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to the leptin mainpage*Possible leptin partners, NPY:
In 1995, Thomas Stephens and his colleagues, at Eli Lilly Co., reported that NYP (neuropeptide Y)production was suppressed by giving the animals external leptin. In contrast, if do not have any leptin, the NPY system is completely unrestrained, and that in turn leads to their obesity. Baskiní s mapping of the brain locations of the leptin receptors fit nearly with this idea, because one of the most locations, the arcuate, is the major site of NYP production.
Richard Palmiterë s group at University of Washington made a puzzling observation in early 1996: The NPY gene inactivated mice appeared in normal body weight, fat levels, and food uptake rather than being thin. Later they mate the NYP knockout mice with ob/ob mutant. They found that the appetite, metabolism, and fat levels of the double mutant offspring were midway between those of normal and ob/ob mice. This result indicated that part, not all, of the weight gain of the ob mouse results from the increased NPY production induced by the animalí s low leptin levels.
Because the NPY defect did not completely counteract the leptin defect in the double mutant offspring, the finding suggests that NPY is not the only obesity regulator responded to the leptin. Here a group of melanocortin and its receptor come as another obesity signal.