The Heartwarming Effect of Brown Adipose Tissue.

Mol Pharmacol

Department of Physiology and Cell Biology (K.M.P., K.I.S.), Center for Diabetes and Metabolism Research Center, Dorothy M. Davis Heart and Lung Research Institute (K.M.P., K.I.S.), and Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio (K.I.S.)

Published: July 2022

Brown adipose tissue (BAT) is a metabolically active tissue that improves glucose metabolism and protects against the development of type 2 diabetes and obesity. However, the role of BAT to improve cardiovascular health has only recently been investigated. In this review, we discuss multiple mechanisms through which both the thermogenic and endocrine functions of BAT mediate cardiac health. -adrenergic stimulation activates the thermogenic function of BAT, resulting in reduced circulating lipids and glucose, and enhanced clearance of hepatic cholesterol-enriched remnants leading to reduced atherosclerotic region size. Additionally, the thermogenic role of BAT has been implicated in activation of the protein kinase B-extracellular-signal-regulated kinase (ERK) 1/2 pathway after myocardial infarction (MI), contributing to reduced injury size. The endocrine function of BAT has also been implicated to improve both systemic metabolic health and cardiac health. Specifically, the batokines fibroblast growth factor 21 (FGF21) and 12,13-diHOME improve cardiovascular health via reduced hypertension, hypertrophy and MI injury size (FGF21) or by directly improving cardiac function via calcium cycling (12,13-diHOME). Finally, we discuss relevant pharmacological treatment methods currently aiming to activate BAT, typically through sympathetic activation. SIGNIFICANCE STATEMENT: This mini-review discusses the role of BAT to improve cardiac health via thermogenic and endocrine effects in both rodents and humans and highlights the need for therapeutic methods which activate or mimic BAT activity.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9341250PMC
http://dx.doi.org/10.1124/molpharm.121.000328DOI Listing

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