BACKGROUND: Dieting in healthy women results in a decrease in the availability of tryptophan (TRP), the amino-acid precursor of serotonin (5-HT), for brain 5-HT synthesis. This is associated with increases in the prolactin response to 5-HT drug challenge suggesting a 'supersensitivity' of 5-HT neuroendocrine responses. The aim of the study was to assess whether increased TRP intake during dieting would prevent the changes in TRP availability and 5-HT neuroendocrine function. METHOD: Fifty female subjects underwent a 1000 kcal daily diet for 3 weeks. In the final week of the diet subjects were randomly allocated to receive either nutritionally-sourced TRP (1.8 g daily) or placebo in a double-blind, parallel group, design. RESULTS:TRP supplementation failed to modify the dieting-induced reduction in fasting TRP availability to the brain. However, in contrast to placebo-treated subjects, subjects receiving additional TRP did not show enhanced prolactin responses to intravenous TRP challenge. CONCLUSIONS: The decrease in TRP availability produced by dieting may be due to increased TRP metabolism rather than decreased TRP intake. While TRP treatment did not increase fasting TRP availability it may have modified the effect of dieting on brain 5-HT function. Further studies will be needed to see if this effect of TRP has consequences for the effectiveness of dieting as means of weight control.
RCT Entities:
BACKGROUND: Dieting in healthy women results in a decrease in the availability of tryptophan (TRP), the amino-acid precursor of serotonin (5-HT), for brain 5-HT synthesis. This is associated with increases in the prolactin response to 5-HT drug challenge suggesting a 'supersensitivity' of 5-HT neuroendocrine responses. The aim of the study was to assess whether increased TRP intake during dieting would prevent the changes in TRP availability and 5-HT neuroendocrine function. METHOD: Fifty female subjects underwent a 1000 kcal daily diet for 3 weeks. In the final week of the diet subjects were randomly allocated to receive either nutritionally-sourced TRP (1.8 g daily) or placebo in a double-blind, parallel group, design. RESULTS:TRP supplementation failed to modify the dieting-induced reduction in fasting TRP availability to the brain. However, in contrast to placebo-treated subjects, subjects receiving additional TRP did not show enhanced prolactin responses to intravenous TRP challenge. CONCLUSIONS: The decrease in TRP availability produced by dieting may be due to increased TRP metabolism rather than decreased TRP intake. While TRP treatment did not increase fasting TRP availability it may have modified the effect of dieting on brain 5-HT function. Further studies will be needed to see if this effect of TRP has consequences for the effectiveness of dieting as means of weight control.
Authors: Barbara Felt; Elias Jimenez; Julia Smith; Agustin Calatroni; Niko Kaciroti; Gloria Wheatcroft; Betsy Lozoff Journal: Pediatr Res Date: 2006-09-11 Impact factor: 3.756
Authors: Abraão Tiago Batista Guimarães; Raissa de Oliveira Ferreira; Joyce Moreira de Souza; Wellington Alves Mizael da Silva; Anderson Rodrigo da Silva; Aline Sueli de LimaRodrigues; Daniela de Melo E Silva; Renata Mazaro E Costa; André Luis da Silva Castro; Guilherme Malafaia Journal: Environ Sci Pollut Res Int Date: 2016-09-30 Impact factor: 4.223
Authors: B T Christian; A S Fox; J A Oler; N T Vandehey; D Murali; J Rogers; T R Oakes; S E Shelton; R J Davidson; N H Kalin Journal: Neuroimage Date: 2009-06-06 Impact factor: 6.556