Vasudevan Abu R, Wu Huaizhu, Xydakis Antonios M, Jones Peter H, Smith E O'Brian, Sweeney John F, Corry David B, Ballantyne Christie M
Division of Diabetes, Endocrinology, and Metabolism, Baylor College of Medicine, Houston, Texas 77030, USA.
J Clin Endocrinol Metab. 2006 Jan;91(1):256-61. doi: 10.1210/jc.2005-1280. Epub 2005 Nov 1.
Asthma and obesity incidence is increasing worldwide, and asthma is often more severe in the obese. Eotaxin, a CC chemokine, is important in extrinsic asthma, an inflammatory disorder.
Our objective was to examine the relation between eotaxin and obesity.
We conducted a comparison study of eotaxin in mice fed high-fat vs. standard chow diet for 26 wk, in obese vs. lean humans, in obese humans before and after 4-6 wk of weight loss, and in sc vs. visceral adipose tissue from patients undergoing bariatric surgery.
Our clinical study occurred in an outpatient weight loss program.
Patients were obese adults with metabolic syndrome (n = 40) and nine morbidly obese bariatric surgery patients.
Intervention was a very-low-calorie diet.
We assessed circulating eotaxin and eotaxin mRNA levels in adipose tissue.
Serum eotaxin levels were significantly higher in obese mice, and adipose mRNA levels correlated positively with serum eotaxin levels. Adipose tissue explants from obese mice showed increased secretion of eotaxin compared with explants from lean mice. In obese patients, plasma eotaxin levels were significantly higher than in lean controls and significantly reduced after weight loss, and eotaxin mRNA levels were 4.7-fold higher in visceral than sc adipose tissue.
Circulating eotaxin and eotaxin mRNA levels in visceral adipose tissue were increased in obesity in mice and humans. Adipose tissue explants secrete eotaxin, and the stromal/vascular component of adipose tissue seems to be the predominant source of eotaxin. Diet-induced weight loss in humans led to reduction in plasma eotaxin levels, demonstrating that clinical interventions that target obesity can modulate systemic eotaxin levels.
哮喘和肥胖症的发病率在全球范围内都在上升,并且哮喘在肥胖者中往往更为严重。嗜酸性粒细胞趋化因子是一种CC趋化因子,在外源性哮喘(一种炎症性疾病)中起重要作用。
我们的目的是研究嗜酸性粒细胞趋化因子与肥胖之间的关系。
我们进行了一项比较研究,比较了喂食高脂饮食与标准饲料26周的小鼠、肥胖者与瘦人、肥胖者在体重减轻4 - 6周前后以及接受减肥手术患者的皮下脂肪组织与内脏脂肪组织中的嗜酸性粒细胞趋化因子。
我们的临床研究在一个门诊减肥项目中进行。
患者为患有代谢综合征的肥胖成年人(n = 40)以及9名病态肥胖的减肥手术患者。
干预措施为极低热量饮食。
我们评估了循环中的嗜酸性粒细胞趋化因子以及脂肪组织中嗜酸性粒细胞趋化因子的mRNA水平。
肥胖小鼠的血清嗜酸性粒细胞趋化因子水平显著更高,脂肪组织中的mRNA水平与血清嗜酸性粒细胞趋化因子水平呈正相关。与瘦小鼠的脂肪组织外植体相比,肥胖小鼠的脂肪组织外植体显示出嗜酸性粒细胞趋化因子分泌增加。在肥胖患者中,血浆嗜酸性粒细胞趋化因子水平显著高于瘦对照组,且在体重减轻后显著降低,并且嗜酸性粒细胞趋化因子的mRNA水平在内脏脂肪组织中比皮下脂肪组织高4.7倍。
在小鼠和人类肥胖状态下,内脏脂肪组织中的循环嗜酸性粒细胞趋化因子和嗜酸性粒细胞趋化因子mRNA水平升高。脂肪组织外植体分泌嗜酸性粒细胞趋化因子,并且脂肪组织的基质/血管成分似乎是嗜酸性粒细胞趋化因子的主要来源。人类饮食诱导的体重减轻导致血浆嗜酸性粒细胞趋化因子水平降低,表明针对肥胖的临床干预可以调节全身嗜酸性粒细胞趋化因子水平。