Why the study?
To clarify whether low-intensity pulsed ultrasound irradiation of the carotid baroreceptor protects against obesity by rebalancing the autonomic nervous system.
Does low-intensity pulsed ultrasound irradiation of the carotid baroreceptor ameliorate metabolic disorders in high-fat diet-induced obese rats?
Does low-intensity pulsed ultrasound irradiation of the carotid baroreceptor ameliorate metabolic disorders in high-fat diet-induced obese rats?
Low-intensity pulsed ultrasound of the carotid baroreceptor ameliorates metabolic disorders in obese rats by rebalancing the autonomic nervous system and rectifying the AMPK/PPAR pathway in adipose tissues.
LIPUS on carotid baroreceptors may improve metabolic parameters in obese rats; leaves open any role in human obesity management.
This study was designed to clarify whether the irradiation of carotid baroreceptor (CB) with low-intensity pulsed ultrasound (LIPUS) protects against obesity by rebalancing the autonomic nervous system (ANS). Obesity was induced using a high-fat diet (HFD) for 8 weeks in Sprague-Dawley rats. Irradiation with LIPUS was daily (20 minutes a day) applied to the right CB. In our study, LIPUS significantly ameliorated metabolic disorders in obese rats. LIPUS partly restored norepinephrine (NE) and acetylcholine (ACH) levels in the perirenal white adipose tissue (PWAT), epididymal white adipose tissue (EWAT), interscapular brown adipose tissue (IBAT), and plasma of obese rats. LIPUS partially rectified the dysregulated AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor (PPAR) α/ɣ pathway in the PWAT, EWAT, and IBAT of obese rats. PPARγ and PPARγ target genes respond more sensitively to HFD and LIPUS in PWAT and EWAT than in IBAT. NE, ACH, uncoupling protein-1, phosphorylated AMPK, PPARα, and PPARα target genes respond more sensitively to HFD and LIPUS in IBAT than in PWAT and EWAT. Conclusion: LIPUS irradiation of CB exerts different metabolic protection in PWAT, EWAT, and IBAT by rebalancing the ANS and rectifying the AMPK/PPARα/ɣ pathway in obese rats.
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Cao et al. (2020) studied this question.
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