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Related Concept Videos

Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
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...
Chronic Pancreatitis I: Introduction01:25

Chronic Pancreatitis I: Introduction

Chronic pancreatitis is a long-standing, relapsing inflammation of the pancreas, characterized by irreversible damage to the gland. It results in progressive destruction of the pancreatic parenchyma, fibrosis, and eventual loss of both exocrine and endocrine function. The disease may evolve gradually after multiple episodes of acute pancreatitis or develop independently.EtiologyChronic pancreatitis can arise from a variety of causes:Alcohol use is the leading cause, accounting for 70–80% of...
Chronic Pancreatitis I: Introduction01:24

Chronic Pancreatitis I: Introduction

The pancreas, an elongated and flat gland situated behind the stomach, serves a vital function in digesting food and managing blood sugar levels.
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Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...
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.
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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...

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A Murine Pancreatic Islet Cell-based Screening for Diabetogenic Environmental Chemicals
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Elevated circulating free fatty acids levels causing pancreatic islet cell dysfunction through oxidative stress.

X Zhang1, Y Bao, L Ke

  • 1Division of Endocrinology and Metabolism, Sichuan University, West China Hospital, Cheng Du, China.

Journal of Endocrinological Investigation
|November 17, 2009
PubMed
Summary

Elevated free fatty acids (FFA) impair pancreatic beta-cell function by increasing oxidative stress. N-acetylcysteine (NAC) partially reversed these effects, suggesting a role for oxidative stress in diabetes development.

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Area of Science:

  • Endocrinology
  • Metabolic Syndrome
  • Diabetes Research

Background:

  • Elevated plasma free fatty acids (FFA) are a predictor of progression to diabetes.
  • Understanding the impact of FFA on pancreatic beta-cell function is crucial for diabetes research.

Purpose of the Study:

  • To assess the effects of prolonged FFA exposure on basal and glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells.
  • To investigate the role of oxidative stress in FFA-induced beta-cell dysfunction.

Main Methods:

  • Rats received 96-h infusions of normal saline, intralipid plus heparin (IH), or IH with N-acetylcysteine (IH+NAC).
  • Measured plasma insulin, malonyldialdehyde (MDA), reduced glutathione (GSH), and oxidized glutathione (GSSG).
  • Performed in vivo intravenous glucose tolerance tests (IVGTT) and ex vivo pancreatic tissue perfusion.

Main Results:

  • FFA infusion (IH group) impaired GSIS, decreased the GSH/GSSG ratio, and increased MDA levels.
  • Increased nuclear factor kappaB and inducible nitric oxide synthase in pancreatic islets of the IH group.
  • N-acetylcysteine (IH+NAC group) partially restored GSH/GSSG ratio and MDA levels, improving GSIS.

Conclusions:

  • Elevated FFA contribute to pancreatic islet cell dysfunction via oxidative stress.
  • Oxidative stress-sensitive pathways are implicated in impaired insulin secretion in obese Type 2 diabetes.