Effect of duodenum-preserving resection of the head of the pancreas on endocrine and exocrine pancreatic function in patients with chronic pancreatitis.

BACKGROUND: Chronic pancreatitis leads to progressive destruction of pancreatic parenchyma affecting exocrine and endocrine function. We prospectively evaluated the effect of duodenum-preserving resection of the head of the pancreas on pancreatic function. METHODS: Exocrine and endocrine function were measured in a combined test including (1) urinary PABA recovery; (2) plasma glucose, glucagon, and C-peptide responses; and (3) plasma pancreatic polypeptide response. Nineteen patients were included. RESULTS: Compared with the preoperative state, plasma glucose levels did not increase postoperatively. Plasma C-peptide levels were reduced postoperatively but the difference was not significant. The percentage of insulin-dependent patients did not increase after operation (32% versus 32%). Glucose tolerance improved in 4 patients and deteriorated in 3 patients. Postoperative basal and-meal stimulated plasma pancreatic polypeptide levels were significantly reduced. Postoperative urinary PABA recovery was not significantly different from preoperative values. CONCLUSIONS: Neither exocrine nor endocrine pancreatic function are negatively influenced by duodenum-preserving pancreatic head resection.

A rare cause of obstructive jaundice and weight loss in Von Recklinghausen's disease.

We present the case of a patient with the rare triad of Von Recklinghausen's disease associated with a somatostatinoma and a gastrointestinal stromal tumour (GIST). The patient had recurrent jaundice, the typical somatostatinoma syndrome, positive MR imaging but negative 68Ga-DOTATOC PET scanning in a histopathology-proven somatostatinoma tumour.

Review article: The gastrointestinal tract: neuroendocrine regulation of satiety and food intake.

BACKGROUND: The gastrointestinal tract elicits numerous signals regulating food intake and satiety, and recently many studies have been performed to elucidate the mechanisms regulating these signals. AIM: To describe the effects of the gastrointestinal tract on satiety, satiation and food intake. METHODS: A PubMed search was performed to identify and select the relevant literature using search terms including 'gastric satiety, intestine + satiety, satiation, cholecystokinin, ghrelin, peptide YY, glucagon-like peptide-1 and ileal brake'. RESULTS: Satiation, satiety and food intake result, among other factors, from signals originating in the stomach caused by distension and signals from the small intestine. These intestinal signals result from nutrient sensing in the gut and activate neural and humoral pathways. Activation of the distal part of the gut, the so called ileal brake, leads to reduction in hunger and food intake, and models of chronic ileal brake activation lead to massive weight loss. CONCLUSION: Gastrointestinal signals are crucial for the regulation of food intake, satiety and satiation. The ileal brake deserves special attention, as both ileal intubation studies and surgical studies demonstrate that activation of the ileal brake reduces food intake. In the surgical models, weight loss occurs without adaptation to the anorectic effects of ileal brake activation.

Effects of somatostatin on human satiety.

Somatostatin (ST) inhibits gastrointestinal motility and exocrine and endocrine secretions. In animals, ST has been demonstrated to decrease food intake. We investigated, in a randomized double-blind investigation in 10 healthy humans, the effects of an intravenous ST infusion compared to saline on subjective hunger feelings. After 1 h, a low dose of fat was given intraduodenally to induce the release of endogenous upper-intestinal satiety factors. Ninety minutes later sandwiches were served and eaten until satiation. In the first hour, when no intraduodenal fat was given, there was a significant decrease in feelings of hunger with ST (p < 0.05). During the intraduodenal fat infusion this pattern reversed with a trend towards less satiety with ST. Food intake during intraduodenal fat infusion tended to be higher during ST (305 +/- 42 g) than during saline (205 +/- 36 g) although not significantly. In the 5 h after the experiment hunger feelings were significantly less after ST. In conclusion, we found evidence for a satiety effect of ST in humans which reversed towards less satiety when intraduodenal intralipid, which presumably produced endogenous satiety factors, was given. Postmeal satiety is higher after ST.

Satiety effects of cholecystokinin in humans.

