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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...
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...
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...
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.
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.
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...
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...

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Updated: Jun 15, 2026

Generation of Scaffold-free, Three-dimensional Insulin Expressing Pancreatoids from Mouse Pancreatic Progenitors In Vitro
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Molecular pathways underlying the pathogenesis of pancreatic alpha-cell dysfunction.

Dan Kawamori1, Hannah J Welters, Rohit N Kulkarni

  • 1Department of Cellular and Molecular Physiology, Joslin Diabetes Center, and Department of Medicine, Harvard Medical School, Boston, MA, USA. dan.kawamori@joslin.harvard.edu

Advances in Experimental Medicine and Biology
|March 11, 2010
PubMed
Summary

Glucagon counteracts insulin to maintain blood sugar, but its secretion is dysregulated in diabetes. Understanding glucagon regulation is key for new diabetes treatments targeting alpha-cell dysfunction.

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Area of Science:

  • Endocrinology
  • Metabolic Research
  • Diabetes Pathophysiology

Background:

  • Glucagon is vital for glucose homeostasis, opposing insulin's effects, particularly during low blood sugar (hypoglycemia).
  • Pancreatic alpha-cell glucagon secretion is influenced by blood sugar levels, neural signals, and adjacent beta-cell secretions.
  • Dysregulated glucagon secretion in diabetes worsens glycemic control and is a target for novel therapeutic strategies.

Purpose of the Study:

  • To elucidate the regulatory mechanisms of glucagon secretion.
  • To understand the molecular basis of alpha-cell dysfunction in diabetes.
  • To identify potential therapeutic targets for managing diabetic hyperglycemia.

Main Methods:

  • Review of current literature on glucagon secretion regulation.
  • Analysis of molecular pathways involved in alpha-cell function.
  • Exploration of therapeutic strategies targeting glucagon signaling.

Main Results:

  • Glucagon secretion is tightly controlled by multiple physiological inputs.
  • Aberrant glucagon secretion contributes significantly to diabetic hyperglycemia.
  • Targeting glucagon excess presents a promising avenue for diabetes management.

Conclusions:

  • A comprehensive understanding of glucagon secretion regulation is essential for addressing alpha-cell dysfunction in diabetes.
  • Developing therapies that modulate glucagon secretion could improve glycemic control in diabetic patients.
  • Further research into the molecular mechanisms governing glucagon release is warranted.