Dietary fat and peroxisome-proliferators affect production of quinolinate in rats, accompanied with suppression of gene expression of α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD)

Yukari Egashira, Hiroyuki Hashimato, Kuniaki Saito, Hiroo Sanada

Research output: Contribution to journalArticle

Abstract

Hepatic α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) plays a key role in regulating NAD biosynthesis from tryptophan. ACMSD also seems to affect the generation of quinolinic acid (QA), a neurotoxin l-tryptophan metabolite. QA is also a potential endogenous toxin. The aim of this study was to evaluate QA concentration and ACMSD mRNA expression after dietary fat or peroxisome-proliferator ingestion. When male Sprague-Dawley rats were fed a clofibrate-free diet (control), or a clofibrate-containing diet for 8 days, hepatic ACMSD mRNA in rats consuming the clofibrate diet was strongly suppressed, as compared with that fed the control. Shifting from the control diet to a clofibrate diet suppressed ACMSD mRNA strongly at day 1 and continued through day 4. However, ACMSD activity decreased gradually. In rats fed with several kinds of peroxisome-proliferator-containing diets, the hepatic ACMSD mRNA was drastically decreased by all the peroxisome-proliferators we used. On the other hand, linoleic acid, clofibrate, bezafibrate and Wy-14,643 affected the serum QA levels. The change of serum QA concentration after peroxisome-proliferator ingestion is suggested to be, in part, due to a decreased ACMSD gene expression. These results suggest that the ingestion of peroxisome-proliferators affect serum QA concentration and that the transcription level of hepatic ACMSD is modulated by peroxisome-proliferators.

Original languageEnglish
Pages (from-to)195-199
Number of pages5
JournalInternational Congress Series
Volume1304
DOIs
Publication statusPublished - 01-11-2007

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Peroxisome Proliferators
Quinolinic Acid
Carboxy-Lyases
Dietary Fats
Clofibrate
Gene Expression
Diet
Messenger RNA
Eating
Liver
Tryptophan
Serum
Bezafibrate
Neurotoxins
Linoleic Acid
NAD
Sprague Dawley Rats

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

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title = "Dietary fat and peroxisome-proliferators affect production of quinolinate in rats, accompanied with suppression of gene expression of α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD)",
abstract = "Hepatic α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) plays a key role in regulating NAD biosynthesis from tryptophan. ACMSD also seems to affect the generation of quinolinic acid (QA), a neurotoxin l-tryptophan metabolite. QA is also a potential endogenous toxin. The aim of this study was to evaluate QA concentration and ACMSD mRNA expression after dietary fat or peroxisome-proliferator ingestion. When male Sprague-Dawley rats were fed a clofibrate-free diet (control), or a clofibrate-containing diet for 8 days, hepatic ACMSD mRNA in rats consuming the clofibrate diet was strongly suppressed, as compared with that fed the control. Shifting from the control diet to a clofibrate diet suppressed ACMSD mRNA strongly at day 1 and continued through day 4. However, ACMSD activity decreased gradually. In rats fed with several kinds of peroxisome-proliferator-containing diets, the hepatic ACMSD mRNA was drastically decreased by all the peroxisome-proliferators we used. On the other hand, linoleic acid, clofibrate, bezafibrate and Wy-14,643 affected the serum QA levels. The change of serum QA concentration after peroxisome-proliferator ingestion is suggested to be, in part, due to a decreased ACMSD gene expression. These results suggest that the ingestion of peroxisome-proliferators affect serum QA concentration and that the transcription level of hepatic ACMSD is modulated by peroxisome-proliferators.",
author = "Yukari Egashira and Hiroyuki Hashimato and Kuniaki Saito and Hiroo Sanada",
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month = "11",
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T1 - Dietary fat and peroxisome-proliferators affect production of quinolinate in rats, accompanied with suppression of gene expression of α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD)

AU - Egashira, Yukari

AU - Hashimato, Hiroyuki

AU - Saito, Kuniaki

AU - Sanada, Hiroo

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N2 - Hepatic α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) plays a key role in regulating NAD biosynthesis from tryptophan. ACMSD also seems to affect the generation of quinolinic acid (QA), a neurotoxin l-tryptophan metabolite. QA is also a potential endogenous toxin. The aim of this study was to evaluate QA concentration and ACMSD mRNA expression after dietary fat or peroxisome-proliferator ingestion. When male Sprague-Dawley rats were fed a clofibrate-free diet (control), or a clofibrate-containing diet for 8 days, hepatic ACMSD mRNA in rats consuming the clofibrate diet was strongly suppressed, as compared with that fed the control. Shifting from the control diet to a clofibrate diet suppressed ACMSD mRNA strongly at day 1 and continued through day 4. However, ACMSD activity decreased gradually. In rats fed with several kinds of peroxisome-proliferator-containing diets, the hepatic ACMSD mRNA was drastically decreased by all the peroxisome-proliferators we used. On the other hand, linoleic acid, clofibrate, bezafibrate and Wy-14,643 affected the serum QA levels. The change of serum QA concentration after peroxisome-proliferator ingestion is suggested to be, in part, due to a decreased ACMSD gene expression. These results suggest that the ingestion of peroxisome-proliferators affect serum QA concentration and that the transcription level of hepatic ACMSD is modulated by peroxisome-proliferators.

AB - Hepatic α-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) plays a key role in regulating NAD biosynthesis from tryptophan. ACMSD also seems to affect the generation of quinolinic acid (QA), a neurotoxin l-tryptophan metabolite. QA is also a potential endogenous toxin. The aim of this study was to evaluate QA concentration and ACMSD mRNA expression after dietary fat or peroxisome-proliferator ingestion. When male Sprague-Dawley rats were fed a clofibrate-free diet (control), or a clofibrate-containing diet for 8 days, hepatic ACMSD mRNA in rats consuming the clofibrate diet was strongly suppressed, as compared with that fed the control. Shifting from the control diet to a clofibrate diet suppressed ACMSD mRNA strongly at day 1 and continued through day 4. However, ACMSD activity decreased gradually. In rats fed with several kinds of peroxisome-proliferator-containing diets, the hepatic ACMSD mRNA was drastically decreased by all the peroxisome-proliferators we used. On the other hand, linoleic acid, clofibrate, bezafibrate and Wy-14,643 affected the serum QA levels. The change of serum QA concentration after peroxisome-proliferator ingestion is suggested to be, in part, due to a decreased ACMSD gene expression. These results suggest that the ingestion of peroxisome-proliferators affect serum QA concentration and that the transcription level of hepatic ACMSD is modulated by peroxisome-proliferators.

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