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  1. Article: Anthranilic Acid, a GPR109A Agonist, and Schizophrenia.

    Oxenkrug, Gregory / Forester, Brent

    International journal of tryptophan research : IJTR

    2024  Volume 17, Page(s) 11786469241239125

    Abstract: Introduction: Limited clinical efficiency of current medications warrants search for new antipsychotic agents. Deorphanized G-protein coupled receptor (GPR)109A has not attracted much of attention of schizophrenia researchers. We analyzed literature and ...

    Abstract Introduction: Limited clinical efficiency of current medications warrants search for new antipsychotic agents. Deorphanized G-protein coupled receptor (GPR)109A has not attracted much of attention of schizophrenia researchers. We analyzed literature and our data on endogenous agonists of GPR109A, beta-hydroxybutyrate (BHB), anthranilic (AA), butyric (BA), and nicotinic (NA) acids, in individuals with schizophrenia.
    Data: Sex specific differences: plasma AA levels were 27% higher in female than in male patients and correlated with PANSS before 6 weeks of antipsychotics treatment (
    Discussion: Upregulation of GPR109A, an anti-inflammatory and neuroprotective receptor, inhibits cytosolic phospholipase A2 (cPLA2), an enzyme that breakdown myelin, lipid-based insulating axonal sheath that protects and promotes nerve conduction. Brain cPLA2 is upregulated in individuals with schizophrenia and subjects at high-risk for development of psychosis. Lower myelin content is associated with cognitive decline in individuals with schizophrenia. Therefore, GPR109A might exert antipsychotic effect via suppression of cPLA2, and, consequently, preservation of myelin integrity. Future research might explore antipsychotic effects of (1) human pegylated kynureninase, an enzyme that catalyzes formation of AA from kynurenine (Kyn); (2) inhibitors of Kyn conversion into kynurenic acid, for example, KYN5356, to patients with already impaired Kyn conversion into 3-hydroxykynurenine; (3) synthetic GPR 109A agonists, for example, MK-1903 and SCH900271 and GSK256073, that underwent clinical trials as anti-dyslipidemia agents. GPR109A expression, that might be a new endophenotype of schizophrenia, especially associated with cognitive impairment, needs thorough assessment.
    Language English
    Publishing date 2024-03-25
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2517435-6
    ISSN 1178-6469
    ISSN 1178-6469
    DOI 10.1177/11786469241239125
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  2. Article ; Online: Extension of life span by down-regulation of enzymes catalyzing tryptophan conversion into kynurenine: Possible implications for mechanisms of aging.

    Oxenkrug, Gregory / Navrotska, Valeriya

    Experimental biology and medicine (Maywood, N.J.)

    2023  Volume 248, Issue 7, Page(s) 573–577

    Abstract: The end products of catabolism of tryptophan (Trp), an essential amino acid, are known to affect mechanism(s) of aging, a neurodegenerative condition. This review focuses on the possible role of the initial step of Trp catabolism, kynurenine (Kyn) ... ...

    Abstract The end products of catabolism of tryptophan (Trp), an essential amino acid, are known to affect mechanism(s) of aging, a neurodegenerative condition. This review focuses on the possible role of the initial step of Trp catabolism, kynurenine (Kyn) formation from Trp, in aging mechanism(s). Rate-limiting enzymes of Trp conversion into Kyn are tryptophan 2,3-dioxygenase 2 (TDO) or indoleamine 2,3-dioxygenase (IDO). Aging is associated with up-regulated production of cortisol, an activator of TDO, and pro-inflammatory cytokines, inducers of IDO. The other rate-limiting enzyme of Kyn formation from Trp is ATP-binding cassette (ABC) transporter that regulates Trp availability as a substrate for TDO. Inhibitors of TDO (alpha-methyl tryptophan) and ABC transporter (5-methyltryptophan) extended life span of wild-type
    MeSH term(s) Animals ; Humans ; Mice ; Tryptophan/metabolism ; Kynurenine/metabolism ; Longevity ; Down-Regulation ; Aging ; Drosophila/metabolism ; Receptors, G-Protein-Coupled/metabolism
    Chemical Substances Tryptophan (8DUH1N11BX) ; Kynurenine (343-65-7) ; GPR35 protein, mouse ; Receptors, G-Protein-Coupled
    Language English
    Publishing date 2023-06-10
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 4015-0
    ISSN 1535-3699 ; 1525-1373 ; 0037-9727
    ISSN (online) 1535-3699 ; 1525-1373
    ISSN 0037-9727
    DOI 10.1177/15353702231179411
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  3. Article ; Online: Low Nitric Oxide and High C-Reactive Protein in Depression: Not a Paradox!

