Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA.
Med Sci Sports Exerc. 2009 Jun;41(6):1255-60. doi: 10.1249/MSS.0b013e318195bad5.
Nampt/pre-B-cell colony-enhancing factor/visfatin (visfatin) release from adipocytes has recently been suggested to be nutrient responsive and linked to systemic nicotinamide adenine dinucleotide biosynthesis and regulation of pancreatic beta-cell function.
We hypothesized that if visfatin does play a role in the insulin response, then the exercise training-induced reduction in insulin response to an oral glucose load would correlate with reduced plasma visfatin.
Sixteen obese men and women (age = 65 +/- 1 yr, body mass index = 33.4 +/- 1.5 kg x m(-2)) volunteered to participate in a 12-wk supervised exercise program (5 d x wk(-1), 60 min x d(-1) at 85% of HRmax). Visceral (VAT) and subcutaneous adipose tissue (SAT) were measured by computed tomographic scans. A 2-h 75-g oral glucose tolerance test was performed to determine the effect of exercise training on the insulin response to a glucose load. Fasting plasma visfatin was measured by enzyme-linked immunosorbent assay.
Exercise training resulted in an increase in (.)VO2max (21.1 +/- 0.9 vs 24.2 +/- 1.1 mL x kg(-1) x min(-1), P < 0.001), a decrease in body weight (96.4 +/- 4.1 vs 92.4 +/- 3.7 kg, P < 0.001), VAT (191 +/- 16 vs 144 +/- 16 cm, P < 0.001), and SAT (369 +/- 34 vs 309 +/- 41 cm, P < 0.02). Area under the glucose (450 +/- 31 vs 392 +/- 33 mmol x L(-1) x 2 h(-1), P < 0.01) and insulin (45,767 +/- 6142 vs 35,277 +/- 4997 pmol x L(-1) x 2 h(-1), P < 0.003) response curves were decreased after training. After intervention, plasma visfatin levels were significantly reduced (16.9 +/- 2.2 vs 14.5 +/- 1.8 ng x mL(-1), P < 0.05), and the change in visfatin was associated with the corresponding change in insulin (r = 0.56, P < 0.05) and glucose AUC (r = 0.53, P < 0.05).
The exercise-induced reduction of plasma visfatin is most likely the result of weight loss and body composition changes. The potential regulatory role of visfatin in mediating the pancreatic insulin response to oral glucose requires further investigation.
如果内脂素确实在胰岛素反应中发挥作用，那么我们推测，运动训练引起的口服葡萄糖负荷后胰岛素反应的降低与血浆内脂素的减少相关。
16 名肥胖男女（年龄=65 ± 1 岁，体重指数=33.4 ± 1.5kg/m2）志愿参加 12 周的监督运动计划（每周 5 天，每天 60 分钟，运动强度为 85%最大心率）。通过计算机断层扫描测量内脏（VAT）和皮下脂肪组织（SAT）。进行 2 小时 75g 口服葡萄糖耐量试验，以确定运动训练对葡萄糖负荷后胰岛素反应的影响。通过酶联免疫吸附试验测量空腹血浆内脂素。
运动训练导致（.）VO2max 增加（21.1 ± 0.9 比 24.2 ± 1.1mL/kg/min，P<0.001）、体重减轻（96.4 ± 4.1 比 92.4 ± 3.7kg，P<0.001）、VAT 减少（191 ± 16 比 144 ± 16cm，P<0.001）和 SAT 减少（369 ± 34 比 309 ± 41cm，P<0.02）。葡萄糖（450 ± 31 比 392 ± 33mmol/L×2h，P<0.01）和胰岛素（45767 ± 6142 比 35277 ± 4997pmol/L×2h，P<0.003）曲线下面积均降低。运动后，血浆内脂素水平显著降低（16.9 ± 2.2 比 14.5 ± 1.8ng/mL，P<0.05），且内脂素的变化与胰岛素（r=0.56，P<0.05）和葡萄糖 AUC（r=0.53，P<0.05）的相应变化相关。
运动引起的血浆内脂素减少很可能是体重减轻和身体成分变化的结果。内脂素在调节口服葡萄糖后胰腺胰岛素反应中的潜在调节作用需要进一步研究。
