Diabetes and its relationship to pancreatic carcinoma.
BACKGROUND
The mechanism of impaired glucose metabolism that develops in most patients with pancreatic cancer (PC) is obscure and the association between PC and diabetes is controversial. According to the published data, about 70% of patients with PC have an impaired glucose tolerance (IGT) or frank diabetes, whereas 30% do not. Up to 60% of the patients with IGT or diabetes show improvement in glucose metabolism after surgery, whereas other patients show only mild or no improvement.


OBJECTIVE
To investigate our theory that there are three types of PC: 1) PC not associated with IGT or diabetes (IGT- subtype, approximately 20-30%); 2) PC associated with IGT or diabetes (IGT+ subtype, approximately 70-80%), in which the abnormality improves postoperatively (IGT+/- subtype, approximately 40-60%); or 3) PC associated with IGT or diabetes that does not improve after the tumor resection (IGT+/+ subtype, approximately 40-60%).


RESULTS
The review of the literature and our own experience, which is the subject of this article, suggests that the reason for impaired glucose metabolism in most patients is the alteration of islet cells, from which, in our view, cancer cells develop. There is a good possibility that the altered islet cells, and/or tumors derived from them, produce diabetogenic substances. The extent of the islet alteration (i.e., focal or diffuse) may determine whether the removal of the tumor alone can improve the metabolic alteration.


CONCLUSIONS
The elucidation of the mechanism is of immense importance for providing an early tumor marker and for developing preventative and therapeutic modalities.
Saruc
Murat
M
UNMC Eppley Cancer Center, University of Nebraska Medical Center, Omaha, Nebraska 68198-6805, USA.
Pour
Parviz M
PM
D001786:Blood Glucose / Q000378:metabolism*; D003920:Diabetes Mellitus / Q000097:blood* / Q000473:pathology; D018149:Glucose Intolerance / Q000097:blood; D006801:Humans; D007515:Islets of Langerhans / Q000473:pathology; D008954:Models, Biological; D010190:Pancreatic Neoplasms / Q000097:blood* / Q000473:pathology
D001786:Blood Glucose