Effect of Adipokine Secretion from Ectopic Fats on The Exercise-Induced Reduction of Arterial Stiffness

Abstract

Aging-induced increase in fat accumulation causes arterial stiffness. Ectopic fat accumulation with aging may be more important than whole-body fat content for predicting cardiovascular disease. Aerobic exercise training （AT） decreases fat accumulation, concomitant with an elevation of serum level of adiponectin, as an anti-inflammatory adipokine, resulting reduction of arterial stiffness. Recently, C1q/TNF-related protein 5 （CTRP5） has been identified as a novel adipokine which is paralog of adiponectin and exerts vasodilator effect. Although AT increases serum CTRP5 levels, concomitant with a reduction of fat accumulation, the differences of AT-induced increases in CTRP5 secretion from ectopic adipose tissues remain unclear.

PURPOSE: This study aimed to clarify whether AT increases mRNA expression level of CTRP5 from ectopic fats in senescence mice.

METHODS: Seventeen 38-week-old senescence-accelerated mouse prone 1 （SAMP1） mice were divided into sedentary control （CON; n=7） and AT （voluntary wheel running for 12-weeks; n=10） groups. Expression level of CTRP5 mRNA in epididymal, perivascular, subscapular subcutaneous and brown fats were measured by using real-time RT-PCR. The vasodilatory response of acetylcholine treatment was assessed by using aortic vascular rings.

RESULTS: Compared with CON group, AT group showed significantly lower epididymal fat mass, and significantly higher vasodilatory response of acetylcholine treatment by using aortic vascular rings. However, there was no significant difference in expression levels of CTRP5 mRNA in epididymal, perivascular, subscapular subcutaneous and brown fats between two groups.

CONCLUSION: These results suggest that AT-induced increases in CTRP5 mRNA may be occurs in tissues other than epididymal, perivascular, subscapular subcutaneous and brown fats.