Volume 3, Issue 4 pp. 234-243

Attenuation of Endocrine-Exocrine Pancreatic Communication in Type 2 Diabetes: Pancreatic Extracellular Matrix Ultrastructural Abnormalities

Melvin R. Hayden MD

Melvin R. Hayden MD

From the Department of Internal Medicine

Diabetes Cardiovascular Center

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Kamlesh Patel MD

Kamlesh Patel MD

Diabetes Cardiovascular Center

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Javad Habibi PhD

Javad Habibi PhD

From the Department of Internal Medicine

Diabetes Cardiovascular Center

The Harry S. Truman VA Medical Center

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Deepa Gupta MD

Deepa Gupta MD

From the Department of Internal Medicine

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Seema S. Tekwani MD

Seema S. Tekwani MD

Diabetes Cardiovascular Center

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Adam Whaley-Connell DO, MSPH

Adam Whaley-Connell DO, MSPH

From the Department of Internal Medicine

Diabetes Cardiovascular Center

The Harry S. Truman VA Medical Center

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James R. Sowers MD

James R. Sowers MD

From the Department of Internal Medicine

Diabetes Cardiovascular Center

The Harry S. Truman VA Medical Center

Department of Physiology and Pharmacology, University of Missouri-Columbia School of Medicine, Columbia, MO

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First published: 24 November 2008
Citations: 58
Melvin R. Hayden, MD, Department of Internal Medicine, University of Missouri-Columbia School of Medicine, D109 Diabetes Center, UHC, One Hospital Drive, Columbia, MO 65121-0001
E-mail:
[email protected]

Abstract

Ultrastructural observations reveal a continuous interstitial matrix connection between the endocrine and exocrine pancreas, which is lost due to fibrosis in rodent models and humans with type 2 diabetes mellitus (T2DM). Widening of the islet-exocrine interface appears to result in loss of desmosomes and adherens junctions between islet and acinar cells and is associated with hypercellularity consisting of pericytes and inflammatory cells in T2DM pancreatic tissue. Organized fibrillar collagen was closely associated with pericytes, which are known to differentiate into myofibroblasts—pancreatic stellate cells. Of importance, some pericyte cellular processes traverse both the connecting islet-exocrine interface and the endoacinar interstitium of the exocrine pancreas. Loss of cellular paracrine communication and extracellular matrix remodeling fibrosis in young animal models and humans may result in a dysfunctional insulino-acinar-ductal–incretin gut hormone axis, resulting in pancreatic insufficiency and glucagon-like peptide deficiency, which are known to exist in prediabetes and overt T2DM in humans.

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