There is now clear evidence that adipocytes are engine rooms producing a large number of factors which can have profound influences upon adjacent tissues. In particular, perivascular fat can influence arterial tone and healthy adipocytes secrete a number of vasorelaxing molecules. Recent evidence has suggested that one of these playing a prominent role is adiponectin and the bioavailability of this adipokine is lost when subjects become obese and develop maturity on-set diabetes or the metabolic syndrome. Adiponectin appears to be released by the stimulation of beta-adrenor receptors located on adipocyte plasma membranes and its actions involve nitric oxide both in the endothelium and in the adipocyte itself. Crucial to the normal functioning of this pathway is the BKCa channel and knockout mice demonstrate no vasorelaxing activity of perivascular fat. In the obese state there is adipocyte hypertrophy and activation of recruited macrophages. Evidence suggests that without the macrophage there is no loss of perivascular vasodilator activity and our most recent data following up patients who have undergone bariatric surgery suggest that this intervention is associated with a loss of inflammation and the restoration of normal perivascular fat function.