Literature DB >> 27300574

Increased Hormone-Negative Endocrine Cells in the Pancreas in Type 1 Diabetes.

Abu Saleh Md Moin1, Sangeeta Dhawan1, Christine Shieh1, Peter C Butler1, Megan Cory1, Alexandra E Butler1.   

Abstract

CONTEXT AND
OBJECTIVE: Type 1 diabetes (T1D) is characterized by a β-cell deficit due to autoimmune inflammatory-mediated β-cell destruction. It has been proposed the deficit in β-cell mass in T1D may be in part due to β-cell degranulation to chromogranin-positive, hormone-negative (CPHN) cells. DESIGN, SETTING, AND PARTICIPANTS: We investigated the frequency and distribution of CPHN cells in the pancreas of 15 individuals with T1D, 17 autoantibody-positive nondiabetic individuals, and 17 nondiabetic controls.
RESULTS: CPHN cells were present at a low frequency in the pancreas from nondiabetic and autoantibody-positive, brain-dead organ donors but are more frequently found in the pancreas from donors with T1D (islets: 1.11% ± 0.20% vs 0.26% ± 0.06 vs 0.27% ± 0.10% of islet endocrine cells, T1D vs autoantibody positive [AA+] vs nondiabetic [ND]; T1D vs AA+, and ND, P < .001). CPHN cells are most commonly found in the single cells and small clusters of endocrine cells rather than within established islets (clusters: 18.99% ± 2.09% vs 9.67% ± 1.49% vs 7.42% ± 1.26% of clustered endocrine cells, T1D vs AA+ vs ND; T1D vs AA+ and ND, P < .0001), mimicking the distribution present in neonatal pancreas.
CONCLUSIONS: From these observations, we conclude that CPHN cells are more frequent in T1D and, as in type 2 diabetes, are distributed in a pattern comparable with the neonatal pancreas, implying a possible attempted regeneration. In contrast to rodents, CPHN cells are insufficient to account for loss of β-cell mass in T1D.

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Year:  2016        PMID: 27300574      PMCID: PMC5010569          DOI: 10.1210/jc.2016-1350

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


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