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控制肥胖的生理学方法。

Physiologic approaches to the control of obesity.

作者信息

Powers M A, Pappas T N

机构信息

Department of Surgery, Duke University Medical Center, Durham, NC 27710.

出版信息

Ann Surg. 1989 Mar;209(3):255-60. doi: 10.1097/00000658-198903000-00001.

DOI:10.1097/00000658-198903000-00001
PMID:2647049
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1493929/
Abstract

Morbid obesity is a major health problem in this country and throughout the world. In addition to its social stigma (in the western world), obesity exacerbates several disease states such as diabetes, hypertension, cardiac disease and restrictive lung disease. When effective medical treatment of obesity becomes available, it will depend in part upon understanding the physiologic factors that control satiety. This review summarizes the information available on brain and gut control mechanisms of satiety. Brain nuclei located in the lateral hypothalamus, ventromedial hypothalamus, and other paraventricular areas are the sites of action for potent neuropeptides, such as cholecystokinin (CCK) and neuropeptide Y, that appear to regulate feeding. Exogenous CCK has been used clinically to decrease meal size in obese patients. The sites of the satiety cascade that are most often manipulated are the gastric and intestinal phases. Physiologic gastric distension is a potent inhibitor of feeding, whereas the intermeal interval may be regulated by intestinal signals released by food in the gut. Jejunal-ileal bypass has fallen from favor and has been replaced by gastric restrictive procedures that create a small proximal gastric pouch that empties into the small bowel (gastric bypass) or the distal stomach (gastroplasty). These operations rely partially on their ability to produce gastric distension in the proximal gastric pouch at an early stage during a meal. Thus, failure results if the pouch compensates by distending or if the stoma widens with subsequent loss of slow emptying. Improved medical and surgical treatment will be designed to intervene at specific sites of the satiety cascade as knowledge of the physiologic control mechanisms of satiety increases.

摘要

病态肥胖是这个国家乃至全世界的一个主要健康问题。除了其社会污名(在西方世界)外,肥胖还会加重多种疾病状态,如糖尿病、高血压、心脏病和限制性肺病。当有效的肥胖医学治疗方法出现时,部分将取决于对控制饱腹感的生理因素的理解。这篇综述总结了关于饱腹感的脑和肠道控制机制的现有信息。位于下丘脑外侧、腹内侧下丘脑和其他室旁区域的脑核是强力神经肽如胆囊收缩素(CCK)和神经肽Y的作用位点,这些神经肽似乎调节进食。外源性CCK已在临床上用于减少肥胖患者的进食量。饱腹感级联反应中最常被操控的阶段是胃和肠道阶段。生理性胃扩张是进食的有力抑制剂,而餐间间隔可能由肠道中食物释放的肠道信号调节。空肠回肠旁路手术已失宠,已被胃限制性手术所取代,后者创建一个小的近端胃囊,该胃囊排入小肠(胃旁路手术)或远端胃(胃成形术)。这些手术部分依赖于它们在进食早期在近端胃囊中产生胃扩张的能力。因此,如果胃囊通过扩张进行代偿或吻合口变宽导致排空减慢,手术就会失败。随着对饱腹感生理控制机制的了解增加,改进的医学和手术治疗将被设计用于在饱腹感级联反应的特定部位进行干预。

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Physiologic approaches to the control of obesity.控制肥胖的生理学方法。
Ann Surg. 1989 Mar;209(3):255-60. doi: 10.1097/00000658-198903000-00001.
2
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Cholecystokinin and control of food intake.胆囊收缩素与食物摄入的控制
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Effect of sham feeding on gastric motor activity of the dog.假饲对犬胃运动活性的影响。
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The feeding response of obese mice (genotype, ob ob) and their wild-type littermates to cholecystokinin (pancreozymin).肥胖小鼠(基因型为ob ob)及其野生型同窝小鼠对胆囊收缩素(胰酶泌素)的摄食反应。
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