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Reduced Liver Mitochondrial Energy Metabolism Impairs Food Intake Regulation Following Gastric Preloads and Fasting. | LitMetric

AI Article Synopsis

  • The liver plays a vital role in regulating food intake, with its anatomical position suggesting it could act as a key sensor for energy levels in the body.
  • Impairments in liver energy metabolism, particularly in certain mouse models, lead to increased meal sizes and reduced inhibition on food intake after eating.
  • This research reinforces the idea that the liver helps manage hunger and satiety by influencing signals related to fullness from the body.

Article Abstract

The capacity of the liver to serve as a peripheral sensor in the regulation of food intake has been debated for over half a century. The anatomical position and physiological roles of the liver suggest it is a prime candidate to serve as an interoceptive sensor of peripheral tissue and systemic energy state. Importantly, maintenance of liver ATP levels and within-meal food intake inhibition is impaired in human subjects with obesity and obese pre-clinical models. We demonstrate that decreased hepatic mitochondrial energy metabolism in liver-specific, heterozygous PGC1a mice results in reduced mitochondrial response to changes in ΔG and tissue ATP following fasting. These impairments in liver energy state are associated with larger and longer meals during chow feeding, impaired dose-dependent food intake inhibition in response to mixed and individual nutrient oral pre-loads, and greater acute fasting-induced food intake. These data support previous work proposing liver-mediated food intake regulation through modulation of peripheral satiation signals.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11565831PMC
http://dx.doi.org/10.1101/2024.10.24.620086DOI Listing

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