    Oxenkrug, Gregory

    The Journal of clinical psychiatry

    2017  Volume 78, Issue 6, Page(s) 732

    MeSH term(s) C-Reactive Protein ; Depression ; Depressive Disorder ; Humans ; Nitric Oxide ; Nutrition Surveys
    Chemical Substances Nitric Oxide (31C4KY9ESH) ; C-Reactive Protein (9007-41-4)
    Language English
    Publishing date 2017-09-05
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 716287-x
    ISSN 1555-2101 ; 0160-6689
    ISSN (online) 1555-2101
    ISSN 0160-6689
    DOI 10.4088/JCP.17lr11532
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  4. Article ; Online: Increased Plasma Levels of Xanthurenic and Kynurenic Acids in Type 2 Diabetes.

    Oxenkrug, Gregory F

    Molecular neurobiology

    2015  Volume 52, Issue 2, Page(s) 805–810

    Abstract: About 350 million people worldwide have type 2 diabetes (T2D). The major risk factor of T2D is impaired glucose tolerance (pre-diabetes) with 10 % of pre-diabetes subjects develop T2D every year. Understanding of mechanisms of development of T2D from pre- ...

    Abstract About 350 million people worldwide have type 2 diabetes (T2D). The major risk factor of T2D is impaired glucose tolerance (pre-diabetes) with 10 % of pre-diabetes subjects develop T2D every year. Understanding of mechanisms of development of T2D from pre-diabetes is important for prevention and treatment of T2D. Chronic stress and chronic low-grade inflammation are prominent risk factors for T2D development in pre-diabetic subjects. However, molecular mechanisms mediating effect of stress and inflammation on development of T2D from pre-diabetes remain unknown. One of such mechanisms might involve kynurenine (KYN) pathway (KP) of tryptophan (TRP) metabolism. We suggested that chronic stress- or chronic low-grade inflammation-induced upregulation of formation of upstream KTP metabolites, KYN and 3-hydroxyKYN, combined with chronic stress- or chronic low-grade inflammation-induced deficiency of pyridoxal 5'-phosphate, a co-factor of downstream enzymes of KTP, triggers overproduction of diabetogenic downstream KYN metabolites, kynurenic acid (KYNA) and 3-hydroxyKYNA (also known as xanthurenic acid (XA)). As the initial assessment of our working hypothesis, we evaluated plasma levels of up- and downstream KP metabolites in the same samples of T2D patients. KYN, XA, and KYNA levels in plasma samples of T2D patients were higher than in samples of non-diabetic subjects. Our results provide further support of "kynurenine hypothesis of insulin resistance and its progression to T2D" that suggested that overproduction of diabetogenic KP metabolites, induced by chronic stress or chronic low-grade inflammation, is one of the mechanisms promoting development of T2D from pre-diabetes. Downstream metabolites of KP might serve as biomarkers of T2D and targets for clinical intervention.
    MeSH term(s) 3-Hydroxyanthranilic Acid/metabolism ; Adult ; Aged ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/drug therapy ; Female ; Humans ; Hypoglycemic Agents/pharmacology ; Hypoglycemic Agents/therapeutic use ; Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism ; Inflammation/blood ; Kynurenic Acid/blood ; Kynurenine/metabolism ; Male ; Metformin/pharmacology ; Metformin/therapeutic use ; Middle Aged ; Prediabetic State/blood ; Pyridoxal Phosphate/physiology ; Stress, Physiological ; Tryptophan/metabolism ; Tryptophan Oxygenase/metabolism ; Xanthurenates/blood
    Chemical Substances Hypoglycemic Agents ; Indoleamine-Pyrrole 2,3,-Dioxygenase ; Xanthurenates ; 3-Hydroxyanthranilic Acid (1UQB1BT4OT) ; Kynurenine (343-65-7) ; xanthurenic acid (58LAB1BG8J) ; Pyridoxal Phosphate (5V5IOJ8338) ; Tryptophan (8DUH1N11BX) ; Metformin (9100L32L2N) ; Tryptophan Oxygenase (EC 1.13.11.11) ; Kynurenic Acid (H030S2S85J)
    Language English
    Publishing date 2015-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-015-9232-0
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  5. Article ; Online: Benserazide, an Inhibitor of Peripheral Kynurenine Metabolism, Attenuates Olanzapine-Induced Weight Gain, Insulin Resistance, and Dyslipidemia in C57Bl/6j Mice.

