Extract

One of the new kids on the block in neuroendocrinology is leptin. One can hardly pick up an endocrine-oriented journal that does not contain at least one article about leptin physiology or its circulating levels in some pathological condition. The story of its discovery, the molecular defect, and the reversal of that defect in the ob/ob mouse is now an old story (for review, see Ref.1). Early on it was thought that this agent or an agonist might be a major player in reversing the marked trend to obesity in man. In fact, in the past few decades there has been a rapid escalation in the prevalence of obesity, including the morbidly obese (2). Although genetic influences are important, with estimates ranging from 20–40% (3), no single important gene has been linked to the obesity syndrome. It is considered that there is a complex interacting“ set” of genes (polygenic); adversive environmental factors acting on this genetic background produce obesity.

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