| Literature DB >> 33450178 |
Nitsan Goldstein1, Aaron D McKnight2, Jamie R E Carty1, Myrtha Arnold3, J Nicholas Betley4, Amber L Alhadeff5.
Abstract
Food intake is tightly regulated by complex and coordinated gut-brain interactions. Nutrients rapidly modulate activity in key populations of hypothalamic neurons that regulate food intake, including hunger-sensitive agouti-related protein (AgRP)-expressing neurons. Because individual macronutrients engage specific receptors in the gut to communicate with the brain, we reasoned that macronutrients may utilize different pathways to reduce activity in AgRP neurons. Here, we revealed that AgRP neuron activity in hungry mice is inhibited by site-specific intestinal detection of different macronutrients. We showed that vagal gut-brain signaling is required for AgRP neuron inhibition by fat. In contrast, spinal gut-brain signaling relays the presence of intestinal glucose. Further, we identified glucose sensors in the intestine and hepatic portal vein that mediate glucose-dependent AgRP neuron inhibition. Therefore, distinct pathways are activated by individual macronutrients to inhibit AgRP neuron activity.Entities:
Keywords: AgRP; fat; food intake; glucose; gut-brain; hepatic portal vein; hypothalamus; intestine; spinal afferents; vagus nerve
Mesh:
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Year: 2021 PMID: 33450178 PMCID: PMC7933100 DOI: 10.1016/j.cmet.2020.12.018
Source DB: PubMed Journal: Cell Metab ISSN: 1550-4131 Impact factor: 27.287