Leptin receptor signaling in POMC neurons is required for normal body weight homeostasis.

By N. Balthasar, R. Coppari, J. McMinn, Shun-Mei Liu, Charlotte E. Lee, V. Tang, Christopher D. Kenny, Robert A. McGovern, S. Chua, J. Elmquist and 1 more. Neuron, 2004

924 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Nutrition and Dietetics, Physiology

View Paper: https://www.semanticscholar.org/paper/ff4110d372e2bfeb5c206ece91c4ed8a76e794a9

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrine and Autonomic Systems

1. M. Myers
2. S. O’Rahilly
3. Bradford B. Lowell
4. I. S. Farooqi
5. A. Coll
6. C. Ye
7. B. Kahn
8. J. Flier

In Nutrition and Dietetics

1. M. Myers
2. Bradford B. Lowell
3. S. O’Rahilly
4. I. S. Farooqi
5. B. Kahn
6. J. Flier
7. A. Coll
8. J. Elmquist

In Physiology

1. Bradford B. Lowell
2. S. O’Rahilly
3. R. Hen
4. B. Kahn
5. J. Flier
6. P. Trayhurn
7. B. Spiegelman
8. Mitchell A. Lazar

Citations in the corpus

• Leptin regulation of the mesoaccumbens dopamine pathway. (2006, positive): “…involving leptin signals within POMC and NPY/AgRP neurons in the arcuate nucleus have been defined through functional neuroanatomy and genetic gain-and loss-of-function approaches (Erickson et al., 1996; Elias et al., 1999; Balthasar et al., 2004; Elmquist et al., 2005; Luquet et al., 2005).”
• Leptin Action on GABAergic Neurons Prevents Obesity and Reduces Inhibitory Tone to POMC Neurons (2011, positive): “Previously established, functionally relevant, first order leptin-responsive neurons include POMC and AgRP neurons in the arcuate nucleus and SF1 neurons in the VMH (Balthasar et al., 2004; Dhillon et al., 2006; van de Wall et al., 2008), and possibly serotonin neurons in the raphe (Yadav et al.”
• A FLEX Switch Targets Channelrhodopsin-2 to Multiple Cell Types for Imaging and Long-Range Circuit Mapping (2008, methodology): “Next, we characterized expression of rAAV-FLEX-rev-ChR2mCherry in pomccre (Balthasar et al., 2004) and agrp-cre (Kaelin et al., 2004) transgenic mice.”
• Neuronal PTP1B regulates body weight, adiposity and leptin action (2006, result): “Recent studies, however, show that LRb-expressing arcuate neurons mediate only part of the effects of leptin on adiposit”
• Leptin directly activates SF1 neurons in the VMH, and this action by leptin is required for normal body-weight homeostasis. (2006, positive): “It was recently shown that steroidogenic factor-1 (SF1) gene knockout mice have abnormal VMH development and are obese, suggesting that SF1 neurons in the VMH play an important role in controlling body weight ( Balthasar et al., 2004; Majdic et al., 2002).”
• Divergence of melanocortin pathways in the control of food intake and energy expenditure. (2005, methodology): “In brief, using previously described recombineering techniques (Balthasar et al., 2004; Lee et al., 2001), Cre-recombinase cDNA was inserted into the ATG of the Sim1 gene in a C57Bl6/J mouse bacterial artificial chromosome (RPCI23-20F11) containing 137.1kb of genomic 5# Sim1 sequences.”
• The Hormonal Control of Food Intake (2007, positive): “For instance, although the selective ablation of leptin receptors in POMC neurons of the arcuate nucleus results in obesity (Balthasar et al., 2004), it is less pronounced than in mice that globally lack leptin receptor.”
• Leptin regulation of bone mass, appetite and energy expenditure relies on its ability to inhibit serotonin synthesis in the brainstem (2009, positive): “Surprisingly however, VMH-specific deletion of ObRb does not affect bone mass (Balthasar et al., 2004).”
• Mechanisms of leptin action and leptin resistance. (2008, background): “Although ablation of AgRP neurons results in hypophagia and ablation of POMC or central melanocortin receptors results in severe obesity (27, 39), deletion of LRb from POMC neurons or the restoration of LRb in the ARC of db/db animals results in only modest alterations in body weight (although these”