Restoring Perivascular Adipose Tissue Function in Obesity Using Exercise

Abstract

Purpose Perivascular adipose tissue (PVAT) exerts an anti-contractile effect which is vital in regulating vascular tone. This effect is mediated via sympathetic nervous stimulation of PVAT by a mechanism which involves noradrenaline uptake through organic cation transporter 3 (OCT3) and β3-adrenoceptor-mediated adiponectin release. In obesity, autonomic dysfunction occurs, which may result in a loss of PVAT function and subsequent vascular disease. Accordingly, we have investigated abnormalities in obese PVAT, and the potential for exercise in restoring function. Methods Vascular contractility to electrical field stimulation (EFS) was assessed ex vivo in the presence of pharmacological tools in ±PVAT vessels from obese and exercised obese mice. Immunohistochemistry was used to detect changes in expression of β3-adrenoceptors, OCT3 and tumour necrosis factor-α (TNFα) in PVAT. Results High fat feeding induced hypertension, hyperglycaemia, and hyperinsulinaemia, which was reversed using exercise, independent of weight loss. Obesity induced a loss of the PVAT anti-contractile effect, which could not be restored via β3-adrenoceptor activation. Moreover, adiponectin no longer exerts vasodilation. Additionally, exercise reversed PVAT dysfunction in obesity by reducing inflammation of PVAT and increasing β3-adrenoceptor and OCT3 expression, which were downregulated in obesity. Furthermore, the vasodilator effects of adiponectin were restored. Conclusion Loss of neutrally mediated PVAT anti-contractile function in obesity will contribute to the development of hypertension and type II diabetes. Exercise training will restore function and treat the vascular complications of obesity.

The Role of Obesity-Induced Perivascular Adipose Tissue (PVAT) Dysfunction in Vascular Homeostasis

“…Noradrenaline, which is the main SNS mediator, induces the expression of β3-adrenoreceptors, which are responsible for adiponectin release, while organic cation transporter 3 (OCT3) separates the excess of NA [38]. Saxton et al reported that obesity contributes to the downregulation of mentioned receptors among mice [123]. However, exercise performed on obese mice turned out to increase the expression of β3-adrenoreceptors and returned control levels of OCT3.…”

Aerobic Exercise Prevents Arterial Stiffness and Attenuates Hyperexcitation of Sympathetic Nerves in Perivascular Adipose Tissue of Mice after Transverse Aortic Constriction

“…Our results showed that aerobic exercise attenuates the hyperexcitation of sympathetic nerves in PVAT, represented by the reduced expression of circulating NE and the distribution of the sympathetic nerve. Exercise training has been shown to normalize sympathetic hyperexcitation in patients with HF [ 16 ], and to restore PVAT function and prevent vascular complications [ 21 ]. Quantitative evidence from HF patients systematically supported this positive influence of exercise [ 22 ].…”

Impact of Rehabilitation Nutrition and Healthy Weight Maintenance in Motor-Complete Tetraplegia Patients

“…It is a confirmed method for muscle mass maintenance in SCI or paralysis-bound patients who cannot actively contract muscles or who are at high risk of muscle atrophy. In this study, the non-obese group with less fat tissue interference [ 34 ] may have benefited more from FES for the contraction of paralyzed muscles than the obese group. In contrast to the muscle-related parameters, fat components including fat mass, fat percentage, and FMI increased during intervention regardless of obesity.…”