Obesity is associated with metabolic derangements such as insulin resistance, 
inflammation and hypercoagulobility which can all be understood as consequences 
of adipose tissue dysfunction. The potential role for adipose tissue derived 
cytokines and adipokines in the development of vascular disease and diabetes may 
produce a clinical need to influence adipose tissue function. Various 
pharmacological and non-pharmacological interventions affect plasma cytokine and 
adipokine levels. The effects of these interventions depend on weight loss per 
se, changes in fat distribution without weight loss and/or direct effects on 
adipose tissue inflammation.Weight loss, as a result of diet, pharmacology and 
surgery, positively influences plasma adipokines and systemic inflammation. 
Several classes of drugs influence systemic inflammation directly through their 
anti-inflammatory actions. PPAR-γ agonism positively influences adipose tissue 
inflammation in several classes of intervention such as the thiazolidinediones 
and perhaps salicylates, CB1-antagonists and angiotensin II receptor blockers. 
Furthermore, within drug classes there are differential effects of individual 
pharmacologic agents on adipose tissue function.It can be concluded that several 
commonly used pharmacological and non-pharmacological interventions have 
unintended influences on adipose tissue function. Improving adipose tissue 
function may contribute to reducing the risk of vascular diseases and the 
development of type 2 diabetes.