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 β-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·m−2) volunteered to participate in a 12-wk supervised exercise program (5 d·wk−1, 60 min·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 V˙O2max (21.1 ± 0.9 vs 24.2 ± 1.1 mL·kg−1·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 cm2, P < 0.001), and SAT (369 ± 34 vs 309 ± 41 cm2, P < 0.02). Area under the glucose (450 ± 31 vs 392 ± 33 mmol·L−1·2 h−1, P < 0.01) and insulin (45,767 ± 6142 vs 35,277 ± 4997 pmol·L−1·2 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·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.
1Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH; 2Department of Physiology, Case Western Reserve University School of Medicine, Cleveland, OH; 3Department of Health and Physical Education, Cleveland State University, Cleveland, OH; 4Department of Obstetrics and Gynecology, Mayo Clinic, Rochester, MN; and 5Department of Gastroenterology/Hepatology, Cleveland Clinic, Cleveland, OH
Address for correspondence: John P. Kirwan, Ph.D., Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Ave/NE-40, Cleveland, OH 44195; E-mail: email@example.com.
Submitted for publication October 2008.
Accepted for publication November 2008.