Millions of years ago visceral fat cells (VFC) started developing from subcutaneous adipocytes. From the early stages of phylogenesis, VFC have fulfilled the biological functions of trophology and homeostasis, endoecology and adaptation. Subcutaneous adipocytes fulfill the phylogenetically later function of locomotion. VFC have no insulin receptors, while subcutaneous adipocytes are insulin-dependent. Within the frames of the biological function of trophology both VFC and subcutaneous adipocytes realize the following biological reactions: exotrophy, deposition, and endotrophy. We believe that impaired deposition of fatty acids (FA) as triglycerides (TG) is the major cause of obesity. Impairedfunction of VFC (metabolic syndrome) andinsulin-dependent adipocytes (obesity) are key factors of metabolic pandemias. Fatty cells absorb FA as nonpolar TG, deposit FA in lipid drops, and secrete them into extracellular medium as polar nonesterified FA. VFC were formed in paracrine communities of enterocytes, where microsomal protein that transports triglycerides formed early chylomicrons. In pathophysiologic, regulatory and functional aspects VFC and adipocytes are different cells; therefore, they should be analyzed separately. Not only VFC, but also all loose connective tissue cells at the level of cell community secrete various humoral mediators of paracrine regulation; there were no other ways of regulation. Leptin is a specific mediator of VFC, and adiponectin--of subcutaneous adipocytes.