Difference in the concentration of tryptophan metabolites between maternal and umbilical foetal blood

Morita, Ikue; Kawamoto, Makoto; Yoshida, Hisanobu

doi:10.1016/0378-4347(92)80208-8

Cited by 43 publications

(47 citation statements)

References 14 publications

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“…The same holds true for QA and 5-HT, as the F/M concentration ratio was consistently >1, but not for l-Kyn. Plasma l-Trp and l-Kyn concentrations increase in sheep fetuses at late gestation (Nicholls et al 1999), and l-Trp from the UV is twofold higher in sheep fetuses than in their mothers, while l-Kyn is fivefold higher in sheep fetuses than in human mothers (Morita et al 1992). However, our study is the first to provide data on multiple tissues, such as AF, FL, UV and FP, in rats.…”

Section: Trp Metabolism In Normal Gestationmentioning

confidence: 95%

Maternal and fetal tryptophan metabolism in gestating rats: effects of intrauterine growth restriction

et al. 2015

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L-Tryptophan (L-Trp) is a precursor for serotonin (5-HT) and nicotinamide adenine dinucleotide (NAD) synthesis. Both 5-HT and NAD may impact energy metabolism during gestation given that recent studies have demonstrated that increased 5-HT production is crucial for increasing maternal insulin secretion, and that sirtuin, an NAD(+)-dependent protein deacetylase, regulates endocrine signaling. Infants born with intrauterine growth restriction (IUGR) are at a higher risk of metabolic disease once they reach adulthood. IUGR is associated with altered maternal-fetal amino acid transfer. Whether IUGR affects L-Trp metabolism in mother and fetus has not been fully elucidated. Recently, we developed an analytical method using stable isotope-labeled L-Trp to explore the metabolism of L-Trp and its main metabolites, L-kynurenine (L-Kyn), 5-HT and quinolinic acid (QA). In this study, dams submitted to dietary protein restriction throughout gestation received intravenous infusions of stable isotope-labeled (15)N2-L-Trp to determine whether L-Trp metabolism is affected by IUGR. Samples were obtained from maternal, fetal and umbilical vein plasma, as well as the amniotic fluid (AF), placenta and liver of the mother and the fetus after isotope infusion. We observed evidence for active L-Trp transfer from mother to fetus, as well as de novo synthesis of 5-HT in the fetus. Plasma 5-HT was decreased in undernourished mothers. In IUGR fetuses, maternal-fetal L-Trp transfer remained unaffected, but conversion to QA was impaired, implying that NAD production also decreased. Whether such alterations in tryptophan metabolism during gestation have adverse consequences and contribute to the increased risk of metabolic disease in IUGR remains to be explored.

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Section: Trp Metabolism In Normal Gestationmentioning

confidence: 95%

Maternal and fetal tryptophan metabolism in gestating rats: effects of intrauterine growth restriction

et al. 2015

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“…Like melatonin, IPA is also found in plasma and cerebrospinal fluid under physiological conditions (20,21). IPA is produced by deamination of L-tryptophan by commensal bacteria in human and animal intestines (45), although its production by other tissues has not been systematically investigated.…”

Section: Discussionmentioning

confidence: 99%

“…In the process of screening indole compounds as neuroprotective agents, new properties were uncovered for an endogenous species, indole-3-propionic acid (IPA). IPA has previously been identified in the plasma and cerebrospinal fluid of humans, but its functions are not known (20,21). IPA has, like melatonin, a heterocyclic aromatic ring structure with high resonance stability, which led us to suspect similar neuroprotective and antioxidant properties.…”

mentioning

confidence: 99%

Potent Neuroprotective Properties against the Alzheimer β-Amyloid by an Endogenous Melatonin-related Indole Structure, Indole-3-propionic Acid

