Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 Oct;15(10):79.
doi: 10.1007/s11892-015-0653-y.

Abnormalities of the Exocrine Pancreas in Type 1 Diabetes

Martha Campbell-Thompson  1 , Teresa Rodriguez-Calvo, Manuela Battaglia
Affiliations
Review

Abnormalities of the Exocrine Pancreas in Type 1 Diabetes

Martha Campbell-Thompson et al. Curr Diab Rep. 2015 Oct.

Abstract

Type 1 diabetes (T1D) is considered a pancreatic beta cell-specific disease that results in absolute insulin deficiency. Nevertheless, clinical studies from 1940 onwards showed that patients with T1D had an abnormal exocrine pancreas due to the presence of subclinical exocrine insufficiency and acinar atrophy. Exocrine abnormalities are an important, and mostly neglected, characteristic associated with T1D. It is however still unclear whether the exocrine dysfunction in T1D is a primary damage caused by the same pathogenic event that led to beta cell destruction or secondary to beta cell loss. In this review, we collect evidence supporting the hypothesis that T1D is a combined endocrine-exocrine disease in which the loss of functional beta cell mass is most clinically apparent.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Exocrine and endocrine pathways to diabetes. 1-3 T3cDM. A “hit” (e.g., environmental, genetic predisposition) (1) leads to acinar injury that stimulates an inflammatory response (2) in which beta cells are lost as innocent bystanders (3). Destruction of sufficient numbers of beta cells leads to insulin deficiency and T3cDM. 4-7 Classical T1D. A “hit” (e.g., environmental, genetic predisposition) leads to beta cell inflammation, release of self antigens (4), and recruitment of immune cells (5) that target the islet leading to beta cell damage and reduced insulin production (6). Lack of insulin, which is an exocrine growth factor, leads to reduction in exocrine tissue (atrophy) (7). 8-10 Simultaneous T1D-exocrine. A “hit” (e.g., environmental) leads to pancreas inflammation (8), which attracts immune cells (9) to both endocrine and exocrine compartments and induces cellular damage (10). As a consequence, both exocrine insufficiency and insulin deficiency occur which eventually resulting in diabetes onset
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Gale EAM. Epidemiology of type 1 diabetes [internet] Diapedia. 2014 Aug 13; 2104085168 rev. no. 39.
    1. Pollard HM, Miller L, Brewer WA. The external secretion of the pancreas and diabetes mellitus. Am J Dig Dis. 1943;10(1):20–3.
    1. Perczak-Dudkowska B, Niewiedziol B. Exocrine function of the pancreas in juvenile onset diabetes mellitus. I. pH, duodenal content volume and bicarbonate concentration and secretion. Pediatr Pol. 1984;59(8):605–12. - PubMed
    1. Gepts W. Pathologic anatomy of the pancreas in juvenile diabetes mellitus. Diabetes. 1965;14(10):619–33. The first report of decreased pancreatic size in patients with T1D. - PubMed
    1. Williams AJ, Thrower SL, Sequeiros IM, Ward A, Bickerton AS, Triay JM, et al. Pancreatic volume is reduced in adult patients with recently diagnosed type 1 diabetes. J Clin Endocrinol Metab. 2012;97(11):E2109–13. - PubMed

MeSH terms