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相关概念视频

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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The ability of induced pluripotent stem cells or iPSCs to differentiate into most body cell types has stimulated repair and regenerative medicine research over the past few decades. iPSC-derived blood cells, hepatocytes, beta islet cells, cardiomyocytes, neurons, and other cell types can repair injuries or regenerate damaged tissue in diseases such as diabetes and neurodegenerative disorders.
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Embryonic and induced pluripotent stem cells are excellent models for disease research because of their ability to self-renew and differentiate into most cell types. Somatic cells from a patient are isolated and reprogrammed into induced pluripotent stem cells or iPSCs. These iPSCs are later differentiated into the desired cell type, which mirrors the diseased cell of the patient. In this way, disease models have been created for investigating diseases such as Down syndrome, type I diabetes,...
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The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
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After cellular or tissue damage, the resident stem cells present in the human body can locally repair and regenerate the damaged tissue or organ. However, even though some tissues do not have stem cells, they can repair and regenerate with the help of pre-existing cells. For example, beta cells of the pancreas and hepatocytes of the liver can divide to renew and regenerate the tissue. Here, both cell division and cell death are well regulated by homeostasis.
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Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
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胰腺小岛细胞的可塑性:致病性或治疗性利用?

Neil Tanday1,2, Andrei I Tarasov1, R Charlotte Moffett1

  • 1Diabetes Research Centre, School of Biomedical Sciences, Ulster University, Coleraine, Northern Ireland.

Diabetes, obesity & metabolism
|October 16, 2023
PubMed
概括

胰腺小岛细胞可以在压力下改变其身份,这是与糖尿病有关的过程. 针对这种可塑性的疗法可能有助于预防β细胞损失和控制糖尿病.

关键词:
糖尿病 糖尿病患者 糖尿病患者这就是内分泌生成 (endocrinogenesis).胰腺小岛是一个小岛.通过转差异化转化.

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科学领域:

  • 内分泌学 在内分泌学.
  • 细胞生物学 细胞生物学
  • 代谢疾病 代谢疾病

背景情况:

  • 胰岛岛内分泌细胞的发育是一个受调节的过程,涉及到成熟细胞表型所必需的转录因子.
  • 在糖尿病,肥胖和怀孕中出现的代谢压力可以改变β细胞转录因子,导致脱差或转差.
  • 这种贝塔细胞身份的丧失与糖尿病的发病有关.

研究的目的:

  • 在实验环境中审查小岛细胞可塑性.
  • 讨论小岛细胞可塑性的生理和治疗方面.
  • 专注于预防β细胞损失和在糖尿病中产生新的β细胞的策略.

主要方法:

  • 审查关于小岛细胞可塑性的现有文献.
  • 对实验环境进行分析,证明细胞可塑性.
  • 讨论治疗剂及其对β细胞脱差和转差的影响.

主要成果:

  • 抗糖尿病药物,包括GLP-1模仿剂和新型,可以防止或逆转β细胞脱差.
  • 这些药物还可能促进非β细胞转基因分化为胰岛素阳性β细胞类细胞.
  • 岛屿细胞可塑性在各种实验模型中表现出来.

结论:

  • 了解小岛细胞可塑性对于开发针对糖尿病的向疗法至关重要.
  • 旨在保护β细胞身份或产生新的β细胞的策略具有治疗潜力.
  • 需要对小岛细胞可塑性的分子机制进行进一步的研究,以对抗糖尿病中的β细胞衰减.