Abstract
Abnormal glucose tolerance and frank diabetes mellitus develop in up to 80% of pancreatic cancer patients. Islets within these tumors show a decreased number of β cells and increased number of α cells. The reduced number of β cells could induce β cell neogenesis in extrainsular tissue to compensate for the loss of insulin in islets. On the other hand, because the β cell depletion in pancreatic cancer seems to be the effect of substances released by cancer cells, suppression of extrainsular endocrine cells is expected. We compared the pattern of extrainsular endocrine cells in pancreatic cancer patients with normal pancreas as well as chronic pancreatitis, which is known to be associated with impaired glucose tolerance or frank diabetes. As in the normal tissue, extrainsular endocrine cells were found in chronic pancreatitis and pancreatic cancer. However, in the chronic pancreatitis specimens insulin cells were the predominant cell type, whereas in pancreatic cancer specimens more glucagon than insulin cells were found, although the differences were statistically insignificant. Thus, our results indicate that the alteration of β cells in pancreatic cancer patients is mainly restricted to the endocrine cells within the islets and that there is no compensatory proliferation of β cells. Teratogenesis Carcinog. Mutagen.
Original language | English |
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Pages (from-to) | 69-81 |
Number of pages | 13 |
Journal | Teratogenesis Carcinogenesis and Mutagenesis |
Volume | 21 |
Issue number | 1 |
DOIs | |
Publication status | Published - 2001 |
Externally published | Yes |
Keywords
- Chronic pancreatitis
- Diabetes mellitus
- Glucose tolerance
- Normal pancreas
- Pancreatic cancer
- α cells
- β cells
ASJC Scopus subject areas
- Oncology
- Genetics
- Toxicology
- Genetics(clinical)
- Health, Toxicology and Mutagenesis