Literature DB >> 9841547

Duodenal nutrient infusions differentially affect sham feeding and Fos expression in rat brain stem.

C B Phifer1, H R Berthoud.   

Abstract

Duodenal infusions of macronutrients inhibit sham and normal feeding. Neural substrates of this response were studied by infusing glucose, linoleic acid, an amino acid mixture, saline, or water into the duodenum of unanesthetized rats and then measuring sham feeding of 30% sucrose or Fos expression in the dorsal vagal complex. Linoleic acid and amino acids (both 1.5 kcal) and glucose (4.5 kcal) suppressed sham feeding relative to control infusions, and all three macronutrients triggered Fos expression in the nucleus of the solitary tract and area postrema. Although there were significant quantitative differences, the subnuclear distribution pattern of Fos-expressing neurons was not different for the three macronutrients and was largely localized to the medial, dorsomedial, and commissural subnuclei of the nucleus of the solitary tract and the area postrema. Linoleic acid suppressed intake and stimulated Fos expression similarly to glucose infusions of three times the caloric value. Amino acids strongly suppressed sham feeding but triggered relatively little Fos expression. These results indicate that the intake-suppressing potency of duodenal macronutrients is dependent on nutrient type, rather than simply caloric value, and that amino acids, although potent inducers of satiety, affect ingestion by processes different from those subserving lipids and carbohydrates. Furthermore, the similar patterns of neuronal activation after different duodenal infusions may indicate a large degree of convergence at the level of primary and second-order sensory neurons, whereas the distinctly different pattern obtained earlier with gastric distension indicates partially separate neural pathways for satiety signals generated by duodenal nutrients and gastric mechanoreceptors.

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Year:  1998        PMID: 9841547     DOI: 10.1152/ajpregu.1998.274.6.R1725

Source DB:  PubMed          Journal:  Am J Physiol        ISSN: 0002-9513


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