Intragastric preloads of l-tryptophan reduce ingestive behavior via oxytocinergic neural mechanisms in male mice
| Autor: | Elizabeth Carpenter, Anica Klockars, Kiriana Isgrove, Allen S. Levine, Pawel K. Olszewski, Fraser Aidney, Colin G. Prosser, Sarah Nicole Gartner |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty media_common.quotation_subject Drinking Appetite Oxytocin c-Fos Satiety Response 03 medical and health sciences chemistry.chemical_compound Eating 0302 clinical medicine Saccharin Dietary Sucrose Internal medicine Hypophagia medicine Animals General Psychology media_common Nutrition and Dietetics biology Tryptophan Brain Water Feeding Behavior Neuropeptide Y receptor Dietary Fats Lipids Mice Inbred C57BL 030104 developmental biology Endocrinology chemistry Hypothalamus Receptors Oxytocin Sweetening Agents Taste Dietary Supplements Taste aversion biology.protein Energy Intake Food Deprivation 030217 neurology & neurosurgery Thirst medicine.drug |
| Zdroj: | Appetite. 125 |
| ISSN: | 1095-8304 |
| Popis: | Human and laboratory animal studies suggest that dietary supplementation of a free essential amino acid, l-tryptophan (TRP), reduces food intake. It is unclear whether an acute gastric preload of TRP decreases consumption and whether central mechanisms underlie TRP-driven hypophagia. We examined the effect of TRP administered via intragastric gavage on energy- and palatability-induced feeding in mice. We sought to identify central mechanisms through which TRP suppresses appetite. Effects of TRP on consumption of energy-dense and energy-dilute tastants were established in mice stimulated to eat by energy deprivation or palatability. A conditioned taste aversion (CTA) paradigm was used to assess whether hypophagia is unrelated to sickness. c-Fos immunohistochemistry was employed to detect TRP-induced activation of feeding-related brain sites and of oxytocin (OT) neurons, a crucial component of satiety circuits. Also, expression of OT mRNA was assessed with real-time PCR. The functional importance of OT in mediating TRP-driven hypophagia was substantiated by showing the ability of OT receptor blockade to abolish TRP-induced decrease in feeding. TRP reduced intake of energy-dense standard chow in deprived animals and energy-dense palatable chow in sated mice. Anorexigenic doses of TRP did not cause a CTA. TRP failed to affect intake of palatable yet calorie-dilute or noncaloric solutions (10% sucrose, 4.1% Intralipid or 0.1% saccharin) even for TRP doses that decreased water intake in thirsty mice. Fos analysis revealed that TRP increases activation of several key feeding-related brain areas, especially in the brain stem and hypothalamus. TRP activated hypothalamic OT neurons and increased OT mRNA levels, whereas pretreatment with an OT antagonist abolished TRP-driven hypophagia. We conclude that intragastric TRP decreases food and water intake, and TRP-induced hypophagia is partially mediated via central circuits that encompass OT. |
| Databáze: | OpenAIRE |
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