馬泰勒蟲免疫熒光試劑盒

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廣州健侖生物科技有限公司

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馬泰勒蟲免疫熒光試劑盒

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【公司名稱】 廣州健侖生物科技有限公司
【】    楊永漢 
【】 
【騰訊 】 2042552662
【公司地址】 廣州清華科技園創(chuàng)新基地番禺石樓鎮(zhèn)創(chuàng)啟路63號二期2幢101-3室
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在胰腺β細胞內(nèi)葡萄糖的代謝對于胰島素基因表達和胞外分泌的賀爾蒙來說是很關(guān)鍵的一環(huán)，但是有越來越多的證據(jù)顯示，葡萄糖代謝途徑同時對于β-細胞發(fā)育和維持成年人的β細胞質(zhì)量非常重要。在小鼠β細胞中針對葡萄糖激酶剃除后不僅防止了葡萄糖所刺激的胰島素分泌，而且也抑制了β細胞的增殖，并與細胞凋亡的增加有關(guān)聯(lián)。在組織培養(yǎng)中，直接操縱胚胎胰臟的葡萄糖可用性實驗則顯示了轉(zhuǎn)錄調(diào)控因子神經(jīng)元素3(Neurog3)和NEUROD對于α和β細胞的發(fā)育是很必要的存在。
針對此主題，帕特爾等人的論文提到丙酮酸脫氫酶α組件是丙酮酸脫氫酶復(fù)合物調(diào)控丙酮酸代謝的速率決定酵素;在老鼠實驗?zāi)Ｊ街刑蕹?beta;細胞的丙酮酸脫氫酶α組件之后，如同預(yù)期的會引起胰島素可用性降低以及葡萄糖敏感性釋放，但是卻也同時觀察到新生老鼠β細胞數(shù)目減少以及Neurog3，NEUROD和的Pdx1的表達。有趣的是，同時也在胰島素免疫陽性，特胰島的內(nèi)分泌小細胞簇中看到數(shù)目的減少，意味著也減少了新生β-細胞的來源。這個新發(fā)現(xiàn)強調(diào)了β-細胞中控制葡萄糖代謝的途徑對于維持β-細胞質(zhì)量以及賀爾蒙和生長因子，例如胰高血糖素樣多肽1(GLP1)是同等重要的。
此研究主題刊登于2014年8月的《實驗生物及醫(yī)學(xué)》，證明了丙酮酸脫氫酶復(fù)合體不僅對于胰島素基因表達和葡萄糖刺激的胰島素分泌非常必要，同時還直接影響β-細胞的生長和成熟，更闡明了葡萄糖代謝會直接調(diào)控β細胞質(zhì)量和可塑性。
紐約州立大學(xué)水牛城分校生物化學(xué)、醫(yī)學(xué)和生物醫(yī)學(xué)科學(xué)學(xué)院的特聘教授，同時也是資深作者的莫成?帕特爾博士說道：“這些發(fā)現(xiàn)顯示了葡萄糖代謝是調(diào)控β細胞質(zhì)量的主要調(diào)控因子，很可能是獨立的訊息傳遞路徑，例如可能不同于胰島素受體作用物2訊息傳遞路徑。”

Glucose metabolism in pancreatic beta cells is a crucial link to hormonal gene expression and extracellular secretion of hormones, but there is growing evidence that glucose metabolism contributes both to beta-cell development and maintenance of adulthood Human β-cell mass is very important. Shaved for glucokinase in mouse beta cells not only prevents glucose-stimulated insulin secretion but also inhibits beta cell proliferation and correlates with increased apoptosis. Glucose availability experiments directly manipulating embryonic pancreas in tissue culture showed that the transcriptional regulators Neurog3 and NEUROD are essential for the development of alpha and beta cells.
In response to this topic, Pa et al.'s paper mentions that the pyruvate dehydrogenase alpha component is a pyruvate dehydrogenase complex that regulates the rate at which pyruvate is metabolized; removing pyruvate from beta cells in experimental models of rats After the hydrogenase α-component, as expected, a decrease in insulin availability and glucose-sensitive release was caused, however, a decrease in the number of β-cells in neonatal mice and the expression of Neurog3, NEUROD and Pdx1 were also observed. Interestingly, a decrease in the number seen also in insulin-immunoreactive, insulinotropic endocrine small cell clusters means that the source of nascent β-cells is also reduced. This new finding emphasizes that the pathways that control glucose metabolism in β-cells are equally important for maintaining β-cell mass and for hormones and growth factors such as glucagon-like polypeptide 1 (GLP1).
The subject of the study, published in August 2014, "Experimental Biology and Medicine," demonstrates that pyruvate dehydrogenase complexes are essential not only for insulin gene expression and glucose-stimulated insulin secretion, but also for β-cell growth and Mature, but also shows that glucose metabolism will directly regulate β-cell quality and plasticity.
Dr. Moblie Pa, Distinguished Professor of Biochemistry, Medical and Biomedical Sciences at the State University of New York at Buffalo, said: "These findings show that glucose metabolism is a major regulator of beta-cell mass, Probably an independent messaging pathway, for example, may differ from the insulin receptor 2 signaling pathway.