Putrescine is involved in the vitamin D action in chick intestine

Shinki, Toshimasa; Tanaka, Hirofumi; Takito, Jiro; Yamaguchi, Akira; Nakamura, Yuichi; Yoshiki, Shusaku; Suda, Toshio

doi:10.1016/0016-5085(91)90590-h

Cited by 24 publications

(12 citation statements)

References 30 publications

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“…We found that 25-OH-D 3 in the maternal diet induced the increase of the villi height in the three segments at hatch. This was in line with previous researchers who reported that 25-OH-D 3 caused longer villi in the small intestine (McCarthy et al, 1984;Shinki et al, 1991). However, Chou et al (2009) showed that 25-OH-D 3 increased the height of villi in the duodenum and jejunum and also the ratio of villi length to crypt depth, while decreased the height of villi in the ileum.…”

Section: Discussionsupporting

confidence: 92%

“…It is well known that calcitriol plays an important role in the intestine, where it promotes Ca 2+ resorption via vitamin D 3 receptormediated genomic mechanisms. Vitamin D 3 may have a role in regulating the morphological and functional development of intestinal villus mucosa (Shinki et al, 1991). It is absorbed through the small intestine and transported in the blood to the liver where it is converted into 25-hydroxycholecalciferol (25-OH-D 3 ), the major circulating form of vitamin D 3 .…”

Section: Introductionmentioning

confidence: 99%

“…The effect of vitamin D 3 on the intestinal morphology of adult fowls have been reported (Shinki et al, 1991;Chou et al, 2009), however, the references to the development of the small intestinal morphology of poult or chick from maternal fed with 25-OH-D 3 , are scarce.…”

Section: Introductionmentioning

confidence: 99%

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Effect of hen diet supplemented with 25-OH-D<sub>3</sub> on the development of small intestinal morphology of chick

Ding¹,

Pirone²,

Lenzi³

et al. 2011

J. Anim. Feed Sci.

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The effect of hen dietary 25-OH-D 3 (added 3000 IU to control diet with 1000 IU) on the morphological changes of the small intestine of Ovambo chicks during prehatch and posthatch period was investigated. After 2 week feeding hens with the experimental diets, eggs were collected and incubated. Results show that the weight, length, thickness of small intestine and the height, perimeter and surface area of villi in small intestine increased with age, and they increased faster in jejunum and duodenum (P<0.05) than in ileum. Comparison with the control diet, 25-OH-D 3 supplement in maternal diet caused the lower weight and shorter length of the small intestine of offspring after hatch (P<0.05). Meanwhile, 25-OH-D 3 of maternal diet induced the increase of the villi height and the crypt depth in the three segments after hatch, in particular in the jejunum and duodenum (P<0.05). We suggest that dietary 25-OH-D 3 can be used as a feed additive in maternal diet to stimulate morphological maturation and in consequence intestinal function in chicks during later incubation and the first week of life.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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Effect of hen diet supplemented with 25-OH-D<sub>3</sub> on the development of small intestinal morphology of chick

Ding¹,

Pirone²,

Lenzi³

et al. 2011

J. Anim. Feed Sci.

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“…Essas enzimas são reguladas pelo 1,25(OH) 2 D 3 , desta maneira se dá a importância da vitamina D sobre a morfologia intestinal (Maeda et al 2002, Ding et al 2011. A falta de putrescina induz a redução no comprimento dos vilos e inibição na absorção de cálcio em pintinhos com deficiência em vitamina D, indicando a relação entre a putrescina, vitamina D e desenvolvimento da mucosa intestinal (Shinki et al 1991).…”

Section: Discussionunclassified

Utilização da vitamina D3 e seus metabólitos na alimentação de frangos de corte sobre parâmetros imunológicos e morfometria intestinal

et al. 2014

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to the ileum (P<0.05). There were no differences (P>0.05) for weight of lymphoid organs, cutaneous basophil hypersensitivity reaction, macrophage activity assessment, measurement of nitric oxide and heterophil profile: lymphocyte. The different sources of vitamin D affect the intestine morphometrics on the villi length in the initial phase, but the effect was not observed in other phases. The immunological parameters were not affected by metabolites of vitamin D.

