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Submitted on January 24, 2006
Accepted on July 19, 2006
Neuroscience Research Program, The Garvan Institute of Medical Research, Sydney, Australia; Bone and Mineral Program, The Garvan Institute of Medical Research, Sydney, Australia; Neurologix Inc, USA. Cornell Medical College, New York, USA
* To whom correspondence should be addressed. E-mail: d.lin{at}garvan.org.au.
Neuropeptide Y (NPY) is a key regulator of energy homeostasis and is implicated in the development of obesity and type 2 diabetes. While it is known that hypothalamic administration of exogenous NPY peptides leads to increased body weight gain, hyperphagia and many hormonal and metabolic changes characteristic of an obesity syndrome, the Y receptor(s) mediating these effects is disputed and unclear. To investigate the role of different Y receptors in the NPY-induced obesity syndrome, we used recombinant adeno-associated viral vector (rAAV) to overexpress NPY in mice deficient of selective single or multiple Y receptors (including Y1, Y2 and Y4). Results from this study demonstrated that long-term hypothalamic overexpression of NPY lead to marked hyperphagia, hypogonadism, body weight gain, enhanced adipose tissue accumulation, hyperinsulinemia and other hormonal changes characteristic of an obesity syndrome. NPY-induced hyperphagia, hypogonadism and obesity syndrome persisted in all genotypes studied (Y1-/-, Y2-/-, Y2Y4-/- and Y1Y2Y4-/- mice). However, triple deletion of Y1, Y2 and Y4 receptors prevented NPY-induced hyperinsulinemia. These findings suggest that Y1, Y2 and Y4 receptors under this condition are not crucially involved in NPY's hyperphagic, hypogonadal and obesogenic effects but they are responsible for the central regulation of circulating insulin levels by NPY.
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