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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...

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Pancreatic function in carboxyl-ester lipase knockout mice.

Mette Vesterhus1, Helge Raeder, Amarnath J Kurpad

  • 1Department of Pediatrics, Haukeland University Hospital, Bergen, Norway.

Pancreatology : Official Journal of the International Association of Pancreatology (IAP) ... [Et Al.]
|August 20, 2010
PubMed
Summary
This summary is machine-generated.

Carboxyl-ester lipase (CEL) knockout mice showed mild glucose intolerance in females on a high-fat diet, but did not fully replicate CEL-MODY. This suggests complex mechanisms beyond simple CEL loss are involved.

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Area of Science:

  • Endocrinology
  • Genetics
  • Metabolic Disorders

Background:

  • CEL-MODY is a rare monogenic diabetes form linked to carboxyl-ester lipase (CEL) gene mutations.
  • It involves both diabetes and exocrine pancreatic insufficiency.
  • Investigating CEL function in vivo is crucial for understanding its role.

Purpose of the Study:

  • To investigate the roles of carboxyl-ester lipase (CEL) in endocrine and exocrine pancreatic function.
  • To characterize a global CEL knockout mouse model (CELKO).

Main Methods:

  • Physiological and histopathological assessment of CELKO mice compared to wild-type littermates.
  • Mice were studied at 7 and 12 months on normal chow and high-fat diets (HFD).
  • High-fat diets varied in fat content (42% and 60% by calories).

Main Results:

  • CELKO mice exhibited normal growth, development, and glucose metabolism on a chow diet.
  • Female CELKO mice on a 60% HFD showed increased random blood glucose (p=0.02) and impaired glucose tolerance.
  • Islet hyperplasia was observed, but islet cell morphology and exocrine function remained normal.

Conclusions:

  • Whole-body CEL knockout in mice resulted in mild glucose intolerance in females on HFD.
  • The study did not fully replicate the human CEL-MODY phenotype.
  • Pathogenic mechanisms for CEL-MODY appear more complex than solely loss of CEL function.