ABSTRACT
AIM: Based on its regulatory action on glucagon-like peptide 1, dipeptidyl peptidase IV (DPP-IV) has increasingly been linked to Type 2 diabetes. However, there is no evidence as to how this normal modulatory enzyme leads to pathology. It is thought that DPP-IV is affected by the development of obesity, which is a common precursor to Type 2 diabetes. Little is known about the relationship between DPP-IV activity in plasma and specific body composition measures. MAIN METHODS: In the current study, plasma DPP-IV activity and body composition measures were collected from 111 healthy subjects between the ages of 19 and 70 years old for analysis. KEY FINDINGS: The mean plasma DPP-IV activity was 35.9U/L ± 12.3, falling within normal reference value range presented by Durinx et al. DPP-IV activity was negatively correlated with absolute body fat mass, but absolute lean mass was positively correlated. Consistent with the findings, DPP-IV activity was also negatively correlated with absolute gynoid fat (p = 0.0047). DPP-IV activity did not have a significant correlation with absolute android fat mass, visceral adipose tissue, BMI, and age. SIGNIFICANCE: From these results, it can be concluded that high activity of DPP-IV is not indicative of pathology, and specific body composition components may influence soluble DPP-IV activity in the blood.
ABSTRACT
Regular physical activity is effective in reducing visceral white adipose tissue (AT) inflammation and oxidative stress, and these changes are commonly associated with reduced adiposity. However, the impact of multiple periods of physical activity, intercalated by periods of inactivity, i.e., intermittent physical activity, on markers of AT inflammation and oxidative stress is unknown. In the present study, 5-wk-old male C57BL/6 mice were randomized into three groups (n = 10/group): sedentary, regular physical activity, and intermittent physical activity, for 24 wk. All animals were singly housed and fed a diet containing 45% kcal from fat. Regularly active mice had access to voluntary running wheels throughout the study period, whereas intermittently active mice had access to running wheels for 3-wk intervals (i.e., 3 wk on/3 wk off) throughout the study. At death, regular and intermittent physical activity was associated with similar reductions in visceral AT mass (approximately -24%, P < 0.05) relative to sedentary. However, regularly, but not intermittently, active mice exhibited decreased expression of visceral AT genes related to inflammation (e.g., monocyte chemoattractant protein 1), immune cell infiltration (e.g., CD68, CD11c, F4/80, CD11b/CD18), oxidative stress (e.g., p47 phagocyte oxidase), and endoplasmic reticulum stress (e.g., CCAAT enhancer-binding protein homologous protein; all P < 0.05). Furthermore, regular, but not intermittent, physical activity was associated with a trend toward improvement in glucose tolerance (P = 0.059). Collectively, these findings suggest that intermittent physical activity over a prolonged period of time may lead to a reduction in adiposity but with retention of a sedentary obese white AT and metabolic phenotype.
