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Abnormal tryptophan metabolism and experimental diabetes by xanthurenic acid (XA).

Kotake Y, +4 more
- 01 Jan 1975 - 
- Vol. 29, pp 236-239
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TLDR
It is found that saturated fat increased urinary xanthurenic acid in vitamin B6 deficiency and reduced insulin activity, and the antigenicity of xanthUREnic acid-insulin was almost same as native insulin.
Abstract
1) Xanthurenic acid-insulin complex reduced insulin activity. 2) The antigenicity of xanthurenic acid-insulin was almost same as native insulin. 3) Saturated fat increased urinary xanthurenic acid in vitamin B6 deficiency.

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Endogenous kynurenines as targets for drug discovery and development

TL;DR: The kynurenine pathway is the main pathway for tryptophan metabolism and generates compounds that can modulate activity at glutamate receptors and possibly nicotinic receptors, in addition to some as-yet-unidentified sites.
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Kynurenines: from the perspective of major psychiatric disorders.

TL;DR: The role of this unbalanced kynurenine metabolism through interactions with other neurochemicals is discussed as a major contributing pathophysiological mechanism in psychiatric disorders and the biomarker role of kynuranine metabolites and future therapeutic opportunities are discussed.
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Metabolic syndrome, age‐associated neuroendocrine disorders, and dysregulation of tryptophan—kynurenine metabolism

TL;DR: KYN–TRY metabolism might be the meeting point for gene‐environment interaction and a new target for prevention and treatment of MetS/AAND.
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The Role of the Microbial Metabolites Including Tryptophan Catabolites and Short Chain Fatty Acids in the Pathophysiology of Immune-Inflammatory and Neuroimmune Disease.

TL;DR: The role of microbial metabolites in the pathophysiology of diabetes type 2 and autism is described and dysbiosis leading to reduced butyrate levels may increase bacterial translocation into the systemic circulation.
Journal ArticleDOI

Insulin resistance and dysregulation of tryptophan-kynurenine and kynurenine-nicotinamide adenine dinucleotide metabolic pathways.

TL;DR: It is proposed 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.
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