Atherosclerosis and pancreatic damage.

Abstract:

:The appearance of diabetes in advanced age may be considered as a part of the involutive processes of aging, and as such, it might have a pathogenesis completely different from that of type 2 diabetes of medium age. As a matter of fact, it has been observed that the pancreas undergoes numerous structural and functional alterations with advancing age, both in exocrine and endocrine parts. The present studies have been performed to reveal the quantity and quality of the pancreatic lesions, which may be attributed to atherosclerosis. We have already studied elderly subjects, therefore, we were now looking for further supports in a population of middle age people, died in complications of malignant hypertension. We investigated the pancreas, kidney and heart of 36 subjects (20 males and 16 females) with mean age of 48.6+/-8.9 years. Of this group, eight subjects (22.2%) became diabetic after the appearance of malignant hypertension. Arteriolar atherosclerosis damage (hyalinosis, thickening and stenosis) of the pancreatic arterioles were found in 92.8% of the non-diabetic, and in 87.5% of the diabetic subjects. Lesions of the pancreatic islets were observed in 32% of the non-diabetics, and in 50% of the diabetic subjects. The pancreas is an organ, which tends particularly to develop atherosclerotic damage. The vascular lesion of atherosclerotic origin, independently from the mechanism of its appearance, causes first only a decrease of the blood flux and hypoxia in the pancreatic islets with a consecutive functional decline of the beta-cells. This is then followed by structural modifications of the islets accompanied by the appearance of hyalinosis, loss of beta-cells, and a further decrease of insulin production.

journal_name

Arch Gerontol Geriatr

authors

Rosso D,Carnazzo G,Giarelli L,Motta L,Maugeri D

doi

10.1016/s0167-4943(00)00088-1

subject

Has Abstract

pub_date

2001-03-01 00:00:00

pages

95-100

issue

2

eissn

0167-4943

issn

1872-6976

pii

S0167-4943(00)00088-1

journal_volume

32

pub_type

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