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Related Concept Videos

Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

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 uptake of...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
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...
Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

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.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...

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Related Experiment Video

Updated: May 22, 2026

Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets
10:09

Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets

Published on: May 11, 2015

Impaired β-cell-β-cell coupling mediated by Cx36 gap junctions in prediabetic mice.

C P F Carvalho1, R B Oliveira, A Britan

  • 1Department of Histology and Embryology, Institute of Biology, University of Campinas, Campinas, São Paulo, Brazil.

American Journal of Physiology. Endocrinology and Metabolism
|May 10, 2012
PubMed
Summary

Impaired gap junctional communication in pancreatic beta cells, mediated by connexin (Cx)36, is observed in prediabetic mice, suggesting a role in early type 2 diabetes development.

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A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
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Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets
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Leprdb Mouse Model of Type 2 Diabetes: Pancreatic Islet Isolation and Live-cell 2-Photon Imaging Of Intact Islets

Published on: May 11, 2015

A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
12:33

A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination

Published on: June 25, 2014

Area of Science:

  • Endocrinology
  • Cell Biology
  • Metabolic Diseases

Background:

  • Gap junctional intercellular communication (GJIC) between pancreatic beta cells is vital for regulating insulin production and release.
  • Connexin 36 (Cx36) is a key protein forming gap junctions (GJs) in beta cells, essential for their coordinated function.

Purpose of the Study:

  • To examine Cx36 protein expression, GJ structure, and function in the pancreatic islets of high-fat diet-induced prediabetic mice.
  • To elucidate the role of Cx36-dependent cell-to-cell communication in early beta cell dysfunction.

Main Methods:

  • C57BL/6 mice were fed a high-fat (HF) or regular diet for 60 days to induce obesity and prediabetes.
  • Assessed insulin resistance, hyperglycemia, hyperinsulinemia, and pancreatic mass.
  • Quantified Cx36 protein levels, analyzed GJ plaque size via electron microscopy, and measured beta cell coupling using ethidium bromide microinjection.

Main Results:

  • HF-fed mice exhibited obesity, insulin resistance, hyperglycemia, and increased islet mass, confirming a prediabetic state.
  • Prediabetic mice showed significantly reduced insulin secretion in response to glucose.
  • A notable decrease in islet Cx36 protein expression and GJ plaque size was observed, alongside a 30% reduction in beta cell-beta cell coupling.

Conclusions:

  • Beta cell-beta cell coupling mediated by Cx36 is impaired in prediabetic mice.
  • Cx36-dependent intercellular communication may play a critical role in the early stages of beta cell dysfunction leading to type 2 diabetes.