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Adipose Tissue ‐ Vasculature Interactions
Author(s) -
Walsh Kenneth
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.75.2
Subject(s) - adipose tissue , adipokine , white adipose tissue , angiogenesis , endocrinology , medicine , inflammation , adipose tissue macrophages , biology , obesity , leptin
Obesity and metabolic dysfunction diminish lifespan, predominantly by increasing the frequency and severity of vascular diseases. It is becoming increasingly recognized that obesity contributes to cardio‐metabolic disease because it promotes the development of a chronic and systemic inflammatory state. Key to the development of this inflammatory state is the status of multiple bioactive substances, referred to as adipokines, that are secreted by adipose tissues. In lean, healthy organisms, adipose tissue produces anti‐inflammatory adipokines that serve to protect the vasculature from stresses. Under conditions of obesity, adipose tissue becomes dysfunctional and produces a pro‐inflammatory repertoire of adipokines that contribute to vascular diseases. In addition to the influence that adipokines have on vascular function, it is also appreciated that adipose tissue vascularity influences adipose tissue function. Recent studies have shown that brown adipose tissue is particularly sensitive to perturbations in its vascular supply. Compared to white adipose tissue that functions to store fat (and is most often associated with obesity), brown adipose tissue possesses abundant mitochondria that consumes fat to produce heat through uncoupled respiration. Recent work has shown that overnutrition leads to the dysfunction of brown adipose tissue, giving it a “whitened” appearance, via a collapse of VEGF‐dependent angiogenesis. These findings highlight the important interplay between the adipose tissue and the vasculature that is mediated by adipokines and angiogenic growth factors.