国际内分泌代谢杂志
國際內分泌代謝雜誌
국제내분비대사잡지
INTERNATIONAL JOURNAL OF ENDOCRINOLOGY AND METABOLISM
2009年
5期
342-345
,共4页
钙离子非依赖性磷脂酶A2β%胰岛β细胞%糖尿病
鈣離子非依賴性燐脂酶A2β%胰島β細胞%糖尿病
개리자비의뢰성린지매A2β%이도β세포%당뇨병
Calcium-independent phospholipase A2β%Pancreatic β-cell%Diabetes mellitus
钙离子非依赖性磷脂酶A2β(iPLA2β()能够催化磷脂sn-2酯酰键水解,释放出游离不饱和脂肪酸和溶血磷脂,在生命活动中发挥重要作用.iPLA2β(的基本结构中包含锚蛋白重复序列、丝氨酸酯酶共有序列和钙调蛋白结合位点等,其活性受钙调蛋白、蛋白激酶C和ATP等多种因素调节.近年来研究发现,该酶在胰岛β(细胞表达水平较高,并参与葡萄糖刺激的胰岛素分泌的调节,其活化、水解膜磷脂释放花生四烯酸(AA),AA作为信号分子引起钙内流和胰岛素分泌.iPLAA2β在β细胞的增殖和凋亡中发挥重要的调节作用,其表达和活性异常导致细胞周期G1期阻滞和细胞凋亡,提示iPLA:B可能与糖尿病的发生、发展密切相关,通过对该酶深入的研究能够为糖尿病的基因治疗和改良胰岛移植治疗提供新的途径.
鈣離子非依賴性燐脂酶A2β(iPLA2β()能夠催化燐脂sn-2酯酰鍵水解,釋放齣遊離不飽和脂肪痠和溶血燐脂,在生命活動中髮揮重要作用.iPLA2β(的基本結構中包含錨蛋白重複序列、絲氨痠酯酶共有序列和鈣調蛋白結閤位點等,其活性受鈣調蛋白、蛋白激酶C和ATP等多種因素調節.近年來研究髮現,該酶在胰島β(細胞錶達水平較高,併參與葡萄糖刺激的胰島素分泌的調節,其活化、水解膜燐脂釋放花生四烯痠(AA),AA作為信號分子引起鈣內流和胰島素分泌.iPLAA2β在β細胞的增殖和凋亡中髮揮重要的調節作用,其錶達和活性異常導緻細胞週期G1期阻滯和細胞凋亡,提示iPLA:B可能與糖尿病的髮生、髮展密切相關,通過對該酶深入的研究能夠為糖尿病的基因治療和改良胰島移植治療提供新的途徑.
개리자비의뢰성린지매A2β(iPLA2β()능구최화린지sn-2지선건수해,석방출유리불포화지방산화용혈린지,재생명활동중발휘중요작용.iPLA2β(적기본결구중포함묘단백중복서렬、사안산지매공유서렬화개조단백결합위점등,기활성수개조단백、단백격매C화ATP등다충인소조절.근년래연구발현,해매재이도β(세포표체수평교고,병삼여포도당자격적이도소분비적조절,기활화、수해막린지석방화생사희산(AA),AA작위신호분자인기개내류화이도소분비.iPLAA2β재β세포적증식화조망중발휘중요적조절작용,기표체화활성이상도치세포주기G1기조체화세포조망,제시iPLA:B가능여당뇨병적발생、발전밀절상관,통과대해매심입적연구능구위당뇨병적기인치료화개량이도이식치료제공신적도경.
Calcium-independent phospholipase A2β (iPLA2β) can catalyze hydrolysis of the sn-2 fatty acyl bond of phospholipids to release free unsaturated fatty acids and lysophospholipids, and plays an im-portant role in life activities. Features of the iPLA2β amino acid sequence include ankyrin-repeats, a serine li-pase consensus sequence and calmodulin-binding domain ,etc. The activity of iPLA213 is regulated by calmod-ulin, protein kinase C (PKC), ATP and some other factors. Studies have found that the expression of iPLA2βin islet β-cells is high, and iPLA2β participates in glucose-stimulated insulin secretion. Arachidonic acid (AA) released from membrane phospholipids by the catalytic action of iPLA2 in β-cells serves as signal mol-ecule to induce calcium influx and insulin secretion. Additionally,recent studies reveal that iPLA2β is in-volved in pathways that contribute to >β-cell proliferation and apoptosis. The abnormal expression and activity of iPLA2β could induce a cell-cycle arrest in G1 phase and apoptosis,which may be correlated with diabetes development. Thus revealing of iPLA2β in β-cells can provide us new ways to treat diabetes, such as gene ther apy and ameliorative islet transplantation.