Is Tryptophan ‘more’ Essential than Other Essential Aminoacids in Development? A Morphologic Study

Imbesi, Rosa; Mazzone, Valeria; Castrogiovanni, Paola

doi:10.1111/j.1439-0264.2009.00955.x

Cited by 5 publications

(5 citation statements)

References 17 publications

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“…Limitation of tryptophan availability for protein synthesis could potentially have adverse consequences for child growth. Dietary tryptophan limitation in Sprague Dawley rats resulted in severe growth restriction of young animals 28 . About 5% of dietary tryptophan is degraded to indole and other derivatives by bacteria in the gut lumen 29 .…”

Section: Discussionmentioning

confidence: 99%

Metabolic alterations in children with environmental enteric dysfunction

Semba

Shardell

Trehan

et al. 2016

Sci Rep

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Environmental enteric dysfunction, an asymptomatic condition characterized by inflammation of the small bowel mucosa, villous atrophy, malabsorption, and increased intestinal permeability, is a major contributor to childhood stunting in low-income countries. Here we report the relationship of increased intestinal permeability with serum metabolites in 315 children without acute malnutrition, aged 12–59 months, in rural Malawi. Increased gut permeability was associated with significant differences in circulating metabolites that included lower serum phosphatidylcholines, sphingomyelins, tryptophan, ornithine, and citrulline, and elevated serum glutamate, taurine, and serotonin. Our findings suggest that environmental enteric dysfunction is characterized by alterations in important metabolites involved in growth and differentiation and gut function and integrity.

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Section: Discussionmentioning

confidence: 99%

Metabolic alterations in children with environmental enteric dysfunction

Semba

Shardell

Trehan

et al. 2016

Sci Rep

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“…More specifically, the low posttraumatic urinary cortisol levels have been identified as a risk factor of posttraumatic stress disorder (PTSD) [74]. Moreover, maternal Trp administration in mice alters the development and function of the HPG axis during offspring's pubertal maturation via regulating the productions of prolactin (PRL) and luteinizing hormone (LH) in the pituitary gland [63, 65,66]. Trp-free diets from gestation to puberty cause hypoandrogenism and hypoprolactinemia in the male progeny [65,66], while maternal administration of Trp-enriched diets increases serum LH in offspring at postnatal (P) 70 days [63].…”

Section: Maternal Tryptophan Fluctuation Alters Behavioral Exhibition...mentioning

confidence: 99%

“…Moreover, maternal Trp administration in mice alters the development and function of the HPG axis during offspring's pubertal maturation via regulating the productions of prolactin (PRL) and luteinizing hormone (LH) in the pituitary gland [63, 65,66]. Trp-free diets from gestation to puberty cause hypoandrogenism and hypoprolactinemia in the male progeny [65,66], while maternal administration of Trp-enriched diets increases serum LH in offspring at postnatal (P) 70 days [63]. Increased serum PRL is associated with a diagnosis of BPD [76], and hyperprolactinemia has been observed in people with neurotic and personality disorders [77].…”

Section: Maternal Tryptophan Fluctuation Alters Behavioral Exhibition...mentioning

confidence: 99%

Gestational Tryptophan Fluctuation Underlying Ontogenetic Origin of Neuropsychiatric Disorders

Huang¹,

Li²,

Cheng³

2023

Cognitive Behavioral Therapy - Basic Principles and Application Areas

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Neuropsychiatry underlies personality development and social functioning. Borderline personality disorder exhibits high trait aggression and is associated with tryptophan hydroxylase polymorphisms. The acute tryptophan depletion reduces plasma and cerebrospinal fluid tryptophan availability and brain serotonin concentrations, leading to alterations in personality and trait-related behaviors. Tryptophan is essential for fatal neurodevelopment and immunomodulation in pregnancy. Gestational tryptophan fluctuation induced by maternal metabolic disorders or drug administrations may account for the maternal-fetal transmission determining neurogenesis and microbial development, consequentially shaping the long-standing patterns of thinking and behavior. However, it is not possible to assess the gestational tryptophan exposure effects on fetal brain and gastrointestinal system in humans for ethical reasons. The maternal–fetal microbe transmission in rodents during gestation, vaginal delivery, and breastfeeding is inevitable. Chicken embryo may be an alternative and evidence from the chicken embryo model reveals that gestational tryptophan fluctuation, i.e., exposed to excessive tryptophan or its metabolite, serotonin, attenuates aggressiveness and affects peer sociometric status. This chapter discusses the gestational tryptophan fluctuation as a risk factor of personality disorders in offspring and the prevention of personality disorders by dietary tryptophan control and medication therapy management during pregnancy.

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“…Pregnant rats deprived of dietary tryptophan gave birth to newborn rats with dwarfism, impaired growth, and low plasma growth hormone concentrations (127,128). Rat pups and lactating dams fed a tryptophan-restricted diet showed growth retardation accompanied by serotonin depletion and reduced developmental plasticity in the brain (129,130).…”

Section: Limitation Of Essential Amino Acids and Growth In Animal Modelsmentioning

confidence: 99%

Perspective: The Potential Role of Essential Amino Acids and the Mechanistic Target of Rapamycin Complex 1 (mTORC1) Pathway in the Pathogenesis of Child Stunting

Semba

Trehan

González-Freire

et al. 2016

Advances in Nutrition

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Stunting is the best summary measure of chronic malnutrition in children. Approximately one-quarter of children under age 5 worldwide are stunted. Lipid-based or micronutrient supplementation has little to no impact in reducing stunting, which suggests that other critical dietary nutrients are missing. A dietary pattern of poor-quality protein is associated with stunting. Stunted children have significantly lower circulating essential amino acids than do nonstunted children. Inadequate dietary intakes of essential amino acids could adversely affect growth, because amino acids are required for synthesis of proteins. The master growth regulation pathway, the mechanistic target of rapamycin complex 1 (mTORC1) pathway, is exquisitely sensitive to amino acid availability. mTORC1 integrates cues such as nutrients, growth factors, oxygen, and energy to regulate growth of bone, skeletal muscle, nervous system, gastrointestinal tract, hematopoietic cells, immune effector cells, organ size, and whole-body energy balance. mTORC1 represses protein and lipid synthesis and cell and organismal growth when amino acids are deficient. Over the past 4 decades, the main paradigm for child nutrition in developing countries has been micronutrient malnutrition, with relatively less attention paid to protein. In this Perspective, we present the view that essential amino acids and the mTORC1 pathway play a key role in child growth. The current assumption that total dietary protein intake is adequate for growth among most children in developing countries needs reevaluation. Adv Nutr 2016;7:853-65.

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Is Tryptophan ‘more’ Essential than Other Essential Aminoacids in Development? A Morphologic Study

Cited by 5 publications

References 17 publications

Metabolic alterations in children with environmental enteric dysfunction

Metabolic alterations in children with environmental enteric dysfunction

Gestational Tryptophan Fluctuation Underlying Ontogenetic Origin of Neuropsychiatric Disorders

Perspective: The Potential Role of Essential Amino Acids and the Mechanistic Target of Rapamycin Complex 1 (mTORC1) Pathway in the Pathogenesis of Child Stunting

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