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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Dr. Frank Rademakers,
View the Slides from this session in ESC Congress 365
Brown and white adipocytes are present in variable ratios throughout the human body and have major metabolic effects which can become abnormal in pre-disease states.
The session's first speaker, Simon Kennedy (Scotland), discussed how activated Protein Kinase (AMPK) acts as a switch to smooth muscle relaxation (K+ channels) and Endothelial Nitric Oxide Synthase (eNOS) production, and can become mutated in disease. In normal circumstances AMKP from perivascular fat has a positive effect on smooth muscle relaxation, which is eliminated in AMPK KO mice. At the same time brown fat content is decreased in these KO mice.
Etto Eringa (The Netherlands) discussed how perivascular adipose tissue (PVAT) also exerts a balanced effect on vascular reactivity through modulation of the insulin effect on perfusion: vasodilation via eNOS production and vasoconstriction through ET-1. In obesity, the insulin resistance causes a decrease in eNOS, resulting in relative vasoconstriction mediated by ET-1.A Western diet causes a 40 fold increase in PVAT in mice, which produces adiponectin and cytokines. These factors are the mediators for abnormalities in perfusion as insulin vasoreactivity is only abnormal in obese mice versus lean mice in the presence of PVAT. In lean mice insulin is a vasodilator; in obese mice, it causes vasoconstiction when exposed to PVAT. The question remains if this can be reversed.
In human studies there are indications that an “outside-to-inside” signaling by inflammatory cytokines is present in perivascular fat, but not in subcutaneous fat, explained the next speaker, Tim Matsurik (Poland). This inflammation can be shown clinically by increased FDG uptake on PET in NSTEMI patients, for example.This FDG uptake correlates with various (negative) plaque characteristics while absolute perivascular fat content does not. How to reverse this localized inflammatory state is still unclear and also the causative role towards the plaque instability remains an issue. Activated plaque itself could also be causing the perivascular fat inflammation rather than the reverse.
Speaker Thomas Schulz (Germany) discussed the recent discovery that humans also have variable amounts of brown adipose tissue (in the neck region and along the spine). In contrast to white adipose tissue (which stores energy) brown adipose has a high density of capillaries and mitochondria, is very metabolically active, expends energy and clears the blood of fatty acids. The trigger is cold exposure which seems to cause cross talk with the neuroendocrine system via Bone Morphogenetic Proteins. This causes a conversion of white adipose cells into “brownish” or Brite cells which have the characteristics of brown adipocytes and increases energy expenditure and decreases body weight. This process is called “browning”. The clinical relevance (there is certainly not less cardiovascular disease in the nordic countries) remains to be established, as well as the possible therapeutic applications.
Proinflammatory activity of adipose tissue
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