Abstract
Neuroanatomical and electrophysiological studies have shown that hypothalamic POMC neurons are targets of the adipostatic hormone leptin. However, the physiological relevance of leptin signaling in these neurons has not yet been directly tested. Here, using the Cre/loxP system, we critically test the functional importance of leptin action on POMC neurons by deleting leptin receptors specifically from these cells in mice. Mice lacking leptin signaling in POMC neurons are mildly obese, hyperleptinemic, and have altered expression of hypothalamic neuropeptides. In summary, leptin receptors on POMC neurons are required but not solely responsible for leptin's regulation of body weight homeostasis.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 983-991 |
| Number of pages | 9 |
| Journal | Neuron |
| Volume | 42 |
| Issue number | 6 |
| DOIs | |
| State | Published - Jun 24 2004 |
| Externally published | Yes |
Bibliographical note
Funding Information:This work was supported by grants from the NIH (PO1 DK56116 to B.B.L. and J.K.E., DK57621 and DK26687 to S.C.C.Jr., MH61583 and DK53301 to J.K.E.) and by Takeda Chemical Industries, Ltd., Japan. N.B was supported by The Wellcome Trust, UK, an EASD-ADA and a BONRC grant. R.C. was supported by Universita' Politecnica delle Marche (previously Universita' di Ancona), Italy. We would like to thank Abby Pullen for expert technical assistance, Satoshi Naganawa for the POMC BAC, T. Williams for colchicine injections, and NIDDK's National Hormone and Peptide Program and A.F. Parlow for providing recombinant mouse leptin.
