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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 pancreas, a vital organ within the abdominal cavity, plays dual roles in the digestive and endocrine systems, collaborating with exocrine and endocrine cells to maintain optimal digestion and blood sugar levels.
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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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Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
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A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
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Nardilysin Is Required for Maintaining Pancreatic β-Cell Function.

Kiyoto Nishi1, Yuichi Sato2, Mikiko Ohno1

  • 1Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto, Japan.

Diabetes
|July 8, 2016
PubMed
Summary
This summary is machine-generated.

Nardilysin (NRDC) is crucial for pancreatic beta-cell function in type 2 diabetes. It regulates glucose-stimulated insulin secretion by controlling the Islet-1-MafA pathway, essential for insulin production.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Metabolic Diseases

Background:

  • Type 2 diabetes (T2D) involves pancreatic beta-cell dysfunction and impaired glucose-stimulated insulin secretion (GSIS).
  • Transcription factors like MafA are key regulators of GSIS in beta-cells.

Purpose of the Study:

  • To investigate the role of nardilysin (N-arginine dibasic convertase; Nrd1 and NRDc) in regulating beta-cell function and its connection to MafA.
  • To elucidate the molecular mechanism by which NRDc influences GSIS and T2D pathogenesis.

Main Methods:

  • Utilized Nrd1 knockout (Nrd1(-/-)) and beta-cell-specific NRDc-deficient (Nrd1(delβ)) mouse models.
  • Assessed glucose tolerance, GSIS, insulin content, and MafA expression in isolated islets and beta-cells.
  • Employed chromatin immunoprecipitation assays to analyze NRDc binding and its interaction with Islet-1 in the MafA enhancer region.

Main Results:

  • Nrd1(-/-) mice exhibited glucose intolerance and significantly reduced GSIS.
  • Nrd1(delβ) mice displayed a diabetic phenotype with markedly impaired GSIS and reduced insulin content.
  • NRDc deficiency led to downregulation of MafA, while NRDc overexpression upregulated MafA and insulin expression in beta-cells.
  • NRDc was found to associate with Islet-1 in the MafA enhancer, controlling Islet-1 and MafA transcription.

Conclusions:

  • Nardilysin (NRDc) plays a critical role in maintaining pancreatic beta-cell function and GSIS.
  • NRDc regulates beta-cell function primarily through the Islet-1-MafA transcriptional pathway.
  • Targeting the NRDc-Islet-1-MafA axis may offer therapeutic strategies for type 2 diabetes.