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Related Concept Videos

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

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.
Insulin and C-peptide are co-secreted in...
Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

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...
Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

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.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment primarily uses...
Renewal of Intestinal Stem Cells01:23

Renewal of Intestinal Stem Cells

The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the goblet,...

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Related Experiment Video

Updated: May 30, 2026

A High-content In Vitro Pancreatic Islet &#946;-cell Replication Discovery Platform
09:35

A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform

Published on: July 16, 2016

ISL1 promotes pancreatic islet cell proliferation.

Ting Guo1, Weiping Wang, Hui Zhang

  • 1Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education of China, Peking University, Beijing, China.

Plos One
|August 11, 2011
PubMed
Summary

Islet 1 (ISL1) promotes adult pancreatic islet cell proliferation by activating c-Myc and CyclinD1 transcription. This transcription factor is crucial for maintaining mature islet cells homeostasis and survival.

Related Experiment Videos

Last Updated: May 30, 2026

A High-content In Vitro Pancreatic Islet &#946;-cell Replication Discovery Platform
09:35

A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform

Published on: July 16, 2016

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • Islet 1 (ISL1), a LIM-homeodomain transcription factor, is vital for pancreatic islet cell proliferation and survival during embryonic and postnatal development.
  • The precise role of ISL1 in adult pancreatic islets remains largely undefined.

Purpose of the Study:

  • To investigate the function of ISL1 in adult pancreatic islet cells.
  • To elucidate the molecular mechanisms by which ISL1 influences islet cell proliferation and survival.

Main Methods:

  • Quantitative mRNA analysis of ISL1 expression in cultured pancreatic cells and diabetic mouse models.
  • ISL1 knockdown experiments in HIT-T15 and primary adult islet cells.
  • Cell cycle analysis (G1, G2/M, S phases) and apoptosis assays.
  • Chromatin immunoprecipitation to assess ISL1 binding to c-Myc and CyclinD1 promoters.

Main Results:

  • ISL1 expression is upregulated in response to glucose stimulation and in type 1 and type 2 diabetes models.
  • ISL1 knockdown increases apoptosis in HIT-T15 cells and promotes cell cycle arrest in G1 phase.
  • ISL1 enhances adult pancreatic islet cell proliferation by upregulating c-Myc and CyclinD1 transcription.
  • ISL1 directly binds to the promoter regions of c-Myc and CyclinD1, activating their transcription.

Conclusions:

  • ISL1 promotes adult pancreatic islet cell proliferation, likely through direct activation of c-Myc and CyclinD1 transcription.
  • These findings highlight ISL1's critical role in maintaining mature islet cell homeostasis.
  • The study provides new insights into the regulatory relationships between ISL1 and growth factors involved in islet cell function.