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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...
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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.
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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...
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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...
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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...
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Imaging Calcium Dynamics in Subpopulations of Mouse Pancreatic Islet Cells
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The calpain system and diabetes.

Muthuraman Pandurangan1, Inho Hwang2, Chinzorio Orhirbat2

  • 1Department of Biomedical Engineering, Dongguk University, Seoul, South Korea.

Pathophysiology : the Official Journal of the International Society for Pathophysiology
|March 18, 2014
PubMed
Summary

Calpains, particularly calpain 10 (CAPN10), are implicated in both insulin-dependent (Type 1) and non-insulin-dependent (Type 2) diabetes. Lifestyle factors like exercise influence calpain expression in diabetes.

Keywords:
CAPN10CalpainsDiabetesRats

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Genetics

Background:

  • Diabetes mellitus is a hyperglycemia syndrome due to insulin deficiency.
  • Global diabetes prevalence is rising, with Type 1 and Type 2 forms having distinct mechanisms.
  • Calpains are implicated in both Type 1 and Type 2 diabetes mellitus.

Purpose of the Study:

  • To review the role of calpains in Non-Insulin Dependent Diabetes Mellitus (NIDDM) and Insulin Dependent Diabetes Mellitus (IDDM).
  • To explore the link between calpain 10 (CAPN10) and NIDDM susceptibility.
  • To examine the influence of lifestyle factors on calpain expression in NIDDM.

Main Methods:

  • Review of existing literature on calpains and diabetes.
  • Analysis of positional cloning studies identifying NIDDM susceptibility genes.
  • Examination of studies on calpain activity in diabetic rat models (ZDF rats).

Main Results:

  • Calpain 10 (CAPN10) is associated with NIDDM susceptibility.
  • Increased calpain activity and leukocyte trafficking observed in ZDF rat microcirculation.
  • Exercise and weight loss reduce calpain expression/increase degradation in NIDDM rat skeletal muscle.

Conclusions:

  • Calpains, especially CAPN10, play a significant role in both NIDDM and IDDM.
  • Non-coding polymorphisms in CAPN10 may contribute to NIDDM.
  • Calpains are linked to glucose metabolism, insulin secretion, and action pathways.