Cholecystokinin is partly responsible for reduced food intake and body weight loss after total gastrectomy in rats

Zittel, Tilman T.; Elm, B.v.; Teichmann, R.; Rabould, Helen E.; Becker, H. D.

doi:10.1016/s0002-9610(99)80148-2

Cited by 17 publications

(15 citation statements)

References 26 publications

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“…13 We have shown that CCK receptor blockade increased food intake and body weight after total gastrectomy in rats. 18 However, the mechanisms and pathways leading to an altered regulation of food intake following gastrectomy are not clear.…”

Section: Discussionmentioning

confidence: 99%

“…CCK-A receptor blockade reduced c-fos protein expression in the NTS and increased food intake in unoperated control rats as well as in gastrectomized rats in this study, and chronic CCK-A receptor blockade increased food intake and body weight after gastrectomy in a previous study. 18 Therefore, it is conceivable that an increased postprandial CCK release might contribute to a reduced body weight after gastrectomy. …”

Section: Discussionmentioning

confidence: 99%

“…Total gastrectomy with Roux-en-Y reconstruction was performed as previously described. 18 In brief, the duodenum was closed by a ligature distal to the pylorus, the stomach was removed, and the jejunum was cut 2 cm distally to the ligament of Treitz. Esophagus and jejunum were anastomosed by single stitches, and an end-to-side jejunal anastomosis (Rouxen-Y) was done about 7 cm distally by a running suture.…”

Section: Surgical Proceduresmentioning

confidence: 99%

“…For example, CCK is released prematurely and at a greater rate after gastrectomy, 10,17 while the inhibitory effects on food intake are preserved after total gastrectomy. 18 Since the number of activated NTS neurons in response to CCK or food is increased after total gastrectomy, we would assume that the food-stimulated neuroendocrine response of the proximal small intestine is decisive for the early initiation of satiety after gastrectomy.…”

Section: Regulation Of Food Intake After Total Gastrectomy In Ratsmentioning

confidence: 99%

“…28,30,51,52 Rather than looking for a perfect reconstruction method, it might be worth looking at pathways that regulate food intake after total gastrectomy. The manipulation of these pathways by defined receptor agonist or antagonist treatments might be an alternative way to increase body weight after total gastrectomy, 18,43,53 possibly alleviating the sequelae of total gastrectomy for these patients.…”

Section: Regulation Of Food Intake After Total Gastrectomy In Ratsmentioning

confidence: 99%

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Total Gastrectomy Severely Alters the Central Regulation of Food Intake in Rats

Zittel¹,

Glatzle²,

Müller³

et al. 2002

Annals of Surgery

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ObjectiveTo investigate the central regulation of food intake by quantifying neuron activation of the nucleus of the solitary tract (NTS) after injection of cholecystokinin (CCK) or food intake in gastrectomized rats. Summary Background DataTotal gastrectomy is followed by early satiety, low calorie intake, and weight loss in the majority of patients. The etiology of these effects is unknown. Sixty percent to 70% of patients remain underweight after total gastrectomy, the weight loss averaging 25% of preoperative body weight. About two thirds of gastrectomized patients report early satiety, and about 60% do not reach the recommended daily calorie intake. The NTS is a brain stem center involved in the regulation of food intake; thus, the extent and pattern of neuronal activation provide information on the process involved in the initiation of satiation and the regulation of food intake. MethodsThe authors investigated neuronal activation in the NTS using c-fos immunohistochemistry following CCK injection or food intake in healthy control rats, sham-operated control rats, age-matched control rats, weight-matched control rats, and vagotomized or gastrectomized rats. ResultsNeuronal activation in the NTS after CCK injection was significantly decreased 21 days after total gastrectomy, but increased by up to 51% 3 months and by up to 102% 12 months after surgery compared to age-matched unoperated control rats. Neuronal activation in the NTS in response to feeding was markedly increased up to fivefold in gastrectomized rats. This increase was early in onset and sustained, and occurred despite significantly reduced food intake. Administration of MK329, a CCK-A receptor antagonist, significantly reduced the number of postprandially activated neurons in both gastrectomized and control rats. ConclusionsThe early postprandial activation of NTS neurons after total gastrectomy in rats may correspond to early satiety reported by patients, while the sustained activation of NTS neurons after a meal could contribute to a reduced daily calorie intake. These data suggest that a disturbed central regulation of food intake might contribute to early satiety, reduced food intake, and weight loss after total gastrectomy.Total gastrectomy is still a mainstay of gastric cancer treatment.1 It is followed by a variety of symptoms and impairments, commonly referred to as postgastrectomy syndromes.2 One important feature of the postgastrectomy syndromes is a considerable loss of body weight.3,4 The loss averages around 25% of preoperative body weight 4,5 and leaves 60% to 70% of patients permanently below ideal body weight. 3,6 While perioperative weight loss due to catabolic metabolism is generally followed by an anabolic phase 3 to 8 days postoperatively with body weight recovery, 7 this is not the case in gastrectomized patients, where weight loss and underweight frequently cause long-lasting morbidity. 4 -6,8 There is evidence that pancreatic insufficiency, resulting in malabsorption and impaired food utilization, contributes Correspon...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Surgical Proceduresmentioning

confidence: 99%

Section: Regulation Of Food Intake After Total Gastrectomy In Ratsmentioning

confidence: 99%