Length of intestinal contact on nutrient-driven satiety

Am J Physiol. 1998 Oct;275(4):R1308-19. doi: 10.1152/ajpregu.1998.275.4.R1308.


Chemosensors throughout small bowel and colon inhibit food intakes when contacted by monomeric nutrients. We postulated that calorie-dependent inhibition of food intakes depended on additions of feedbacks from sensors in proximal and distal bowel contacted after high intakes of nutrients. Therefore, we determined how feedback from sensors in proximal gut interacted with feedback from simultaneously contacted sensors in distal bowel and whether suppression of nutrient intakes by intestinally perfused nutrients depended on length of gut contacted. Suppression of food intakes by maltose simply added to that from dodecanoate when both were present together either in proximal or distal small bowel. When dodecanoate was infused into proximal gut while maltose was infused distally, suppression of intake was threefold higher and was thus potentiated. Limiting contact of slowly absorbed lactose or oleate to 35 cm of jejunum nearly abolished the satiating potencies each exhibited during access to whole gut. The observations were consistent with our hypothesis.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Chemoreceptor Cells / physiology
  • Colon / physiology*
  • Dose-Response Relationship, Drug
  • Duodenum / physiology
  • Eating / physiology*
  • Energy Intake
  • Feedback
  • Galactose / pharmacology
  • Glucose / pharmacology
  • Intestine, Small / physiology*
  • Lactose / pharmacology
  • Lauric Acids / pharmacology
  • Male
  • Maltose / pharmacology
  • Organ Specificity
  • Rats
  • Rats, Sprague-Dawley
  • Satiety Response / drug effects
  • Satiety Response / physiology*
  • Trehalose / pharmacology


  • Lauric Acids
  • lauric acid
  • Maltose
  • Trehalose
  • Glucose
  • Lactose
  • Galactose