BACKGROUND/AIMS: Cholecystokinin (CCK) inhibits gastric emptying and may exert satiety effects in several species, including humans. Because the effects of physiological doses of CCK on satiety in humans is unclear, the satiety effects of CCK-33 in physiological levels in lean and obese subjects were studied. METHODS: CCK-33 was infused intravenously to 32 healthy men or women (14 obese, all women; 18 lean, 4 men and 14 women) in doses that elicited plasma CCK concentrations in the physiological range. The effects of these infusions on feelings of hunger, wish to eat, fullness, and prospective feeding intentions were measured on visual analogue scales and compared with saline during a 1-hour infusion period. RESULTS: The CCK infusions induced significant decreases in hunger feelings, wish to eat, and prospective feeding intentions (P < 0.05), whereas fullness tended to be increased (P = 0.054). No clear differences between lean and obese subjects were observed apart from a more marked decrease in fullness and increase in prospective feeding intentions during the 1-hour saline infusion in the lean group (P < 0.05). CONCLUSIONS: CCK infusion leading to physiological plasma levels significantly increases satiety in humans.

Gallbladder responses to modified sham feeding: effects of the composition of a meal.

Changes in gallbladder contraction and plasma cholecystokinin release were studied following modified sham feeding of 3 different isocaloric meals rich in either fat, protein or carbohydrates in healthy volunteers, and results were compared with those following real feeding of comparable meals. In contrast to carbohydrate-rich meals (8 +/- 19 ml/120 min), fat- (-412 +/- 46 ml/120 min) and protein-rich meals (-352 +/- 42 ml/120 min) reduced integrated gallbladder volume (P < 0.05) in response to modified sham feeding. Plasma cholecystokinin levels were not significantly influenced by modified sham feeding of fat, protein or carbohydrates. Real feeding of a carbohydrate-rich meal also failed to significantly reduce gallbladder volume and to stimulate cholecystokinin release (-45 +/- 40 ml/120 min and 51 +/- 11 pmol/120 min, respectively), while real feeding of both fat- and protein-rich meals distinctly reduced gallbladder volume (-679 +/- 76 and -564 +/- 53 ml/120 min, respectively; P < 0.05) and increased cholecystokinin release (651 +/- 72 and 504 +/- 43 pmol/120 min, respectively; P < 0.05). This study demonstrates that gallbladder contraction during the cephalic phase of meal stimulation is dependent on the fat, protein and carbohydrate percentages of a meal, and is activated by different mechanisms than the intestinal phase of a meal.

Gallbladder motility after duodenum-preserving resection of the head of the pancreas.

BACKGROUND: Duodenum-preserving resection of the head of the pancreas (DPRHP) is performed in patients with chronic pancreatitis (CP) localized in the head of the pancreas. It has been suggested that functional integrity of the upper digestive tract is preserved after DPRHP. We tested this hypothesis with regard to gallbladder motility. METHODS: Gallbladder motility and cholecystokinin (CCK) secretion were studied fasting, after cephalic vagal stimulation with sham feeding, and after regular feeding in 9 patients after DPRHP, in 6 unoperated patients with CP, and 9 healthy control subjects. RESULTS: Mean fasting gallbladder volume in patients after DPRHP (49 +/- 10 cm3) and patients with CP (53 +/- 10 cm3) was larger than in controls (33 +/- 3 cm3). Sham-feeding gallbladder contraction did not differ between patients after DPRHP, patients with CP, and controls. Both postprandial CCK secretion and gallbladder contraction in patients after DPRHP (78 +/- 16 pM. 120 min; 47% +/- 6%) and patients with CP (72 +/- 18 pM.120 min; 40% +/- 7%) were significantly reduced (P < 0.05) compared with controls (151 +/- 13 pM.120 min; 74% +/- 4%). Fasting gallbladder volume, sham feeding, and regular-feeding-induced gallbladder contraction and postprandial CCK secretion did not differ between operated and unoperated patients with CP. CONCLUSIONS: Gallbladder motility and CCK secretion are reduced in patients with pancreatic insufficiency. A DPRHP procedure does not further influence these results. These findings support the concept that gallbladder motor function is preserved after DPRHP.