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Perivascular fat, AMP ‐activated protein kinase and vascular diseases
Author(s) -
Almabrouk T A M,
Ewart M A,
Salt I P,
Kennedy S
Publication year - 2014
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/bph.12479
Subject(s) - ampk , adipose tissue , paracrine signalling , adipokine , metformin , endocrinology , stromal vascular fraction , vascular smooth muscle , medicine , adipocyte , amp activated protein kinase , protein kinase a , diabetes mellitus , biology , microbiology and biotechnology , insulin resistance , kinase , receptor , smooth muscle
Perivascular adipose tissue ( PVAT ) is an active endocrine and paracrine organ that modulates vascular function, with implications for the pathophysiology of cardiovascular disease ( CVD ). Adipocytes and stromal cells contained within PVAT produce mediators (adipokines, cytokines, reactive oxygen species and gaseous compounds) with a range of paracrine effects modulating vascular smooth muscle cell contraction, proliferation and migration. However, the modulatory effect of PVAT on the vascular system in diseases, such as obesity, hypertension and atherosclerosis, remains poorly characterized. AMP ‐activated protein kinase ( AMPK ) regulates adipocyte metabolism, adipose biology and vascular function, and hence may be a potential therapeutic target for metabolic disorders such as type 2 diabetes mellitus (T2DM) and the vascular complications associated with obesity and T2DM. The role of AMPK in PVAT or the actions of PVAT have yet to be established, however. Activation of AMPK by pharmacological agents, such as metformin and thiazolidinediones, may modulate the activity of PVAT surrounding blood vessels and thereby contribute to their beneficial effect in cardiometabolic diseases. This review will provide a current perspective on how PVAT may influence vascular function via AMPK . We will also attempt to demonstrate how modulating AMPK activity using pharmacological agents could be exploited therapeutically to treat cardiometabolic diseases.