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Quantitative morphology of B, A, D, and PP cells in infants of diabetic mothers
Insights
Infants of diabetic mothers (IDM) show increased pancreatic islet cells, including B cells, A cells, and PP cells. This suggests maternal hyperglycemia may stimulate multiple islet cell types, not just B cells.
Area of Science:
- Endocrinology
- Developmental Biology
- Histology
Background:
- Maternal diabetes can affect fetal development.
- Infants of diabetic mothers (IDM) may exhibit pancreatic abnormalities.
Purpose of the Study:
- To investigate pancreatic islet cell composition in infants of diabetic mothers (IDM).
- To determine if maternal hyperglycemia specifically causes B cell hyperplasia in fetuses.
Main Methods:
- Histological examination of pancreatic specimens from 34 IDM and 32 control infants.
- Immunocytochemical staining for insulin (B cells), glucagon (A cells), somatostatin (D cells), and pancreatic polypeptide (PP cells).
- Automatic image analysis and point counting to quantify fractional areas of endocrine cells in PP-rich and PP-poor regions.
Main Results:
- IDM showed significantly higher fractional areas of B cells in both pancreatic regions.
- Increased fractional areas of A cells (PP-poor) and PP cells (PP-rich) were observed in IDM.
- Total endocrine cell fractional area was higher in IDM in PP-poor regions, but not PP-rich regions.
Conclusions:
- Results do not support the hypothesis of specific fetal B cell hyperplasia due to maternal hyperglycemia.
- Hyperplasia of B, A, and PP cells in IDM may result from diverse stimuli.
- A single stimulus acting on a pluripotential stem cell is a possible explanation for observed cell hyperplasia.
Abstract:
Pancreatic specimens from 34 infants of diabetic mothers (IDM) and 32 control infants of gestational ages 26-44 wk were examined histologically using immunocytochemical stains for insulin, glucagon, somatostatin, and pancreatic polypeptide (PP). Each section was divided into PP-rich and PP-poor regions that are thought to be derived from the ventral and dorsal lobes of the gland, respectively. In some of these, the fractional area (%) occupied by positively stained B, A, and PP cells was determined by automatic image analysis, and the area occupied by D cells was determined by conventional point counting. The B cell fractional area was significantly higher in the IDM in both PP-poor and PP-rich areas (P less than 0.02). the fractional area of A cells in PP-poor areas and of PP cells in PP-rich areas was also significantly greater in IDM (P less than 0.02). The total endocrine cell fractional area was significantly greater in IDM in PP-poor but not in PP-rich regions of the pancreas. These results are not compatible with the hypothesis that maternal hyperglycemia results in specific fetal B cell hyperplasia and raise the possibility that hyperplasia of B, A, and PP cells in IDM may result from a variety of stimuli or that one stimulus acts on a pluripotential stem cell.