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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.
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
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...
Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...
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...

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Related Experiment Video

Updated: May 20, 2026

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

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First phase insulin secretion and type 2 diabetes.

K Cheng1, S Andrikopoulos, J E Gunton

  • 1Diabetes and Transcription Factors Group, Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, Sydney, NSW 2010, Australia.

Current Molecular Medicine
|July 28, 2012
PubMed
Summary
This summary is machine-generated.

Type 2 diabetes involves impaired first phase insulin secretion. Restoring this critical function improves glucose control by reducing liver glucose production and enhancing glucose uptake.

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Isolation of Human Islets from Partially Pancreatectomized Patients
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Last Updated: May 20, 2026

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

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Published on: July 30, 2011

Area of Science:

  • Endocrinology
  • Metabolic Disorders
  • Molecular Biology

Background:

  • Type 2 diabetes (T2D) is characterized by pancreatic beta-cell dysfunction and inadequate insulin secretion, leading to glucose imbalance.
  • Loss of first phase insulin secretion is a key predictor of T2D onset and impairs glucose homeostasis.
  • Restoring first phase insulin secretion can improve blood glucose levels in T2D by modulating hepatic glucose production and peripheral glucose uptake.

Purpose of the Study:

  • To review the initiation of first phase insulin secretion.
  • To detail recent findings on novel regulatory factors influencing first phase insulin secretion and glucose homeostasis.

Main Methods:

  • Literature review of recent studies on first phase insulin secretion regulation.
  • Analysis of novel regulatory factors including hypoxia-inducible factor 1α, von Hippel-Lindau, factor inhibiting HIF, nicotinamide phospho-ribosyl-transferase, and sirtuins.

Main Results:

  • First phase insulin secretion is initiated by a classical triggering pathway involving multiple stimulatory signals.
  • Several novel factors, including HIF-1α, VHL, PHDs, NAMPT, and sirtuins, play crucial roles in regulating first phase insulin secretion.
  • These factors are critical for maintaining glucose homeostasis in the context of T2D.

Conclusions:

  • Understanding the regulation of first phase insulin secretion is vital for developing T2D therapies.
  • Novel regulatory factors present promising targets for interventions aimed at restoring insulin secretion and improving glucose control.
  • Further research into these pathways could lead to significant advancements in T2D management.