Cobalamin deficiency results in severe metabolic disorder of serine and threonine in rats

Ebara, Shuhei; Toyoshima, Shigeki; Matsumura, Tomoko; Adachi, Satoko; Takenaka, Shigeo; Yamaji, Ryoich; Watanabe, Fumio; Miyatake, Kazutaka; Inui, Hiroshi; Nakano, Yoshihisa

doi:10.1016/s0304-4165(01)00207-0

Cited by 26 publications

(30 citation statements)

References 26 publications

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“…2C), as has been reported previously ( 18 ). In the Cbl-supplemented rats, the level of hepatic PCNA expression was decreased to near the level of the Cbl-sufficient rats (Fig.…”

Section: Resultssupporting

confidence: 88%

“…Methylmalonic acid concentration in urine was determined by high-performance liquid chromatography according to a previous paper ( 18 ). Triacylglycerols in the liver were extracted with isopropanol and measured using a commercial kit ( L -Type Wako TG-H; Wako Pure Chemical Industries, Ltd., Osaka, Japan) according to the manufacturer's instructions.…”

Section: Animals and Treatmentsmentioning

confidence: 99%

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Abnormal Increase in the Expression Level of Proliferating Cell Nuclear Antigen (PCNA) in the Liver and Hepatic Injury in Rats with Dietary Cobalamin Deficiency

Nakao

Kono

Adachi

et al. 2006

J Nutr Sci Vitaminol

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Summary Dietary cobalamin (Cbl; vitamin B 12 ) deficiency resulted in severe growth retardation in rats, and body weight in the Cbl-deficient rats at 20 wk of age was significantly lower compared with the age-matched Cbl-sufficient control rats. In contrast, liver weight, when normalized to body weight, was greater in the Cbl-deficient rats than in the controls ( p Ͻ 0.05). The expression level of proliferating cell nuclear antigen (PCNA), a marker for cell proliferation, in the liver was significantly enhanced in the deficient rats, suggesting that cell proliferation is abnormally activated in the liver under Cbl-deficient conditions. In addition, plasma alanine aminotransferase (ALT) activity, a marker for hepatic injury, was also significantly elevated in the deficient rats. When L -carnitine, which is used clinically for the treatment of Cbl-deficient patients with methylmalonic aciduria, was administered to the Cbl-deficient rats by intraperitoneal injection twice per day for 2 wk (each 0.5 mmol), the amount of methylmalonic acid excreted into the urine was significantly reduced, and the plasma ALT activity was lowered to a normal level. However, the PCNA expression in the liver was barely influenced by the treatment with carnitine. In contrast, when the deficient rats were fed an L -methionine-supplemented diet (4 g of L -methionine per kg of the diet) for 2 wk, the increased expression of PCNA was normalized.

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“…2C), as has been reported previously ( 18 ). In the Cbl-supplemented rats, the level of hepatic PCNA expression was decreased to near the level of the Cbl-sufficient rats (Fig.…”

Section: Resultssupporting

confidence: 88%

Section: Animals and Treatmentsmentioning

confidence: 99%

Abnormal Increase in the Expression Level of Proliferating Cell Nuclear Antigen (PCNA) in the Liver and Hepatic Injury in Rats with Dietary Cobalamin Deficiency

Nakao

Kono

Adachi

et al. 2006

J Nutr Sci Vitaminol

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“…In fact, Ueatrongchit and Asano (13) showed that CnThrDH reacts with only two compounds, L-Thr and DL-␣-amino ␤-hydroxyvalerate, and has no activity toward 36 other compounds, including other amino acids and their derivatives. Because of its high specificity for L-Thr, CnThrDH can be used to quantitate the L-Thr concentration in blood plasma; the plasma level of L-Thr reflects the symptom of certain diseases and can therefore be a criterion for diagnosis of these conditions (13)(14)(15). Yoneda et al (16) were the first to determine the crystal structure of the SDR-like L-ThrDH from Flavobacterium frigidimaris KUC-1 (FfThrDH); they showed that the overall structure of FfThrDH is similar to other GalE structures.…”

Section: The Atomic Coordinates and Structure Factors (Codes 3wmw Andmentioning

confidence: 99%

Binding of NAD+ and l-Threonine Induces Stepwise Structural and Flexibility Changes in Cupriavidus necator l-Threonine Dehydrogenase

Nakano

Okazaki

Tokiwa

et al. 2014

Journal of Biological Chemistry

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“…A lack or deficiency of these vitamins has devastating consequences to the organism, particularly the unborn child [4,19]. The norm requirements for these vitamins are relatively low, however, an imbalance or undersupply may easily occur due to morning sickness (hyperemesis gravidarum).…”

Section: General Significance Of Vitaminsmentioning

confidence: 99%

“…Ein Fehlen oder eine Unterversorgung dieser Vitamine hat verheerende Folgen für den Organismus, insbesondere auch für das noch ungeborene Kind [4,19]. Die Bedarfsnormen für diese Vitamine sind relativ gering, jedoch kann bei einem Schwangerschaftsvomitus (Hyperemesis gravidarum) leicht eine Imbalance bzw.…”

Section: Allgemeine Bedeutung Der Vitamineunclassified

Induction and Prevention of Cleft Lip, Alveolus and Palate and Neural Tube Defects with Special Consideration of B Vitamins and the Methylation Cycle

et al. 2007

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Previous studies on the development of cleft lip, alveolus, palate, and velum and neural tube defects have revealed several shared multifactorial causes. Both anomalies emerge at different times during embryonic development and are not associated with each other unless there is a genetic component to the etiology. Vitamin deficiency disorders are one of several factors contributing to the etiology of these anomalies.Vitamins B6, folic acid and B12 play an essential role in the methylation cycle. A lack of or deficiency in these vitamins thus has severe consequences for the organism, especially the unborn child. Due to its short half-life, vitamin B6 is particularly important for undisturbed embryogenesis and should be taken along with folic acid as a periconceptional supplement to prevent embryonic deformities. This paper is intended to provide the orthodontist (as a member of the interdisciplinary cleft team) with an overview of the issues and etiological significance of vitamin B deficiencies as possible inducers of these embryopathies. This may encourage comprehensive counselling, particularly of parents of children born with deformities who wish to have more children.

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Cobalamin deficiency results in severe metabolic disorder of serine and threonine in rats

Cited by 26 publications

References 26 publications

Abnormal Increase in the Expression Level of Proliferating Cell Nuclear Antigen (PCNA) in the Liver and Hepatic Injury in Rats with Dietary Cobalamin Deficiency

Abnormal Increase in the Expression Level of Proliferating Cell Nuclear Antigen (PCNA) in the Liver and Hepatic Injury in Rats with Dietary Cobalamin Deficiency

Binding of NAD+ and l-Threonine Induces Stepwise Structural and Flexibility Changes in Cupriavidus necator l-Threonine Dehydrogenase

Induction and Prevention of Cleft Lip, Alveolus and Palate and Neural Tube Defects with Special Consideration of B Vitamins and the Methylation Cycle

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