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

Autor: Ekkehard C. Jehle, Jörg Glatzle, Mario Müller, Horst D. Becker, Helen E. Raybould, Tilman T. Zittel, Martin E. Kreis
Rok vydání: 2002
Předmět:
Zdroj: Annals of Surgery. 236:166-176
ISSN: 0003-4932
DOI: 10.1097/00000658-200208000-00004
Popis: 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 to weight loss after gastrectomy. 9–11 In addition, several studies have shown a reduced food intake after gastrectomy, 3,12 but the reasons for this are not clear. Gastrointestinal peptides contribute to the regulation of food intake by activating specific brain centers. 13 We have recently shown that cholecystokinin (CCK) injection or food intake stimulated neurons in the nucleus of the solitary tract (NTS), 14 a brain stem center known to be involved in the regulation of food intake. 15,16 A strong correlation between the CCK dose injected or the amount of food intake and neuronal activation in the NTS was observed, indicating that the activation of these brain stem neurons probably reflects the initiation of satiation. 14 After gastrectomy, gut peptides that inhibit food intake are released at considerably increased amounts in response to a meal. For example, CCK release is increased after gastrectomy, 10,17 and CCK is known to suppress food intake under physiologic conditions. 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. In the present study, we investigated the central regulation of food intake by quantifying NTS neuron activation after CCK injection or food intake in gastrectomized rats. We obtained evidence that the central regulation of food intake is altered after total gastrectomy; these changes might reflect the disturbances in food intake and satiation clinically observed after total gastrectomy.
Databáze: OpenAIRE