Differential Effects of Biotin Deficiency and Replenishment on Rat Liver Pyruvate and Propionyl-CoA Carboxylases and on Their mRNAs

Rodriguez-Melendez, Rocio; Pérez-Andrade, Martha Elva; Dı́az, Alejandra; Deolarte, Alejandra; Camacho‐Arroyo, Ignacio; Cicerón, Isabel; Ibarra, Isabel; Velázquez, Antonio

doi:10.1006/mgme.1998.2777

Cited by 36 publications

(25 citation statements)

References 29 publications

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“…The reduction in protein-bound biotin in liver was likely caused by a combination of a decrease in carboxylase levels because of reduced synthesis and impairment in carboxylase biotinylation because of reduced synthesis of HCS. The latter is in keeping with the previous detection of accumulated unbiotinylated carboxylases (apocarboxylases) in the liver of biotin-deficient rats (40,41). Thus, through the expedient of repression of mRNA synthesis, the reduction in biotinylated carboxylases in liver could be doubly assured through down-regulation in the synthesis of both apocarboxylases and HCS.…”

Section: Biotin Availability Regulates Mrna Levels Of the Biotin Utilsupporting

confidence: 85%

Paradoxical Regulation of Biotin Utilization in Brain and Liver and Implications for Inherited Multiple Carboxylase Deficiency

Pacheco‐Alvarez

Solorzano–Vargas

Gravel

et al. 2004

Journal of Biological Chemistry

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Holocarboxylase synthetase (HCS) catalyzes the biotinylation of five carboxylases in human cells, and mutations of HCS cause multiple carboxylase deficiency (MCD). Although HCS also participates in the regulation of its own mRNA levels, the relevance of this mechanism to normal metabolism or to the MCD phenotype is not known. In this study, we show that mRNA levels of enzymes involved in biotin utilization, including HCS, are down-regulated during biotin deficiency in liver while remaining constitutively expressed in brain. We propose that this mechanism of regulation is aimed at sparing the essential function of biotin in the brain at the expense of organs such as liver and kidney during biotin deprivation. In MCD, it is possible that some of the manifestations of the disease may be associated with downregulation of biotin utilization in liver because of the impaired activity of HCS and that high dose biotin therapy may in part be important to overcoming the adverse regulatory impact in such organs.

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Section: Biotin Availability Regulates Mrna Levels Of the Biotin Utilsupporting

confidence: 85%

Paradoxical Regulation of Biotin Utilization in Brain and Liver and Implications for Inherited Multiple Carboxylase Deficiency

Pacheco‐Alvarez

Solorzano–Vargas

Gravel

et al. 2004

Journal of Biological Chemistry

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“…25) Furthermore, the mRNA expression of the biotin transporter sodiumdependent multivitamin transporter (SMVT) and pyruvate carboxylase was also decreased in biotin-deficient rat liver and human leukocytes. [26][27][28][29][30] In addition to these genes, the mRNA level of biotinidase was analyzed by quantitative RT-PCR. The abundance of mRNAs of HCS and SMVT remained unchanged by the biotin treatment in STZ rats (Fig.…”

Section: Effects Of Biotin On the Expression Of Transcription Factorsmentioning

confidence: 99%

Effect of Biotin Treatment on Hepatic Gene Expression in Streptozotocin-Induced Diabetic Rats

Sugita

Shirakawa

Sugimoto

et al. 2008

Bioscience, Biotechnology, and Biochemistry

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“…In biotin-deficient mice, activity of 3-methylcrotonylCoA carboxylase (MCC) is reduced in the liver, 20,[26][27][28] resulting in high excretion of 3-HIA, which is a metabolite of L-leucine in the urine. 20,25,26) MCC catalyzes the metabolism of 3-methylcrotonyl-CoA to 3-methylglutaconyl-CoA, which involves with L-leucine catabolism 6,19) Reduction in this enzyme reaction like biotin deficiency leads to the accumulation of the substrate 3-methylcrotonyl-CoA.…”

Section: Discussionmentioning

confidence: 99%

“…20,25,26) MCC catalyzes the metabolism of 3-methylcrotonyl-CoA to 3-methylglutaconyl-CoA, which involves with L-leucine catabolism 6,19) Reduction in this enzyme reaction like biotin deficiency leads to the accumulation of the substrate 3-methylcrotonyl-CoA. Accordingly, accumulated 3-methylcrotonyl-CoA is hydrolyzed to form 3-hydroxyisovaleroyl-CoA by enoyl-CoA hydrolase and then converted to 3-HIA, which is quickly eliminated through urine.…”

Section: Discussionmentioning

confidence: 99%

Biotin-deficient diet induces chromosome misalignment and spindle defects in mouse oocytes

Tsuji

Nakamura

Shibata

2015

Bioscience, Biotechnology, and Biochemistry

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Increased abnormal oocytes due to meiotic chromosome misalignment and spindle defects lead to elevated rates of infertility, miscarriage, and trisomic conceptions. Here, we investigated the effect of biotin deficiency on oocyte quality. Three-week-old female ICR mice were fed a biotin-deficient or control diet (0, 0.004 g biotin/kg diet) for 21 days. On day 22, these mouse oocytes were analyzed by immunofluorescence. Due to biotin, undernutrition increased the frequency of abnormal oocytes (the biotin deficient vs. control: 40 vs. 16%). Next, the remaining mice in the biotin-deficient group were fed a control or biotin-deficient diet from day 22 to 42. Although biotin nutritional status in the recovery group was restored, the frequency of abnormal oocytes in the recovery group was still higher than that in the control group (48 vs. 18%). Our results indicate that steady, sufficient biotin intake is required for the production of high-quality oocytes in mice.

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Differential Effects of Biotin Deficiency and Replenishment on Rat Liver Pyruvate and Propionyl-CoA Carboxylases and on Their mRNAs

Cited by 36 publications

References 29 publications

Paradoxical Regulation of Biotin Utilization in Brain and Liver and Implications for Inherited Multiple Carboxylase Deficiency

Paradoxical Regulation of Biotin Utilization in Brain and Liver and Implications for Inherited Multiple Carboxylase Deficiency

Effect of Biotin Treatment on Hepatic Gene Expression in Streptozotocin-Induced Diabetic Rats

Biotin-deficient diet induces chromosome misalignment and spindle defects in mouse oocytes

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