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Ingestion of a meal causes the release of cholecystokinin and neurotensin into the circulation, but little is known about the duration of this release.Six healthy volunteers were studied. Blood samples for cholecystokinin, neurotensin and gastrin assessment were drawn before and after consumption of a typical Italian lunch. Postprandial samples were obtained every hour for a total of 10 hours. All peptides were measured using previously validated radioimmunoassays.Ingestion of the meal caused a prompt and significant increase in plasma levels of all three peptides. Cholecystokinin remained elevated for about 7 hours and then tended to return towards basal values, whereas the increase of neurotensin persisted for the entire period of the study (10 hours). Gastrin remained elevated for about 5 hours and then declined. The integrated CCK and gastrin responses during the initial postprandial hours were greater than those in the late hours, whereas the integrated neurotensin response during the initial hours was lower than that in the late hours.The results indicate that, after an ordinary meal, cholecystokinin is released into the circulation for about 7 hours, much longer than previously reported (3-4 hours). The release of neurotensin begins soon after the meal and persists even longer, for at least 10 hours. Possible physiological implications of these findings are discussed.

Current data regarding an association between cholelithiasis, cholecystectomy, or gastrectomy and pancreatic cancer are conflicting. We evaluated the frequency with which these factors were present in 720 patients with newly diagnosed pancreatic cancer and in 720 matched controls. All subjects were interviewed personally and in detail about their clinical history. Cholelithiasis was present in 126 patients with pancreatic cancer (17.5%) and in 95 controls (13.2%), constituting a statistically significant association (odds ratio, 1.39; 95% confidence interval, 1.04–1.86); however, considering only the patients and controls in whom the diagnosis of cholelithiasis was made more than one year before cancer diagnosis or interview, the association was no longer significant (odds ratio, 1.04; 95% confidence interval, 0.75–1.44). Cholecystectomy had been performed in 93 patients with pancreatic cancer (12.9%) and in 71 controls (9.9%). When all subjects were considered, the odds ratio was mildly, although not significantly, increased (odds ratio, 1.35; 95% confidence interval, 0.97–1.87); when only subjects who underwent cholecystectomy one year or more before the cancer diagnosis or interview were considered, the odds ratio fell to unity. Gastrectomy had been performed in 28 patients with pancreatic cancer (3.9%) and in 25 controls (3.5%); analysis revealed no significant association between these two factors (odds ratio, 1.14; 95% confidence interval, 0.64–2.05). In conclusion, our study, one of the largest on this topic, has found no evidence for an association between cholelithiasis, cholecystectomy, or gastrectomy and pancreatic cancer.

While cigarette smoking is a well-established risk factor for pancreatic cancer, the role of alcohol, coffee, and tea consumption remains controversial. In view of this, and because of the limited information on possible environmental risk factors of pancreatic cancer in Italy, we carried out this study. Five hundred seventy patients with newly diagnosed pancreatic cancer and 570 controls from 14 Italian centers were studied. Using a standardized questionnaire, all were interviewed personally about their smoking habits, as well as habitual alcohol, coffee, and tea consumption throughout their lives prior to clinical onset of the disease. Details were also obtained on exposure to potential occupational carcinogens. A moderate association, statistically significant only in women (odds ratio, 2.18; 95% confidence interval, 1.30-3.68), was found between pancreatic cancer and cigarette smoking, but none was observed with alcohol or tea consumption or with any particular occupational exposure. Consumption of 1 or 2 cups of coffee per day was not associated with increased risk; 3 coffees per day increased the risk, but not significantly (odds ratio, 1.49; 95% confidence interval, 0.97-2.30); with consumption of more than 3 coffees per day the increase in risk was highly significant (odds ratio, 2.53; 95% confidence interval, 1.53-4.18). A statistically significant dose-response relationship (p < 0.001) was observed in each sex. The association between coffee use and pancreatic cancer still held after controlling for potential confounding factors such as cigarette smoking or alcohol use, and when the analysis was restricted to nonsmoking coffee drinkers. The results of this study, one of the largest of its type so far published, suggest that a causal relationship may exist between coffee consumption and pancreatic cancer.

Summary Aims: Diabetes occurs more frequently in patients with pancreatic cancer than in the general population, and it has repeatedly been claimed that it is a risk factor for this tumor. However in most of the studies on this subject the duration of diabetes before the diagnosis of pancreatic cancer was not ascertained. In an attempt to clarify the cause of the association between these two pathologic conditions and to determine whether diabetes is a risk factor for pancreatic cancer we recently studied this association in a large number of patients with pancreatic cancer. Methods: A total of 720 patients with newly diagnosed pancreatic cancer (415 men and 305 women; mean age 62.6 years, range 22 to 79 years) and 720 controls matched for sex, age, social class, and geographic region, were enrolled in the study. All subjects were interviewed personally and in detail about their clinical history. The diagnosis of diabetes was based on criteria recommended by the American Diabetes Association. Results: One hundred sixty-four patients with pancreatic cancer (22.8 %) and 60 controls (8.3 %) had diabetes. In the majority of the patients with pancreatic cancer (56.1 %), diabetes was diagnosed either concomitantly with the cancer (in 40.2 %), or within two years before the diagnosis of cancer (in 15.9 %). The association between the two conditions was significant (odds ratio, 3.04; 95 % confidence interval, 2.21 to 4.17). However, when only patients with diabetes of three or more years' duration were considered, the association was no longer significant (odds ratio, 1.43; 95 % confidence interval, 0.98 to 2.07). All the patients with pancreatic cancer whose diabetes had been diagnosed before the cancer had non-insulin-dependent diabetes; all but one of the control patients with diabetes had the non-insulin-dependent form of the disease. Conclusions: Diabetes in patients with pancreatic cancer is frequently of recent onset and is presumably caused by the tumor. Diabetes is not a risk factor for pancreatic cancer.

The aim of the present review was to evaluate the effects of neurotensin on the exocrine pancreatic secretion. Neurotensin immunoreactivity has been identified in the central nervous system and also in the digestive system, where it is found in specific endocrine cells of the intestinal mucosa (N cells), in nerve fibers of the enteric nervous system and in intrapancreatic ganglia (both in nerves and cell bodies). Studies in laboratory animals and in humans have demonstrated that the ingestion of a meal causes a significant release of neurotensin into the circulation and that exogenous administration of low doses of the peptide strongly stimulates exocrine pancreatic secretion. These findings, together with the demonstration that the immunoneutralization of circulating neurotensin significantly reduces the pancreatic secretory response to a meal, suggest that neurotensin is a physiological regulator of exocrine pancreatic secretion.