Institute of Nutrition Josué de Castro, Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Institute of Nutrition Josué de Castro, Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Nutrition. 2019 Nov-Dec;67-68:110547. doi: 10.1016/j.nut.2019.06.027. Epub 2019 Jul 2.
Obesity is a multifactorial, complex, and public health problem worldwide. Interaction between genes and environment as associated with diet may predispose an individual to obesity. In this sense, nutrigenetics appears to be a strategy that can improve understanding of the gene-diet interaction. The aim of this literature review was to summarize data from studies of genes involved in the regulation of energy intake (melanocortin 4 receptor [MC4R], fat mass and obesity-associated [FTO], ghrelin [GHRL], leptin [LEP], and cholecystokinin [CCK]) and diet interaction in obesity. The presence of polymorphisms in MC4R, FTO, leptin, and the respective receptor appear to be associated with higher energy and total lipid consumption. Polymorphisms in FTO, leptin, and leptin receptor are also related to increased intake of saturated fatty acids. Individuals with the MC4R, FTO, and ghrelin polymorphisms, who submitted themselves for weight loss intervention, appeared to achieve weight loss similar to individuals without polymorphisms in these genes. Additionally, protein seems to interact with these genes, which increases or decreases appetite, or to drive or lessen body weight recovery. Additionally, polymorphisms in these genes were found to be associated with inappropriate eating behaviors, such as increased consumption of sweets and snacks, consumption of large food portions, desire to eat, and eating associated with emotional issues. Preliminary data has supported the gene-diet interaction in determining weight loss and gain in individuals with polymorphisms in the genes involved in energy intake. Despite the advent of nutrigenetics in obesity, it is still too early to define the dietary management for weight loss based on the presence or absence of obesity polymorphisms.
肥胖是一个多因素、复杂的全球性公共健康问题。基因与环境的相互作用与饮食有关，可能使个体易患肥胖症。在这个意义上，营养遗传学似乎是一种可以增进对基因-饮食相互作用理解的策略。本文综述的目的是总结参与能量摄入调节的基因（黑皮质素 4 受体 [MC4R]、脂肪量和肥胖相关 [FTO]、生长激素释放肽 [GHRL]、瘦素 [LEP]和胆囊收缩素 [CCK]）以及肥胖症中饮食相互作用的研究数据。MC4R、FTO、瘦素和相应受体中的基因多态性的存在似乎与更高的能量和总脂质消耗有关。FTO、瘦素和瘦素受体的基因多态性也与饱和脂肪酸摄入量增加有关。接受减肥干预的 MC4R、FTO 和生长激素释放肽基因多态性个体似乎与这些基因中无多态性的个体体重减轻相似。此外，蛋白质似乎与这些基因相互作用，增加或减少食欲，或驱动或减轻体重恢复。此外，这些基因的多态性与不适当的饮食行为有关，如甜食和零食摄入量增加、大量食物摄入、食欲和与情绪问题相关的进食。初步数据支持基因-饮食相互作用在决定具有能量摄入相关基因多态性个体的体重减轻和增加方面的作用。尽管营养遗传学在肥胖症中的应用已经出现，但根据肥胖症多态性的存在与否来确定减肥的饮食管理还为时过早。