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“…1) Recently, Khan et al 47) reported that KCl depolarizationinduced serotonin release from fish brain synaptosomes is mediated by KCl-stimulated influx of Ca 2+ into the synaptosomes from the extracellular medium and that DFMOpretreatment resulted in decreases of both Ca 2+ influx and serotonin release which were restored by putrescine, the tissue content of which is higher than those of spermidine and spermine in various parts of fish brain. Shinki et al 48) reported that in vitamin D-deficient chick small intestine, treatment with calcitriol resulted in marked elevation of the putrescine level, mainly due to back-conversion of spermidine, 17) and stimulation of Ca 2+ absorption that is thought to be accompanied by enhanced Ca 2+ passage across both mucous and serous membranes of the epithelial cells. Lowering of the putrescine level by inhibitors of polyamine oxidase and ornithine decarboxylase decreased Ca 2+ absorption.…”

Section: Discussionmentioning

confidence: 99%

Putrescine‐stimulated Intracellular Ca²⁺ Release for Invasiveness of Rat Ascites Hepatoma Cells

Ashida

Ueno

Miwa

et al. 1998

Japanese Journal of Cancer Research

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Our previous study showed that treatment of highly invasive rat ascites hepatoma (LC-AH) cells with α α α α-difluoromethylornithine (DFMO), an inhibitor of ornithine decarboxylase, decreased both their intracellular level of putrescine and their in vitro invasion of a monolayer of calf pulmonary arterial endothelial (CPAE) cells, and that both these decreases were completely reversed by exogenous putrescine, but not spermidine or spermine. Here we show that all adhering control (DFMOuntreated) cells migrated beneath CPAE monolayer with morphological change from round to cauliflower-shaped cells (migratory cells ] i by inhibiting endoplasmic Ca 2+ -ATPase, indicating that thapsigargin mimics the effects of putrescine. These results support the idea that putrescine is a cofactor for Ca 2+ release through the Ca 2+ channel in the endoplasmic reticulum that is inhibited by ryanodine, this release being initiated by cell adhesion and being a prerequisite for tumor cell invasion. Key words: Putrescine -Tumor invasion -Difluoromethylornithine -Ryanodine -ThapsigarginThe polyamines spermidine and spermine, and the diamine putrescine, as well as normal constituents of all animal cells. On the basis of their metabolism under various physiological conditions as well as the effects of specific inhibitors of polyamine biosynthesis, polyamines have been suggested to be important in various cellular functions such as proliferation, differentiation, 1-4) cytoskeleton construction, 5) membrane transport 6, 7) and receptor responses.8, 9) However, their physiological roles are not yet well defined at the molecular level.We previously reported that pretreatment of a highly invasive tumor cell line, LC-AH cells, with DFMO, a specific irreversible inhibitor of ornithine decarboxylase (EC 4.1.1.17), decreased both their intracellular level of putrescine and their invasion beneath a CPAE cell monolayer, without change in their viability, proliferative activity or levels of spermidine and spermine. 10) We also showed that these DFMO-induced decreases were completely reversed by putrescine added to the culture medium during pretreatment with DFMO or during invasion assay in which LC-AH cells were co-cultured with a CPAE cell layer for 24 h.Moreover, these reverses were observed only with putrescine, not with 1,3-diaminopropane, spermidine or spermine. 10)The LC-AH cells used in these studies have a very high cellular putrescine level (73 nmol/mg DNA) which is similar to their spermidine level (70 nmol/mg DNA). 10) This high putrescine level is a characteristic of these highly invasive LC-AH cells, the putrescine levels in a variety of other tumor cells such as Ehrlich ascites, 11) B16 melanoma, 12) Lewis lung carcinoma, 13) and leukemia 14) cells being less than 30% of their spermidine levels. Pretreatment with 0.5 mM DFMO for 5 h induced a 64% decrease in their putrescine level without significant changes in their intracellular levels of spermidine and spermine. 10) Although 0.5 mM DFMO completely inhibited the ornithine decarboxylase ...

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Putrescine is involved in the vitamin D action in chick intestine

Cited by 24 publications

References 30 publications

Effect of hen diet supplemented with 25-OH-D<sub>3</sub> on the development of small intestinal morphology of chick

Effect of hen diet supplemented with 25-OH-D<sub>3</sub> on the development of small intestinal morphology of chick

Utilização da vitamina D3 e seus metabólitos na alimentação de frangos de corte sobre parâmetros imunológicos e morfometria intestinal

Putrescine‐stimulated Intracellular Ca²⁺ Release for Invasiveness of Rat Ascites Hepatoma Cells

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Putrescine is involved in the vitamin D action in chick intestine

Cited by 24 publications

References 30 publications

Effect of hen diet supplemented with 25-OH-D<sub>3</sub> on the development of small intestinal morphology of chick

Effect of hen diet supplemented with 25-OH-D<sub>3</sub> on the development of small intestinal morphology of chick

Utilização da vitamina D3 e seus metabólitos na alimentação de frangos de corte sobre parâmetros imunológicos e morfometria intestinal

Putrescine‐stimulated Intracellular Ca2+ Release for Invasiveness of Rat Ascites Hepatoma Cells

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Putrescine‐stimulated Intracellular Ca²⁺ Release for Invasiveness of Rat Ascites Hepatoma Cells