Brown Institute of Molecular Medicine at McGovern Medical School and Neuroscience Program of MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
School of Sport Science, Beijing Sport University, Beijing 100084, China.
Cell Rep. 2023 Jul 25;42(7):112789. doi: 10.1016/j.celrep.2023.112789. Epub 2023 Jul 8.
In addition to their role in promoting feeding and obesity development, hypothalamic arcuate agouti-related protein/neuropeptide Y (AgRP/NPY) neurons are widely perceived to be indispensable for maintaining normal feeding and body weight in adults, and consistently, acute inhibition of AgRP neurons is known to reduce short-term food intake. Here, we adopted complementary methods to achieve nearly complete ablation of arcuate AgRP/NPY neurons in adult mice and report that lesioning arcuate AgRP/NPY neurons in adult mice causes no apparent alterations in ad libitum feeding or body weight. Consistent with previous studies, loss of AgRP/NPY neurons blunts fasting refeeding. Thus, our studies show that AgRP/NPY neurons are not required for maintaining ad libitum feeding or body weight homeostasis in adult mice.
除了在促进进食和肥胖发展中的作用外，下丘脑弓状核 agouti 相关蛋白/神经肽 Y（AgRP/NPY）神经元被广泛认为对于维持成人体重和正常进食是不可或缺的，而且，急性抑制 AgRP 神经元已知会减少短期食物摄入。在这里，我们采用互补的方法来实现成年小鼠弓状核 AgRP/NPY 神经元的几乎完全消融，并报告称成年小鼠弓状核 AgRP/NPY 神经元的损伤不会导致自由进食或体重出现明显变化。与之前的研究一致，AgRP/NPY 神经元的缺失削弱了禁食再进食。因此，我们的研究表明，AgRP/NPY 神经元对于维持成年小鼠的自由进食或体重稳态不是必需的。
