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Citations to this article

Leptin receptor expression in hindbrain Glp-1 neurons regulates food intake and energy balance in mice
Michael M. Scott, … , Charlotte E. Lee, Joel K. Elmquist
Michael M. Scott, … , Charlotte E. Lee, Joel K. Elmquist
Published May 23, 2011
Citation Information: J Clin Invest. 2011;121(6):2413-2421. https://doi.org/10.1172/JCI43703.
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Research Article

Leptin receptor expression in hindbrain Glp-1 neurons regulates food intake and energy balance in mice

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Abstract

Leptin is an adipose-derived hormone that signals to inform the brain of nutrient status; loss of leptin signaling results in marked hyperphagia and obesity. Recent work has identified several groups of neurons that contribute to the effects of leptin to regulate energy balance, but leptin receptors are distributed throughout the brain, and the function of leptin signaling in discrete neuronal populations outside of the hypothalamus has not been defined. In the current study, we produced mice in which the long form of the leptin receptor (Lepr) was selectively ablated using Cre-recombinase selectively expressed in the hindbrain under control of the paired-like homeobox 2b (Phox2b) promoter (Phox2b Cre Leprflox/flox mice). In these mice, Lepr was deleted from glucagon-like 1 peptide–expressing neurons resident in the nucleus of the solitary tract. Phox2b Cre Leprflox/flox mice were hyperphagic, displayed increased food intake after fasting, and gained weight at a faster rate than wild-type controls. Paradoxically, Phox2b Cre Leprflox/flox mice also exhibited an increased metabolic rate independent of a change in locomotor activity that was dependent on food intake, and glucose homeostasis was normal. Together, these data support a physiologically important role of direct leptin action in the hindbrain.

Authors

Michael M. Scott, Kevin W. Williams, Jari Rossi, Charlotte E. Lee, Joel K. Elmquist

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Year: 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 Total
Citations: 5 9 4 9 6 7 3 9 5 10 9 11 11 4 102
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