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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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Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular...
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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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A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
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Islet-1 Is essential for pancreatic β-cell function.

Benjamin N Ediger1, Aiping Du2, Jingxuan Liu2

  • 1Department of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, PA Department of Medicine and Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.

Diabetes
|July 17, 2014
PubMed
Summary
This summary is machine-generated.

Islet-1 (Isl-1) is crucial for pancreatic beta-cell function after birth. Loss of Isl-1 impairs insulin secretion and glucose tolerance by directly regulating key genes like Pdx1 and Slc2a2.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Genetics

Background:

  • Islet-1 (Isl-1) is vital for pancreatic endocrine progenitor development and survival.
  • Isl-1 expression persists in adult pancreatic endocrine cells, but its postnatal role remains undefined.

Purpose of the Study:

  • To investigate the specific function of Isl-1 in postnatal pancreatic beta-cells.
  • To identify direct transcriptional targets of Isl-1 in mature beta-cells.

Main Methods:

  • Generated a tamoxifen-inducible, beta-cell-specific Isl-1 knockout mouse model (Isl-1(L/L); Pdx1-CreER(Tm)).
  • Performed physiological and morphometric analyses, RNA sequencing, and chromatin immunoprecipitation sequencing (ChIP-seq).
  • Validated direct gene regulation using luciferase reporter assays.

Main Results:

  • Beta-cell-specific ablation of Isl-1 impaired glucose tolerance and insulin secretion.
  • No significant changes in beta-cell mass or apoptosis were observed.
  • Isl-1 directly regulates the expression of Pdx1 and Slc2a2, affecting the beta-cell transcriptome.

Conclusions:

  • Isl-1 is essential for maintaining normal postnatal beta-cell function.
  • Isl-1 directly controls Pdx1 and Slc2a2, contributing to a distinct mature beta-cell gene regulatory network.
  • Isl-1's function in adult beta-cells differs from its role in progenitor cells.