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Related Experiment Videos

Phosphate loading prevents the decrease in ATP and increase in food intake produced by 2,5-anhydro-D-mannitol

N E Rawson1, M I Friedman

  • 1Monell Chemical Senses Center, Philadelphia, Pennsylvania 19104.

The American Journal of Physiology
|June 1, 1994
PubMed
Summary
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The fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) stimulates feeding by depleting liver phosphate and ATP. Pre-loading with phosphate blocked this effect, confirming the mechanism.

Area of Science:

  • Biochemistry
  • Physiology
  • Neuroscience

Background:

  • The fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) is known to trigger feeding behavior in rats.
  • This feeding response is thought to be mediated by the liver's metabolic processes.

Purpose of the Study:

  • To investigate the role of hepatic phosphate depletion and reduced adenosine triphosphate (ATP) levels in the feeding response induced by 2,5-AM.
  • To determine if manipulating hepatic phosphate levels can prevent the 2,5-AM-induced feeding behavior.

Main Methods:

  • Rats were administered excess sodium phosphate prior to injection with 2,5-AM.
  • Hepatic inorganic phosphate and ATP levels were measured.
  • Food and water intake were monitored.
  • Eating responses to insulin and 2-deoxy-D-glucose were assessed for specificity.

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Main Results:

  • Phosphate loading successfully prevented the increase in food intake typically caused by 2,5-AM.
  • Phosphate loading also prevented the decrease in liver ATP levels observed after 2,5-AM administration.
  • The changes in plasma fuels induced by 2,5-AM were not affected by phosphate loading.
  • Water intake and feeding responses to other stimuli (insulin, 2-deoxy-D-glucose) remained unaffected, indicating behavioral specificity.

Conclusions:

  • The data strongly suggest that 2,5-AM elicits feeding behavior by a mechanism involving the depletion of hepatic inorganic phosphate and subsequent reduction of liver ATP.
  • This phosphate trapping mechanism is specific to 2,5-AM and not a general stress response or malaise effect.