In this brief overview the central role of the endocrine aberrations of visceral obesity has been emphasized. Indeed, it may provide not only a background to the pronounced insulin resistance seen in that condition, but also explain why lipid accumulates in visceral depots. It is possible that this lipid accumulation actually amplifies and widens the metabolic derangements via hepatic mechanisms induced by an excess of FFA in the portal vein. This chain of events has not been conclusively established. There is, however, considerable experimental support for several crucial parts of it, providing an interesting hypothesis for further work. Intervention studies will probably be of value for further evaluation and these are already being carried out.