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Related Concept Videos

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 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...
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...
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...
Diabetic Neuropathy01:22

Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
Chronic Pancreatitis II: Pathophysiology01:21

Chronic Pancreatitis II: Pathophysiology

Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...

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Related Experiment Video

Updated: May 10, 2026

Sustained Administration of &#946;-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres
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Published on: November 5, 2016

Update on the protective molecular pathways improving pancreatic beta-cell dysfunction.

Alessandra Puddu1, Roberta Sanguineti, François Mach

  • 1Department of Internal Medicine, University of Genoa, Viale Benedetto XV 6, 16132 Genova, Italy.

Mediators of Inflammation
|June 6, 2013
PubMed
Summary

Maintaining pancreatic beta-cell function is key to preventing diabetes. This review explores molecular regulators that preserve beta-cell mass and function, offering potential therapeutic targets for diabetes treatment.

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Sustained Administration of &#946;-cell Mitogens to Intact Mouse Islets Ex Vivo Using Biodegradable Poly(lactic-co-glycolic acid) Microspheres
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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

A High-content In Vitro Pancreatic Islet &#946;-cell Replication Discovery Platform
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12:32

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds

Published on: January 23, 2018

Area of Science:

  • Endocrinology
  • Metabolic diseases
  • Cell biology

Background:

  • Pancreatic beta-cells are crucial for insulin production and glucose homeostasis.
  • Impaired beta-cell function leads to hyperglycemia and diabetes mellitus.
  • Protecting beta-cells from damage is vital for diabetes management.

Purpose of the Study:

  • To review recent molecular regulators of beta-cell mass and function.
  • To identify potential therapeutic targets for diabetes treatment.
  • To highlight novel pathways for improving beta-cell dysfunction.

Main Methods:

  • Narrative review of existing scientific literature.
  • Analysis of recently identified molecular regulators.
  • Synthesis of evidence on beta-cell preservation and recovery.

Main Results:

  • Several molecular regulators have been identified that preserve beta-cell mass.
  • Evidence suggests these regulators can promote beta-cell function recovery.
  • Novel molecular pathways show promise for enhancing beta-cell function.

Conclusions:

  • Targeting molecular regulators offers a promising therapeutic strategy for diabetes.
  • Preserving beta-cell function and mass is critical for diabetes treatment.
  • Further research into novel pathways could lead to improved diabetes therapies.