UCP2 mediates ghrelin’s action on NPY/AgRP neurons by lowering free radicals

By Z. Andrews, Zhong-Wu Liu, Nicholas Walllingford, D. Erion, Erzsébet Borók, J. Friedman, Matthias Tschöp, M. Shanabrough, G. Cline, Gerald I. Shulman and 4 more. Nature, 2009

382 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/afadd22593836a20095b210a3302024d2fc5552f

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Citations in the corpus

• Mitochondrial ROS signaling in organismal homeostasis. (2015, background): “Knocking out UCP2 diminished the ability of AgRP neurons to inhibit mtROS production and maintain low levels of cellular ROS, which, in turn, impairs their neuronal functions (Andrews et al., 2008).”
• Reactive Oxygen Species in Health and Disease (2012, background): “On the other hand, UCP2 (ubiquitously expressed at low levels) and UCP3 (preferentially expressed in skeletal muscle) maintain their original function of decreasing ROS production through uncoupling and hence buffering ROS levels and do not appear to play a thermogenic role [43–45].”