Human Nutrition Unit, University of Auckland, Auckland, New Zealand; School of Biological Sciences, University of Auckland, Auckland, New Zealand.
Physiol Behav. 2013 Aug 15;120:114-23. doi: 10.1016/j.physbeh.2013.07.008. Epub 2013 Aug 1.
The gastrointestinal (GI) tract and specifically the most distal part of the small intestine, the ileum, has become a renewed focus of interest for mechanisms targeting appetite suppression. The 'ileal brake' is stimulated when energy-containing nutrients are delivered beyond the duodenum and jejunum and into the ileum, and is named for the feedback loop which slows or 'brakes' gastric emptying and duodeno-jejunal motility. More recently it has been hypothesized that the ileal brake also promotes secretion of satiety-enhancing GI peptides and suppresses hunger, placing a 'brake' on food intake. Postprandial delivery of macronutrients to the ileum, other than unavailable carbohydrates (CHO) which bypass absorption in the small intestine en route to fermentation in the large bowel, is an uncommon event and hence this brake mechanism is rarely activated following a meal. However the ability to place a 'brake' on food intake through delivery of protected nutrients to the ileum is both intriguing and challenging. This review summarizes the current clinical and experimental evidence for activation of the ileal brake by the three food macronutrients, with emphasis on eating behavior and satiety as well as GI function. While clinical studies have shown that exposure of the ileum to lipids, CHOs and proteins may activate GI components of the ileal brake, such as decreased gut motility, gastric emptying and secretion of GI peptides, there is less evidence as yet to support a causal relationship between activation of the GI brake by these macronutrients and the suppression of food intake. The predominance of evidence for an ileal brake on eating comes from lipid studies, where direct lipid infusion into the ileum suppresses both hunger and food intake. Outcomes from oral feeding studies are less conclusive with no evidence that 'protected' lipids have been successfully delivered into the ileum in order to trigger the brake. Whether CHO or protein may induce the ileal brake and suppress food intake has to date been little investigated, although both clearly have GI mediated effects. This review provides an overview of the mechanisms and mediators of activation of the ileal brake and assesses whether it may play an important role in appetite suppression.
胃肠道（GI）道，特别是小肠的最远端部分，回肠，已成为针对抑制食欲的机制的新的关注焦点。当含有能量的营养素被输送到十二指肠和空肠之外并进入回肠时，“回肠制动”就会被刺激，它的命名是因为这个反馈回路会减缓或“制动”胃排空和十二指肠-空肠运动。最近，人们假设回肠制动还可以促进饱腹感增强的胃肠道肽的分泌，并抑制饥饿感，从而对食物摄入施加“制动”。除了在小肠中无法吸收的碳水化合物（CHO）之外，将大量营养素输送到回肠是一种不常见的情况，因此，这种制动机制在进食后很少被激活。然而，通过将保护的营养素输送到回肠来抑制食物摄入的能力既有趣又具有挑战性。本综述总结了目前关于三种食物宏量营养素通过回肠制动的临床和实验证据，重点关注进食行为和饱腹感以及胃肠道功能。虽然临床研究表明，回肠暴露于脂肪、CHO 和蛋白质可能会激活回肠制动的胃肠道成分，例如降低肠道蠕动、胃排空和胃肠道肽的分泌，但目前还没有更多的证据支持这些宏量营养素激活胃肠道制动与抑制食物摄入之间存在因果关系。关于回肠制动对进食的抑制作用的证据主要来自于脂质研究，其中直接将脂质输注到回肠会抑制饥饿感和食物摄入。口服喂养研究的结果不太确定，没有证据表明“保护”脂质已成功输送到回肠以触发制动。迄今为止，CHO 或蛋白质是否会引发回肠制动并抑制食物摄入的研究较少，尽管它们显然都有胃肠道介导的作用。本综述提供了回肠制动的激活机制和调节剂的概述，并评估了它是否可能在抑制食欲方面发挥重要作用。