Chyan

Pöeggeler

Omar

et al. 1999

Journal of Biological Chemistry

348

254

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Widespread cerebral deposition of a 40 -43-amino acid peptide called the amyloid ␤-protein (A␤) in the form of amyloid fibrils is one of the most prominent neuropathologic features of Alzheimer's disease. Numerous studies suggest that A␤ is toxic to neurons by free radical-mediated mechanisms. We have previously reported that melatonin prevents oxidative stress and death of neurons exposed to A␤. In the process of screening indole compounds for neuroprotection against A␤, potent neuroprotective properties were uncovered for an endogenous related species, indole-3-propionic acid (IPA). This compound has previously been identified in the plasma and cerebrospinal fluid of humans, but its functions are not known. IPA completely protected primary neurons and neuroblastoma cells against oxidative damage and death caused by exposure to A␤, by inhibition of superoxide dismutase, or by treatment with hydrogen peroxide. In kinetic competition experiments using free radical-trapping agents, the capacity of IPA to scavenge hydroxyl radicals exceeded that of melatonin, an indoleamine considered to be the most potent naturally occurring scavenger of free radicals. In contrast with other antioxidants, IPA was not converted to reactive intermediates with pro-oxidant activity. These findings may have therapeutic applications in a broad range of clinical situations.Brains of patients afflicted with Alzheimer's disease show abnormal expression of numerous oxidative stress indicators (1-5) as well as extensive evidence of oxidative damage to proteins (6) and nucleic acids (7,8). A prominent feature of the Alzheimer's disease brain is the widespread cerebral deposition of a 40 -43-amino acid peptide called the amyloid ␤-protein (A␤) 1 in the form of amyloid fibrils within senile plaques and in cerebral and meningeal blood vessels (9, 10). A large body of data suggests that A␤ causes neuronal degeneration and death by mechanisms that involve reactive oxygen species reviewed in Ref. 15).Since the severity of the dementia in Alzheimer's disease has been correlated best with the extent of synaptic loss and the degree of neuronal death (16, 17), enhancing neuronal survival has been a primary objective of many therapeutic strategies. We have recently reported that melatonin prevents oxidative stress and death of neurons exposed to the amyloid peptide (18,19). In the process of screening indole compounds as neuroprotective agents, new properties were uncovered for an endogenous species, indole-3-propionic acid (IPA). IPA has previously been identified in the plasma and cerebrospinal fluid of humans, but its functions are not known (20,21). IPA has, like melatonin, a heterocyclic aromatic ring structure with high resonance stability, which led us to suspect similar neuroprotective and antioxidant properties. Here, we report that IPA prevented oxidative stress and death of primary neurons and neuroblastoma cells exposed to A␤. In addition, IPA also showed a strong level of neuroprotection in two other paradigms of oxidative stress. We found...

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“…Indole-3-propionic acid (IPA) is a deamination product of tryptophan and is found in plasma and cerebrospinal fluid [69,70]. IPA has been shown to be a powerful antioxidant [71] and has been considered as a possible treatment for Alzheimer's disease [72] due to its ability to protect neurons and neuroblastoma cells against oxidative damage and death [73,74].…”

Section: Indole-3-propionic Acidmentioning

confidence: 99%

Bacterial Neuroactive Compounds Produced by Psychobiotics

Wall

Cryan

Ross

et al. 2014

Advances in Experimental Medicine and Biology

276

156

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We recently coined the phrase 'psychobiotics' to describe an emerging class of probiotics of relevance to psychiatry [Dinan et al., Biol Psychiatry 2013;74(10):720-726]. Such "mind-altering" probiotics may act via their ability to produce various biologically active compounds, such as peptides and mediators normally associated with mammalian neurotransmission. Several molecules with neuroactive functions such as gamma-aminobutyric acid (GABA), serotonin, catecholamines and acetylcholine have been reported to be microbially-derived, many of which have been isolated from bacteria within the human gut. Secreted neurotransmitters from bacteria in the intestinal lumen may induce epithelial cells to release molecules that in turn modulate neural signalling within the enteric nervous system and consequently signal brain function and behaviour of the host. Consequently, neurochemical containing/producing probiotic bacteria may be viewed as delivery vehicles for neuroactive compounds and as such, probiotic bacteria may possibly have the potential as a therapeutic strategy in the prevention and/or treatment of certain neurological and neurophysiological conditions.

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Difference in the concentration of tryptophan metabolites between maternal and umbilical foetal blood

Cited by 43 publications

References 14 publications

Maternal and fetal tryptophan metabolism in gestating rats: effects of intrauterine growth restriction

Maternal and fetal tryptophan metabolism in gestating rats: effects of intrauterine growth restriction

Potent Neuroprotective Properties against the Alzheimer β-Amyloid by an Endogenous Melatonin-related Indole Structure, Indole-3-propionic Acid

Bacterial Neuroactive Compounds Produced by Psychobiotics

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