Habitual Exercise Decreases Serum Angiopoietin-related Growth Factor Levels In Healthy Human Subjects

Abstract

It is known that angiopoietin-related growth factor (AGF/Angptl6) potently regulates lipid, glucose, and energy metabolism. Previous studies in animal subjects suggest that AGF might be a potential regulator of metabolic homeostasis by counteracting obesity. However, human studies are lacking and the effect of regular exercise in AGF levels in humans has not yet been reported. PURPOSE: The objective of this study was to determine whether an association exists between AGF levels and exercise in healthy human subjects. METHODS: 18 healthy subjects (age 45.33±10.43) performed 50 minutes of supervised aerobic exercise four to five times per week for 12-weeks. Pre and post-training measurements were made. Body composition and body fat were measured by BoCA X1 analyzer. The predicted VO2max was determined using a treadmill test. Enzyme-linked immunosorbent assay (ELISA) was used to measure the AGF level in human serum. RESULTS: After the 12-week training program, there was a significant increase in maximal exercise capacity (VO2max=37.75±0.42) compared to before training (VO2max=33.54±0.36). Serum AGF concentrations decreased after 12 weeks training from 364.08±5.7 to 308.4±3.96 ng/ml (P=0.012). The decrease was inversely related to changes in BMI (P<0.0001), body fat (P<0.0001), waist-to-hip ratio (P<0.0007) and serum triglycerides (P<0.0029). In contrast, changes in serum AGF were positively related to serum HDL cholesterol (P<0.0012). Insulin sensitivity was also improved post training compared to before training from 4.29±0.15 to 2.25±0.09, as indicated by HOMA-IR. CONCLUSIONS: There have been no previous studies on AGF levels in healthy human subjects. Our study shows that habitual exercise significantly decreases serum AGF levels in humans. This finding is contrary to many former animal studies. Further studies in human subjects are warranted to validate these findings. In the future, AGF may be used as a therapeutic target for metabolic syndrome.