-1和IL-6系统，包含与老年男性脂肪量而非瘦体重相关的基因多态性。
