大阪大学 · 医学
島井伊佐夫教授の研究室は、腎疾患や代謝異常に関連するポリアミン代謝、ビタミンD機能、および血管・腎臓における石灰化のメカニズムを解明することを主眼としています。特に、肝障害や腎障害に伴うポリアミン代謝の変化、ビタミンDの腎細胞保護作用、およびフェトウインAによる腎石灰化抑制機構の解明が進んでいます。また、必須アミノ酸補給が血管石灰化に与える影響についても、動物モデルを用いた実験的アプローチを展開しています。
Figures are computed from collected data and may differ slightly.
A cytosolic spermidine N-acetyltransferase has been partially purified from livers of rats treated with carbon tetrachloride or thioacetamide.This enzyme formed N'-acetylspermidine when incubated with spermidine and acetyl-coA.The enzyme was also able to acetylate spermine, norspermidine, norspermine and, at a much slower rate, 1,3-diaminopropane.Putrescine, cadaverine, homospermidine, and histones were not substrates ( ~2 % activity of spermidine) distinguishing this enzyme from a previously de
Combined use of two markers is useful for the risk stratification of renal outcome.
We demonstrated the breakdown of the vitamin D activation system in podocyte injury, and established a preventative role for vitamin D in podocyte injury.
Vascular calcification (VC) is a life-threatening complication of CKD. Severe protein restriction causes a shortage of essential amino acids, and exacerbates VC in rats. Therefore, we investigated the effects of dietary l-lysine, the first-limiting amino acid of cereal grains, on VC. Male Sprague-Dawley rats at age 13 weeks were divided randomly into four groups: low-protein (LP) diet (group LP), LP diet+adenine (group Ade), LP diet+adenine+glycine (group Gly) as a control amino acid group, and
Treatment of rats with dimethylnitrosamine (30 mg/kg) or diethylnitrosamine (200 mg/kg) produced a rapid increase in the activity of spermidine N1-acetyltransferase which peaked at values 7-fold greater than did control at 48 hr after exposure. This increase led to a small accumulation of N1-acetylspermidine in the liver but produced a more striking effect on putrescine which increased 30- to 40-fold after 2 days. Most of this increase appeared to be due to the conversion of N1-acetylspermidine
The serum glycoprotein fetuin-A is an important inhibitor of extraosseous calcification. The importance of fetuin-A has been confirmed in fetuin-A null mice, which develop widespread extraosseous calcification including the kidney. However, the mechanism how fetuin-A protects kidneys from nephrocalcinosis remains uncertain. Here, we demonstrate that intratubular fetuin-A plays a role in the prevention of nephrocalcinosis in the proximal tubules. Although normal rat kidney did not express mRNA fo
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