Erlanson-Albertsson Charlotte
Two views are being debated around fat-rich food and appetite regulation. One is that fat intake has a weak satiety-signaling property, with the consequence being a passive overconsumption of fat-rich food, in turn leading to obesity (Westerterp, 2006). The other view is that fat intake is tightly regulated through specific signals, which when overstimulated leads to aversion (Jebb et al., 2006). Fat intake depends not only on the quantity but more importantly on the quality of fat ingested, whether it is saturated, monounsaturated, or polyunsaturated fat (Casas-Agustench et al., 2008). Another important feature relates to whether the fat is eaten with sucrose or with something that has a sweet taste (Erlanson-Albertsson, 2005a). In general this will lead to a blunted response. Endocannabinoids released after palatable food ingestion, such as food containing fat and sucrose, will promote hunger and energy storage. The following hormones have been found to regulate the appetite for fat. Galanin (Gaysinskaya et al., 2007), agouti-related peptide (AgRP) (Tracy et al., 2007), and ghrelin (Shimbara et al., 2004) stimulate fat intake, while enterostatin (Berger et al., 2004), apolipoprotein A-IV (Apo A-IV) (Tso and Liu, 2004a), peptide YY (PYY) (Boey et al., 2008), cholecystokinin (CCK) (Beglinger and Degen, 2004), and neuropeptide Y (NPY) (Primeaux et al., 2005) inhibit fat intake. Both galanin (Schneider et al., 2007) and ghrelin (Jerlhag et al., 2007) also stimulate the intake of ethanol, via pathways involving a link to the reward system. The inhibition of fat intake occurs through reduced gastric emptying and serotonin release (Ritter, 2004). A proper satiety for fat is possible only with complete fat digestion, fatty acids being important to release satiety hormones (Feinle-Bisset et al., 2005). For proper control of fat intake, fat digestion needs to be retarded without being inhibited (Albertsson et al., 2007). Why we overeat fat? Energy dense. Gastrointestinal processing too rapid. Satiety signals too weak. Hunger signals too strong.
关于富含脂肪的食物与食欲调节,存在两种观点并引发了争论。一种观点认为,脂肪摄入具有较弱的饱腹感信号特性,其结果是被动地过度食用富含脂肪的食物,进而导致肥胖(韦斯特特普,2006年)。另一种观点则认为,脂肪摄入是通过特定信号严格调节的,当这些信号受到过度刺激时会导致厌恶(杰布等人,2006年)。脂肪摄入不仅取决于摄入量,更重要的是取决于所摄入脂肪的质量,无论是饱和脂肪、单不饱和脂肪还是多不饱和脂肪(卡萨 - 阿古斯特恩奇等人,2008年)。另一个重要特征涉及脂肪是与蔗糖一起食用还是与有甜味的东西一起食用(埃兰森 - 阿尔伯特松,2005a)。一般来说,这会导致反应迟钝。摄入美味食物(如含有脂肪和蔗糖的食物)后释放的内源性大麻素会促进饥饿感和能量储存。已发现以下激素可调节对脂肪的食欲。甘丙肽(盖辛斯卡娅等人,2007年)、刺鼠相关肽(AgRP)(特雷西等人,2007年)和胃饥饿素(岛原等人,2004年)会刺激脂肪摄入,而肠抑胃肽(伯杰等人,2004年)、载脂蛋白A-IV(Apo A-IV)(曹和刘,2004a)、肽YY(PYY)(博伊等人,2008年)、胆囊收缩素(CCK)(贝格林格和德根,2004年)以及神经肽Y(NPY)(普里莫等人,2005年)会抑制脂肪摄入。甘丙肽(施耐德等人,2007年)和胃饥饿素(耶尔哈格等人,2007年)还会通过涉及与奖励系统相关联的途径刺激乙醇摄入。对脂肪摄入的抑制是通过减少胃排空和血清素释放来实现的(里特,2004年)。只有在脂肪完全消化的情况下才可能产生适当的脂肪饱腹感,脂肪酸对于释放饱腹感激素很重要(费内尔 - 比塞特等人,2005年)。为了适当控制脂肪摄入,脂肪消化需要减缓但不能被抑制(阿尔伯特松等人,2007年)。我们为什么会过量摄入脂肪?能量密度高。胃肠道消化过程过快。饱腹感信号过弱。饥饿信号过强。