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Curr Hypertens Rep. 2018 Sep 18;20(11):96. doi: 10.1007/s11906-018-0894-7.

Adipose Tissue and Modulation of Hypertension.

Author information

1
Translational Medicine Program, The Hospital for Sick Children Research Institute, Toronto, Ontario, M5G 0A4, Canada.
2
Department of Microbiology, Siliguri College, North Bengal University, Siliguri, West Bengal, 734001, India.
3
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada.
4
Department of Physiology, University of Toronto, Toronto, Canada.
5
Translational Medicine Program, The Hospital for Sick Children Research Institute, Toronto, Ontario, M5G 0A4, Canada. hoon-ki.sung@sickkids.ca.
6
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada. hoon-ki.sung@sickkids.ca.
7
Banting and Best Diabetes Centre, University of Toronto, Toronto, Canada. hoon-ki.sung@sickkids.ca.

Abstract

PURPOSE OF REVIEW:

Obesity is a major risk factor for the development of hypertension (HTN), a leading cause of cardiovascular morbidity and mortality. Growing body of research suggests that adipose tissue function is directly associated with the pathogenesis of obesity-related HTN. In this review, we will discuss recent research on the role of adipose tissue in blood pressure (BP) regulation and activation of brown adipose tissue (BAT) as a potentially new therapeutic means for obesity-related HTN.

RECENT FINDINGS:

Adipose tissue provides mechanical protection of the blood vessels and plays a role in regulation of vascular tone. Exercise and fasting activate BAT and induce browning of white adipose tissue (WAT). BAT-secreted FGF21 lowers BP and protects against HTN. Browning of perivascular WAT improves HTN. New insights on WAT browning and BAT activation can open new avenues of potential therapeutic interventions to treat obesity-related HTN.

KEYWORDS:

Batokine; Blood pressure and endothelial cells; Brown adipose tissue; Hypertension; Obesity

PMID:
30229358
DOI:
10.1007/s11906-018-0894-7
[Indexed for MEDLINE]

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