Endoscopic ultrasonography is a highly sensitive and specific procedure for the localization of pancreatic endocrine tumors. It should be considered for the preoperative localization of such tumors once the clinical and laboratory diagnosis has been established.

Endoscopic ductal decompression therapy offers relief of pain in two-thirds of the patients when it is used as the only form of treatment. One-quarter of the patients have to undergo surgery.

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Ghrelin is an orexigenic gastric hormone that decreases in peripheral blood after carbohydrate-rich meals but increases after protein ingestion. In the present study plasma ghrelin was determined together with hunger and satiety ratings and with insulin and glucose concentrations after the ingestion of satiating quantities of carbohydrate-, fat-, protein-, fruit-, and vegetable-rich meals in 14 healthy subjects. Four hours later, standardized sandwiches were consumed. After carbohydrate, ghrelin decreased, whereas fat, protein, fruit, and vegetable ingestion significantly increased ghrelin levels. Considering all test meals, no significant correlation existed between changes of ghrelin levels and satiety ratings (r = 0.05; not significant), whereas a significant inverse relationship was observed between plasma ghrelin and insulin levels (r = -0.44; P < 0.001). During the second meal, sandwich consumption was significantly greater after the preceding fruit and vegetable meals, which was significantly correlated with the fourth-hour increase of ghrelin (r = 0.44; P < 0.001). In conclusion, after an overnight fast, ghrelin release depends on the ingested macronutrients and is most likely not a major regulator of acute food intake, although it is of greater importance for the recurrence of hunger and subsequent meal size.

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To gain further insight into the regulatory role of insulin and leptin on plasma ghrelin, 56 normal weight, 128 normoinsulinemic obese, 121 hyperinsulinemic obese, and 30 type 2 diabetic normoinsulinemic and 75 type 2 diabetic hyperinsulinemic obese patients were examined. In the obese subjects, basal hyperinsulinemia was associated with significantly lower ghrelin independent of BMI, age, and leptin. In normoinsulinemic (normal weight and normoinsulinemic obese) subjects, ghrelin was inversely related to stepwise increasing leptin. Multiple regression analysis and matching for insulin revealed a significant negative interaction of ghrelin with leptin but not insulin. In type 2 diabetic normoinsulinemic subjects, ghrelin was significantly lower compared with that in normoinsulinemic obese subjects. In type 2 diabetic hyperinsulinemic subjects, ghrelin was significantly lower than in normoinsulinemic subjects, whereas no further reduction was observed compared with hyperinsulinemic obese subjects. The postprandial decrease was significantly attenuated in normoinsulinemic obese and hyperinsulinemic obese subjects (؊214.8 ؎ 247 pg/ml [normal weight], ؊137.6 ؎ 107 pg/ml [normoinsulinemic obese], ؊85.5 ؎ 69 pg/ml [hyperinsulinemic obese], P < 0.001; mean ؎ SD), whereas type 2 diabetes had no independent postprandial effect. In conclusion, the present data support the concept that leptin could be of importance for suppression of basal ghrelin during moderate weight gain in normoinsulinemic subjects, whereas hyperinsulinemia but not leptin is responsible in more severe obesity. Postprandial suppression of ghrelin is attenuated by as yet unknown mechanisms that are related to body weight but not to insulin or type 2 diabetes. Diabetes