    Oxenkrug, Gregory / Summergrad, Paul

    Molecular neurobiology

    2019  Volume 57, Issue 1, Page(s) 135–138

    Abstract: Schizophrenia (Sz) patients, especially treated with atypical antipsychotics, are at high risk of the development of metabolic syndrome that increases morbidity and mortality and impairs compliance with treatment. Mechanism of the high association of ... ...

    Abstract Schizophrenia (Sz) patients, especially treated with atypical antipsychotics, are at high risk of the development of metabolic syndrome that increases morbidity and mortality and impairs compliance with treatment. Mechanism of the high association of metabolic syndrome with the use of atypical antipsychotics is not clear. Literature and our data suggest that chronic inflammation- or stress-induced dysregulation of the peripheral down-stream kynurenine (Kyn) metabolism, shared by both Sz and metabolic syndrome, contributes to the development of metabolic syndrome in Sz patients treated with atypical antipsychotics. Correction of dysregulation of the peripheral down-stream metabolism of Kyn would prevent/treat metabolic syndrome. This is a pre-clinical trial of the effect of benserazide (BRZ), an inhibitor of the key enzymes of Kyn metabolism, on olanzapine-induced mouse model of metabolic syndrome. Olanzapine is one of the most effective atypical antipsychotics but has high potential to induce metabolic syndrome. Olanzapine (4 mg/kg, p.o) and/or BRZ (100 mg/day, p.o.) were administered to 6-week-old C57Bl/6 female mice, 5 days/week, for 10 weeks. The study was approved by the Tufts Medical Center Institutional Animal Care and Use Committee. BRZ attenuated olanzapine-induced excessive weight gain, impairment of glucose tolerance, and elevation of plasma cholesterol and triglycerides. Present results suggest that peripheral down-stream Kyn metabolism is a new target for prevention/treatment of olanzapine-induced metabolic syndrome. BRZ has a high translational potential as medication already approved for human use.
    MeSH term(s) Animals ; Antipsychotic Agents/pharmacology ; Benserazide/pharmacology ; Dyslipidemias/chemically induced ; Female ; Insulin Resistance/physiology ; Kynurenine/pharmacology ; Metabolic Syndrome/blood ; Mice, Inbred C57BL ; Obesity/metabolism ; Olanzapine/pharmacology ; Weight Gain/drug effects ; Weight Gain/physiology
    Chemical Substances Antipsychotic Agents ; Kynurenine (343-65-7) ; Benserazide (762OS3ZEJU) ; Olanzapine (N7U69T4SZR)
    Language English
    Publishing date 2019-09-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-019-01763-x
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  6. Article ; Online: Serotonin-kynurenine hypothesis of depression: historical overview and recent developments.

    Oxenkrug, Gregory

    Current drug targets

    2013  Volume 14, Issue 5, Page(s) 514–521

    Abstract: This mini-review focuses on the studies of late Prof. IP Lapin (1903 - 2012) and his research team on the role of methoxyindole and kynurenine (KYN) pathways of tryptophan (TRP) metabolism in the pathogenesis of depression and action mechanisms of ... ...

    Abstract This mini-review focuses on the studies of late Prof. IP Lapin (1903 - 2012) and his research team on the role of methoxyindole and kynurenine (KYN) pathways of tryptophan (TRP) metabolism in the pathogenesis of depression and action mechanisms of antidepressant effect. In the late 60s of the last century Prof. IP Lapin suggested that "intensification of central serotoninergic processes is a determinant of the thymoleptic (mood elevating) component" while "activation of noradrenergic processes is responsible for psychoenergetic and motor-stimulating component of the clinical antidepressant effect". The cause of serotonin deficiency in depression was attributed to the shunt of TRP "metabolism away from serotonin production towards KYN production" due to cortisol-induced activation of liver enzyme, tryptophan 2,3- dioxygenase, the rate-limiting enzyme of TRP - KYN pathway. Prof. Lapin suggested and discovered that KYN and its metabolites affect brain functions, and proposed the role of neurokynurenines in pathogenesis of depression and action mechanisms of antidepressant effect (kynurenine hypothesis). Further research suggested the antidepressant and cognition- enhancing effects of post-serotonin metabolite, N-acetylserotonin (NAS), an agonist to tyrosine kinase B (TrkB) receptor; and link between depression and chronic inflammation-associated disorders (e.g., insulin resistance, hepatitis C virus) via inflammation-induced activation of indoleamine 2,3- dioxygenase, brain located rate-limiting enzyme of TRY - KYN metabolism. NAS and kynurenines might be the targets for prevention and treatment of depression and associated conditions.
    MeSH term(s) Animals ; Antidepressive Agents/chemistry ; Antidepressive Agents/therapeutic use ; Brain/drug effects ; Brain/metabolism ; Brain/physiopathology ; Cognition ; Depression/diagnosis ; Depression/drug therapy ; Depression/history ; Depression/metabolism ; Depression/physiopathology ; Depression/psychology ; Drug Design ; Emotions ; History, 20th Century ; History, 21st Century ; Humans ; Kynurenine/metabolism ; Serotonin/analogs & derivatives ; Serotonin/deficiency ; Serotonin/metabolism ; Signal Transduction/drug effects
    Chemical Substances Antidepressive Agents ; Serotonin (333DO1RDJY) ; Kynurenine (343-65-7) ; N-acetylserotonin (P4TO3C82WV)
    Language English
    Publishing date 2013-01-03
    Publishing country United Arab Emirates
    Document type Historical Article ; Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2064859-5
    ISSN 1873-5592 ; 1389-4501
    ISSN (online) 1873-5592
    ISSN 1389-4501
    DOI 10.2174/1389450111314050002
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  7. Article ; Online: Insulin resistance and dysregulation of tryptophan-kynurenine and kynurenine-nicotinamide adenine dinucleotide metabolic pathways.

