The current concept of the pathogenesis of obesity relates to the inflammation caused by excess of adipose tissue. Regulatory T cells accumulated in visceral adipose tissue (VAT-resident Tregs) are also involved in this pathogenesis. In the present paper the mechanisms responsible for alterations in the number and function of VAT-resident Tregs T in obesity are described. The role of Tregs in inflammation, insulin resistance, atherogenesis, and also the influence on VAT-resident Tregs of adipocytokines and insulin are reviewed.