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J Clin Endocrinol Metab. 2016 Feb;101(2):523-32. doi: 10.1210/jc.2015-3566. Epub 2015 Dec 23.

β-Cell Deficit in Obese Type 2 Diabetes, a Minor Role of β-Cell Dedifferentiation and Degranulation.

Author information

1
Larry L. Hillblom Islet Research Center (A.E.B., S.D., J.H., M.C., K.Z., P.C.B.), David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095-7073; Institute of Pathology (H.F.), Division of Clinical and Functional Anatomy, Medical University of Innsbruck, A-6020 Innsbruck, Austria; St Josef Hospital of the Ruhr-University Bochum (J.J.M.), 44791 Bochum, Germany; and Division of Endocrinology, Diabetes, Metabolism, and Nutrition (R.A.R.), Mayo Clinic College of Medicine, Rochester, Minnesota 55905.

Abstract

CONTEXT:

Type 2 diabetes is characterized by a β-cell deficit and a progressive defect in β-cell function. It has been proposed that the deficit in β-cells may be due to β-cell degranulation and transdifferentiation to other endocrine cell types.

OBJECTIVE:

The objective of the study was to establish the potential impact of β-cell dedifferentiation and transdifferentiation on β-cell deficit in type 2 diabetes and to consider the alternative that cells with an incomplete identity may be newly forming rather than dedifferentiated.

DESIGN, SETTING, AND PARTICIPANTS:

Pancreata obtained at autopsy were evaluated from 14 nondiabetic and 13 type 2 diabetic individuals, from four fetal cases, and from 10 neonatal cases.

RESULTS:

Whereas there was a slight increase in islet endocrine cells expressing no hormone in type 2 diabetes (0.11 ± 0.03 cells/islet vs 0.03 ± 0.01 cells/islet, P < .01), the impact on the β-cell deficit would be minimal. Furthermore, we established that the deficit in β-cells per islet cannot be accounted for by an increase in other endocrine cell types. The distribution of hormone negative endocrine cells in type 2 diabetes (most abundant in cells scattered in the exocrine pancreas) mirrors that in developing (embryo and neonatal) pancreas, implying that these may represent newly forming cells.

CONCLUSIONS:

Therefore, although we concur that in type 2 diabetes there are endocrine cells with altered cell identity, this process does not account for the deficit in β-cells in type 2 diabetes but may reflect, in part, attempted β-cell regeneration.

PMID:
26700560
PMCID:
PMC4880126
DOI:
10.1210/jc.2015-3566
[Indexed for MEDLINE]
Free PMC Article

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