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Atherosclerosis and pancreatic damage.

D Rosso1, G Carnazzo, L Giarelli

  • 1Institute of Internal Medicine and Geriatrics, Azienda Ospedaliera "Cannizzaro", University of Catania, Via Messina 829, 95125, Catania, Italy

Archives of Gerontology and Geriatrics
|April 21, 2001
PubMed
Summary

Atherosclerosis significantly impacts the pancreas, contributing to diabetes development in middle-aged individuals. Pancreatic arteriolar damage and islet lesions were prevalent, leading to reduced beta-cell function and insulin production.

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Area of Science:

  • Pathology
  • Endocrinology
  • Gerontology

Background:

  • Diabetes in older adults may stem from aging processes, differing from type 2 diabetes.
  • The aging pancreas exhibits structural and functional changes in both exocrine and endocrine tissues.
  • Atherosclerosis is a potential contributor to pancreatic dysfunction in aging populations.

Purpose of the Study:

  • To investigate pancreatic lesions attributable to atherosclerosis in middle-aged individuals.
  • To compare the prevalence and nature of pancreatic damage in diabetic versus non-diabetic subjects with malignant hypertension.

Main Methods:

  • Examined the pancreas, kidneys, and heart of 36 middle-aged subjects (mean age 48.6 years) who died from malignant hypertension.
  • Assessed arteriolar atherosclerosis in pancreatic vessels and lesions within pancreatic islets.

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  • Correlated findings with diabetic status.

    • Main Results:

    • Pancreatic arteriolar atherosclerosis (hyalinosis, thickening, stenosis) was found in 92.8% of non-diabetics and 87.5% of diabetics.
    • Pancreatic islet lesions were observed in 50% of diabetics compared to 32% of non-diabetics.
    • Eight subjects (22.2%) developed diabetes following malignant hypertension.

    Conclusions:

    • The pancreas is susceptible to atherosclerotic damage, impacting pancreatic islet function.
    • Atherosclerotic vascular lesions reduce blood flow and oxygen to islets, impairing beta-cell function and insulin production.
    • This process can lead to structural islet changes, beta-cell loss, and decreased insulin secretion, contributing to diabetes.