Lee AeJin, Jeon Kyeong Jin, Kim Min Soo, Kim Hye-Kyeong, Han Sung Nim
Department of Food and Nutrition, College of Human Ecology, Seoul National University, Seoul, Korea.
Department of Food Science and Nutrition, The Catholic University of Korea, Bucheon, Korea.
Nutr Res. 2015 Apr;35(4):301-8. doi: 10.1016/j.nutres.2015.02.004. Epub 2015 Feb 24.
Obesity has been reported to impair immune functions and lead to low-grade long-term inflammation; however, studies that have investigated the impact of weight loss on these among the young and slightly obese are limited. Thus, we investigated the effect of a 12-week weight management program with behavioral modifications on cell-mediated immune functions and inflammatory responses in young obese participants. Our hypothesis was that weight loss would result in improved immune functions and decreased inflammatory responses. Sixty-four participants (45 obese and 19 normal weight) finished the program. Obese (body mass index ≥25) participants took part in 5 group education and 6 individual counseling sessions. Normal-weight (body mass index 18.5-23) participants only attended 6 individual sessions. The goal for the obese was to lose 0.5 kg/wk by reducing their intake by 300 to 500 kcal/d and increasing their physical activity. Program participation resulted in a modest but significant decrease in weight (2.7 ± 0.4 kg, P < .001) and lipopolysaccharide-stimulated interleukin-1β production (from 0.85 ± 0.07 to 0.67 ± 0.07 ng/mL, P < .05) in the obese. In the obese group, increase in phytohemagglutinin-stimulated interleukin-10 production, a TH2 and anti-inflammatory cytokine, approached significance after program participation (from 6181 ± 475 to 6970 ± 632 pg/mL, P = .06). No significant changes in proliferative responses to the optimal concentration of concanavalin A or phytohemagglutinin were observed in the obese after program participation. Collectively, modest weight loss did not change the cell-mediated immune functions significantly but did attenuate the inflammatory response in young and otherwise healthy obese adults.
据报道,肥胖会损害免疫功能并导致低度长期炎症;然而,研究年轻人和轻度肥胖者体重减轻对这些方面影响的研究有限。因此,我们研究了一项为期12周、包含行为调整的体重管理计划对年轻肥胖参与者细胞介导免疫功能和炎症反应的影响。我们的假设是体重减轻将导致免疫功能改善和炎症反应降低。64名参与者(45名肥胖者和19名正常体重者)完成了该计划。肥胖(体重指数≥25)参与者参加了5次小组教育和6次个人咨询会议。正常体重(体重指数18.5 - 23)参与者仅参加了6次个人会议。肥胖者的目标是通过每天减少300至500千卡热量摄入并增加身体活动,每周减重0.5千克。参与该计划使肥胖者体重适度但显著下降(2.7±0.4千克,P <.001),脂多糖刺激的白细胞介素 - 1β产生量也下降(从0.85±0.07降至0.67±0.07纳克/毫升,P <.05)。在肥胖组中,参与计划后,植物血凝素刺激的白细胞介素 - 10产生量增加,白细胞介素 - 10是一种TH2和抗炎细胞因子,接近显著水平(从6181±475升至6970±632皮克/毫升,P = .06)。参与计划后,肥胖者对最佳浓度伴刀豆球蛋白A或植物血凝素的增殖反应未观察到显著变化。总体而言,适度体重减轻并未显著改变细胞介导免疫功能,但确实减弱了年轻且其他方面健康的肥胖成年人的炎症反应。