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Updated: Nov 9, 2025

Isolating and Analyzing Cells of the Pancreas Mesenchyme by Flow Cytometry
Published on: January 28, 2017
Chromogranin A-positive hormone-negative endocrine cells in pancreas in human pregnancy
Abu Saleh Md Moin1, Kylie Zeng2, Robert A Rizza3
1Diabetes Research Center (DRC), Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), Doha, Qatar.
Introduction:
We sought to determine whether chromogranin A-positive hormone-negative (CPHN) endocrine cells are increased in the pancreas of pregnant women, offering potential evidence in support of neogenesis.
Methods:
Autopsy pancreata from pregnant women (n = 14) and age-matched non-pregnant control women (n = 9) were obtained. Staining of pancreatic sections for chromogranin A, insulin and a cocktail of glucagon, somatostatin, pancreatic polypeptide and ghrelin was undertaken, with subsequent evaluation for CPHN cell frequency.
Results:
The frequency of clustered β-cells was increased in pregnant compared to non-pregnant subjects (46.6 ± 5.0 vs. 31.8 ± 5.0% clustered β-cells of total clustered endocrine cells, pregnant vs. non-pregnant, p < .05). Frequency of endocrine cocktail cells was lower in pregnant women than non-pregnant women (36.2 ± 4.0 vs. 57.0 ± 6.8% clustered endocrine cocktail cells of total clustered endocrine cells, pregnant vs. non-pregnant, p < .01). No difference in frequency of CPHN cells was found in islets, nor in clustered or single cells scattered throughout the exocrine pancreas, between pregnant and non-pregnant women. The frequency of CPHN cells in pregnancy was independent of the number of pregnancies (gravidity).
Conclusions:
Our findings of no increase in CPHN cell frequency in pancreas of pregnant women suggest that this potential β-cell regenerative mechanism is not that by which the increased β-cell mass of pregnancy is achieved. However, an increase in the percentage of clustered β-cells was found in pregnancy, with decreased frequency of other endocrine cells in clusters, suggesting a compensatory shift from other pancreatic endocrine cell types to β-cells as a mechanism to meet the increased insulin demands of pregnancy.
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