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Comment
. 2001 Apr 10;98(8):4279-81.
doi: 10.1073/pnas.091101498.

Circumventing leptin resistance for weight control

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Comment

Circumventing leptin resistance for weight control

S P Kalra. Proc Natl Acad Sci U S A. .
No abstract available

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Figures

Figure 1
Figure 1
Schematic representation of hypothalamic signaling pathways in the regulation of appetite and energy expenditure. NPY, AgrP, and GABA, the appetite-stimulating signals, are coproduced in the perikarya located in the ARC. Likewise, the appetite-inhibiting peptides, α-MSH and CART, are coproduced in the POMC/CART coexpressing perikarya in the ARC. These distinct populations of neurons project into the two subdivisions of the PVN, the mPVN and pPVN, to activate their corresponding receptors for regulation of appetite and energy expenditure. NPY-producing neurons also contact the POMC/CART neurons locally in the ARC to curtail their tonic restraint on appetite. Leptin inhibits appetite through leptin-Rb located on the NPY/AgrP/GABA- and POMC/CART-expressing cell bodies in the ARC and at postsynaptic sites in the PVN where it regulates release of these signals and enhances energy expenditure through the sympathetic nervous system. The results show that CNTF/CNTFAx15, through activation of the CNTFRα located in the ARC and PVN, markedly diminish the availability of NPY for release in the PVN by suppressing its synthesis in the ARC and concurrently attenuating postsynaptic NPYergic signaling by decreasing NPY Y1 receptor and pCREB abundance.

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