2008
DOI: 10.1249/mss.0b013e31816c091d
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Low-Intensity Exercise Exerts Beneficial Effects on Plasma Lipids via PPARγ

Abstract: We propose that the net effect of these changes may be to increase oxLDL uptake, to stimulate RCT, and thus to promote clearance of proatherogenic lipids from the vasculature, ultimately contributing to the cardiovascular benefits of low-intensity aerobic exercise.

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Cited by 116 publications
(130 citation statements)
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“…Irisin may modulate the PPARα signaling pathway, a key regulator of lipid metabolism that coordinates fat oxidation through a thermogenesis mechanism (5). Previous studies have reported an increase in PPARα following physical training (26,49,50). It seems practicable that endurance training and resistance training are beneficial in adipose metabolism by elevating the expression of FNDC5 and the subsequent increase in PPARα expression stimulation.…”
Section: Discussionmentioning
confidence: 96%
“…Irisin may modulate the PPARα signaling pathway, a key regulator of lipid metabolism that coordinates fat oxidation through a thermogenesis mechanism (5). Previous studies have reported an increase in PPARα following physical training (26,49,50). It seems practicable that endurance training and resistance training are beneficial in adipose metabolism by elevating the expression of FNDC5 and the subsequent increase in PPARα expression stimulation.…”
Section: Discussionmentioning
confidence: 96%
“…This suggests that the improvements observed in AIx in the current study (which suggest an improvement in endothelial function) may also occur as a result of exercise-induced activation of PPARγ. Thus, while due to an association with increased risk of death from CV causes [51], the prescription of RSG has fallen dramatically in recent years [52], exercise may provide a safe alternative to RSG as a method of inducing beneficial PPARγ-dependent effects [36,37]. Therefore, with regard to the current study's findings, we propose that an exerciseinduced activation of the nuclear receptor PPARγ may cause the observed down-regulation in the expression of the elastin-degrading gene MMP-9 (and also possibly improve endothelial function), which in turn may ameliorate physical inactivity-related vascular remodelling.…”
Section: Discussionmentioning
confidence: 99%
“…Finally, given previous reports that participation in exercise is associated with generation of natural ligands for the nuclear receptor protein peroxisome proliferator-activated receptor-gamma (PPARγ) within the vasculature [36,37], that pharmacological activators of the nuclear receptor PPARγ are associated with decreased MMP-9 secretion from human monocytes [38], and that PPARγ may bring about this effect by antagonistic transrepression at nuclear factor-kappa Beta response elements (NFkB-RE) and activator protein-1 sites [39,40], we performed bioinformatics screens of the human MMP-9 promoter (accession code: NG_011468.1) for peroxisome proliferator response elements (PPRE), NFkB-RE and AP-1 consensus sequences. No PPREs were found within ~5Kbp of the MMP-9 start site, but sequences were found resembling the reported consensus sequences for NFkB-RE [41] and AP-1 [42] at positions -4076bp, -637bp, -408bp, -349bp; and positions -1680bp, -556bp, respectively.…”
Section: Walk Registers and Ipaq Met-minutes Revealed That 19 Of The 36mentioning
confidence: 99%
“…PGC-1 has been shown to mediate the beneficial effects of exercise 38) . Butcher et al reported that 8-week low-intensity exercise significantly increased leukocyte mRNA expression for PPAR , LXR, and ABCA1, and plasma HDL-C in sedentary adults 39) . These suggest that aerobic exercise training might play an important role for affect HDL transport and/or metabolism through PPARs, LXR, and ABC A1.…”
Section: Correlation Coefficients Between Cholesterol Efflux Capacitymentioning
confidence: 99%