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Intragastric preloads of l-tryptophan reduce ingestive behavior via oxytocinergic neural mechanisms in male mice.
Appetite. 2018 06 01; 125:278-286.A

Abstract

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.

Authors+Show Affiliations

University of Waikato, Hamilton, New Zealand.University of Waikato, Hamilton, New Zealand.University of Waikato, Hamilton, New Zealand.Dairy Goat Co-operative (NZ) Ltd, Hamilton, New Zealand.Dairy Goat Co-operative (NZ) Ltd, Hamilton, New Zealand.University of Waikato, Hamilton, New Zealand.Department of Food Science and Nutrition, University of Minnesota, St. Paul, MN, USA.University of Waikato, Hamilton, New Zealand; Department of Food Science and Nutrition, University of Minnesota, St. Paul, MN, USA. Electronic address: pawel@waikato.ac.nz.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29471071

Citation

Gartner, Sarah N., et al. "Intragastric Preloads of L-tryptophan Reduce Ingestive Behavior Via Oxytocinergic Neural Mechanisms in Male Mice." Appetite, vol. 125, 2018, pp. 278-286.
Gartner SN, Aidney F, Klockars A, et al. Intragastric preloads of l-tryptophan reduce ingestive behavior via oxytocinergic neural mechanisms in male mice. Appetite. 2018;125:278-286.
Gartner, S. N., Aidney, F., Klockars, A., Prosser, C., Carpenter, E. A., Isgrove, K., Levine, A. S., & Olszewski, P. K. (2018). Intragastric preloads of l-tryptophan reduce ingestive behavior via oxytocinergic neural mechanisms in male mice. Appetite, 125, 278-286. https://doi.org/10.1016/j.appet.2018.02.015
Gartner SN, et al. Intragastric Preloads of L-tryptophan Reduce Ingestive Behavior Via Oxytocinergic Neural Mechanisms in Male Mice. Appetite. 2018 06 1;125:278-286. PubMed PMID: 29471071.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Intragastric preloads of l-tryptophan reduce ingestive behavior via oxytocinergic neural mechanisms in male mice. AU - Gartner,Sarah N, AU - Aidney,Fraser, AU - Klockars,Anica, AU - Prosser,Colin, AU - Carpenter,Elizabeth A, AU - Isgrove,Kiriana, AU - Levine,Allen S, AU - Olszewski,Pawel K, Y1 - 2018/02/19/ PY - 2017/09/29/received PY - 2018/02/09/revised PY - 2018/02/15/accepted PY - 2018/2/23/pubmed PY - 2019/6/20/medline PY - 2018/2/23/entrez KW - Amino acids KW - Food intake KW - Oxytocin KW - Tryptophan KW - c-Fos SP - 278 EP - 286 JF - Appetite JO - Appetite VL - 125 N2 - 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. SN - 1095-8304 UR - https://www.unboundmedicine.com/medline/citation/29471071/Intragastric_preloads_of_l_tryptophan_reduce_ingestive_behavior_via_oxytocinergic_neural_mechanisms_in_male_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0195-6663(17)31445-9 DB - PRIME DP - Unbound Medicine ER -