    Oxenkrug, Gregory

    Molecular neurobiology

    2013  Volume 48, Issue 2, Page(s) 294–301

    Abstract: Insulin resistance (IR) underlines aging and aging-associated medical (diabetes, obesity, dyslipidemia, hypertension) and psychiatric (depression, cognitive decline) disorders. Molecular mechanisms of IR in genetically or metabolically predisposed ... ...

    Abstract Insulin resistance (IR) underlines aging and aging-associated medical (diabetes, obesity, dyslipidemia, hypertension) and psychiatric (depression, cognitive decline) disorders. Molecular mechanisms of IR in genetically or metabolically predisposed individuals remain uncertain. Current review of the literature and our data presents the evidences that dysregulation of tryptophan (TRP)-kynurenine (KYN) and KYN-nicotinamide adenine dinucleotide (NAD) metabolic pathways is one of the mechanisms of IR. The first and rate-limiting step of TRP-KYN pathway is regulated by enzymes inducible by pro-inflammatory factors and/or stress hormones. The key enzymes of KYN-NAD pathway require pyridoxal-5-phosphate (P5P), an active form of vitamin B6, as a cofactor. Deficiency of P5P diverts KYN-NAD metabolism from production of NAD to the excessive formation of xanthurenic acid (XA). Human and experimental studies suggested that XA and some other KYN metabolites might impair production, release, and biological activity of insulin. We propose that one of the mechanisms of IR is inflammation- and/or stress-induced upregulation of TRP-KYN metabolism in combination with P5P deficiency-induced diversion of KYN-NAD metabolism towards formation of XA and other KYN derivatives affecting insulin activity. Monitoring of KYN/P5P status and formation of XA might help to identify subjects at risk for IR. Pharmacological regulation of the TRP-KYN and KYN-NAD pathways and maintaining of adequate vitamin B6 status might contribute to prevention and treatment of IR in conditions associated with inflammation/stress-induced excessive production of KYN and deficiency of vitamin B6, e.g., type 2 diabetes, obesity, cardiovascular diseases, aging, menopause, pregnancy, and hepatitis C virus infection.
    MeSH term(s) Biomarkers/metabolism ; Humans ; Insulin Resistance ; Kynurenine/metabolism ; Metabolic Networks and Pathways ; NAD/metabolism ; Tryptophan/metabolism
    Chemical Substances Biomarkers ; NAD (0U46U6E8UK) ; Kynurenine (343-65-7) ; Tryptophan (8DUH1N11BX)
    Language English
    Publishing date 2013-06-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-013-8497-4
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  8. Article ; Online: Interferon-gamma - Inducible Inflammation: Contribution to Aging and Aging-Associated Psychiatric Disorders.

    Oxenkrug, Gregory

    Aging and disease

    2011  Volume 2, Issue 6, Page(s) 474–486

    Abstract: Aging is associated with the chronic, low grade, Th-1 type inflammation. The key Th-1 type, pro-inflammatory cytokine, interferon-gamma (IFNG), transcriptionally induces the rate-limiting enzyme of tryptophan (TRY) - kynurenine (KYN) pathway, indoleamine ...

