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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...
Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

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.
In addition to accelerating glucose uptake and utilization, insulin has...
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...
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...

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Related Experiment Video

Updated: May 31, 2026

Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres
09:31

Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres

Published on: November 5, 2016

Eicosanoids, β-cell function, and diabetes.

Pengcheng Luo1, Mong-Heng Wang

  • 1Department of Nephrology, Renmin Hospital of Wuhan University, China.

Prostaglandins & Other Lipid Mediators
|July 16, 2011
PubMed
Summary
This summary is machine-generated.

Eicosanoids derived from arachidonic acid (AA) impact pancreatic beta-cell function in diabetes. Inhibiting soluble epoxide hydrolase (sEH) to stabilize epoxyeicosatrienoic acids (EETs) shows promise for improving beta-cell function and reducing apoptosis.

Related Experiment Videos

Last Updated: May 31, 2026

Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres
09:31

Sustained Administration of β-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres

Published on: November 5, 2016

Area of Science:

  • Biochemistry
  • Endocrinology
  • Metabolic Diseases

Background:

  • Arachidonic acid (AA) is metabolized into eicosanoids by cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP) enzymes.
  • Eicosanoids play crucial roles in various diseases, including type 1 and type 2 diabetes, particularly in pancreatic beta-cell function and survival.
  • Accumulating evidence highlights the significance of eicosanoids in the pathogenesis of diabetes and its complications.

Purpose of the Study:

  • To review recent findings on the role of eicosanoid pathways in diabetes and its complications.
  • To discuss the therapeutic potential of targeting eicosanoid metabolism for diabetes treatment.
  • To explore the impact of specific eicosanoid metabolites on pancreatic beta-cell function and apoptosis.

Main Methods:

  • Review of existing literature on eicosanoid metabolism in diabetes.
  • Analysis of studies involving animal models with targeted gene deletions.
  • Examination of research on specific enzymatic inhibitors for eicosanoid pathways.

Main Results:

  • Prostaglandin E(2) (PGE(2)) from the COX pathway is implicated in beta-cell dysfunction and destruction.
  • 12-LOX eicosanoids are involved in cytokine-mediated inflammation in pancreatic beta cells.
  • Stabilizing epoxyeicosatrienoic acids (EETs) by inhibiting soluble epoxide hydrolase (sEH) improves beta-cell function and reduces apoptosis in diabetes models.

Conclusions:

  • Eicosanoid pathways, including COX, LOX, and CYP, are critical in diabetes pathogenesis.
  • Targeting sEH to modulate EET levels presents a potential therapeutic strategy for diabetes.
  • Further research using genetic models and enzymatic inhibitors can identify novel targets for diabetes treatment.