Obesity has emerged as a major health problem with 1.6 bil- lion adults classified as overweight and obese. The condition is associated with type 2 diabetes, cardiovascular diseases, and several cancers [1] and is characterized by an increase in the size and number of adipocytes. Peroxisome proliferator- activated receptors (PPARs) act as lipid sensors and therefore represent critical molecular targets for the treatment of obesity. Thus, agonists of peroxisome proliferator-activated receptor γ (PPARγ, also known as NR1C3) are used to treat non-insulin-dependent diabetes type 2. PPARγ belongs to the superfamily of nuclear receptors; it acts as a critical transcription factor in the regulation of adipose
differentiation, lipid storage, and of genes involved in energy storage and utilisation. One putative mechanism through which PPARγ enhances insulin sensitivity is its ability to channel fatty acids into adipose tissue, thus decreasing plasma fatty acid concentration. PPARγ can also affect insulin sensitivity by regulating hormones, cytokines, and proteins that are involved in insulin resistance [2]. It exists as two forms encoded by multiple transcript variants. PPARγ1 is the predominant isoform in humans; it is highly expressed in adipose tissue but is also expressed in many other cell types in which it plays important functions, particularly intestine and immune cells. PPARγ1 is the main isoform found in liver. PPARγ2 is found at high levels in different adipose tissues [3]. Hepatic PPARγ represents only 10–30%