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Related Concept Videos

Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

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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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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.
Insulin and C-peptide are...
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Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

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Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
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Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

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Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
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Insulin: Biosynthesis, Chemistry, and Preparation01:25

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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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Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
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Related Experiment Video

Updated: Aug 31, 2025

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
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Gut-derived bacterial flagellin induces beta-cell inflammation and dysfunction.

Torsten P M Scheithauer1,2, Hilde Herrema1, Hongbing Yu3

  • 1Department of (Experimental) Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.

Gut Microbes
|August 19, 2022
PubMed
Summary

Bacterial flagellin, more abundant in type 2 diabetes (T2D) patients, triggers inflammation in pancreatic islets. This leads to beta-cell dysfunction, suggesting flagellin as a novel therapeutic target for T2D.

Keywords:
Gut microbiotabeta-cell functionflagellininflammationtype 2 diabetes

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Area of Science:

  • Endocrinology
  • Microbiology
  • Immunology

Background:

  • Type 2 diabetes (T2D) is linked to pancreatic beta-cell failure, with the gut microbiota's role unclear.
  • Obesity is a significant risk factor for T2D and beta-cell dysfunction.

Purpose of the Study:

  • To investigate the causal link between gut microbiota composition and beta-cell dysfunction in T2D.
  • To explore the role of flagellin, a bacterial component, in T2D pathogenesis.

Main Methods:

  • Analysis of gut microbiota in obese individuals with and without T2D from Dutch cohorts.
  • In vitro and in vivo studies using mouse pancreatic islets and obese mice.
  • Investigation of flagellin's effect on pancreatic islets via Toll-like receptor 5 (TLR-5) signaling.

Main Results:

  • Enterobacteriaceae, a source of flagellin, were more abundant in individuals with T2D.
  • Flagellin induced a pro-inflammatory response in pancreatic islets via TLR-5.
  • This inflammation impaired beta-cell function, reducing insulin gene expression and affecting insulin processing.

Conclusions:

  • Increased systemic flagellin in T2D contributes to beta-cell failure.
  • Flagellin-induced islet inflammation represents a novel therapeutic target for T2D.