    Abstract Aging is associated with the chronic, low grade, Th-1 type inflammation. The key Th-1 type, pro-inflammatory cytokine, interferon-gamma (IFNG), transcriptionally induces the rate-limiting enzyme of tryptophan (TRY) - kynurenine (KYN) pathway, indoleamine 2,3- dioxygenase (IDO). Activation of IDO shunts TRY metabolism from production of serotonin (substrate of antidepressant effect) and its derivatives: N-acetylserotonin (an agonist to the receptors of brain derived neurotropic factor), and melatonin (regulator of sleep and other circadian rhythms), towards production of KYN and its derivatives (anxiogenic, neurotoxic and pro-oxidant factors). Some of kynurenines up-regulate nitric oxide synthase (NOS). Concurrently with activation of IDO, IFNG induces guanosine triphosphate cyclohydrolase I (GTPCH), the rate limiting enzyme of GTP conversion into BH2 (and increases formation of a stable derivative of BH2, neopterin, at the expense of production of BH4, the mandatory co-factor of NOS). Combination of increased NOS activity (by kynurenines) with decreased formation of BH4 leads to the uncoupling of NOS with consequent shift of arginine metabolism from biosynthesis of NO to formation of superoxide anion and other free radicals, and exacerbation of depression, anxiety and cognitive impairment caused by kynurenines. Polymorphism of IFNG (+874) T/A gene, that encodes production of IFNG protein, impacts the IDO and GTPCH activity that might be assessed in humans by KYN/TRY ratio and neopterin concentrations in biological fluids (e.g., blood, urine and spinal fluid). The hypothesis of IFNG inducible IDO/GTPCH inflammation cascade helps to understand the increased association between aging, inflammation and aging-associated psychiatric and medical (insulin resistance, obesity) disorders. Evaluation of markers of IFNG-inducible inflammation cascade might be used to assess the severity of corresponding behavioral and cognitive changes and the efficacy of pharmacological interventions (e.g., IDO inhibitors).
    Language English
    Publishing date 2011-12-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2625789-0
    ISSN 2152-5250 ; 2152-5250
    ISSN (online) 2152-5250
    ISSN 2152-5250
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  9. Article ; Online: Kynurenine and hypotension: historic perspectives.

    Oxenkrug, Gregory F

    Critical care medicine

    2012  Volume 40, Issue 6, Page(s) 2006; author reply 2006–7

    MeSH term(s) Female ; Humans ; Hypotension/etiology ; Kynurenine/biosynthesis ; Male ; Shock, Septic/complications ; Tryptophan/metabolism
    Chemical Substances Kynurenine (343-65-7) ; Tryptophan (8DUH1N11BX)
    Language English
    Publishing date 2012-06
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 197890-1
    ISSN 1530-0293 ; 0090-3493
    ISSN (online) 1530-0293
    ISSN 0090-3493
    DOI 10.1097/CCM.0b013e31824e1e3b
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  10. Article: Effect of kynurenic acid on development and aging in wild type and vermilion mutants of

    Navrotskaya, Valeriya / Oxenkrug, Gregory

    Pharmacology, drug development & therapeutics

    2016  Volume 1, Issue 1

    Abstract: Background: Up-regulation of tryptophan (Trp) conversion into kynurenine (Kyn) and increased formation of down-stream metabolites of Kyn is one of the mechanisms of aging and neurodegenerative disorders. Kyn is an immediate precursor of kynurenic acid ( ... ...

    Abstract Background: Up-regulation of tryptophan (Trp) conversion into kynurenine (Kyn) and increased formation of down-stream metabolites of Kyn is one of the mechanisms of aging and neurodegenerative disorders. Kyn is an immediate precursor of kynurenic acid (KYNA), an antagonist to NMDA and α7nAChR receptors and activator of aryl hydrocarbon receptor. Increased formation of KYNA ameliorates neurodegeneration and eclosion defect in Drosophila model of Huntington's Disease.
    Aims: Effect of KYNA on pupae viability and life span was evaluated in wild type (Canton-S, CS) and
    Methods: Vermilion mutants were transferred into the Canton-S genetic background (v-CS). KYNA effect on viability (number of filial generation pupae and %% of their lethality) was assessed in pupae maintained at standard temperature (23°C). KYNA effect on life span was evaluated in adult (imago) flies maintained at 28°C (accelerated aging).
    Results: KYNA drastically increased (4 fold from 8.36 to 33.62) %% of dead pupae in Canton-S but not in
    Discussion: This the first (to the best of our knowledge) observation of the toxic effect of KYNA in Drosophila pupae. KYNA effect on high-temperature induced aging acceleration was gender dependent. Present data support the role of downstream Kyn metabolites in aging mechanisms.
    Language English
    Publishing date 2016-12-08
    Publishing country England
    Document type Journal Article
    ISSN 2399-7389
    ISSN 2399-7389
    DOI 10.15761/PDDT.1000104
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