Department of Genetics, Texas Biomedical Research Institute, San Antonio, TX 78245-0549, USA.
Am J Primatol. 2013 May;75(5):491-9. doi: 10.1002/ajp.22125. Epub 2013 Jan 11.
Nutrient composition of a diet (D) has been shown to interact with genetic predispositions (G) to affect various lipid phenotypes. Our aim in this study was to confirm G × D interaction and determine whether the interaction extends to other cardiometabolic risk factors such as glycemic measures and body weight. Subjects were vervet monkeys (Chlorocebus aethiops sabaeus; n = 309) from a multigenerational pedigreed colony initially fed with a plant-based diet, standard primate diet (18% calories from protein, 13% from fat, and 69% from carbohydrates), and subsequently challenged for 8 weeks with a diet modeled on the typical American diet (18% calories from protein, 35% from fat, and 47% from carbohydrates). Our results showed that although exposure to the challenge diet did not result in significant changes in weight, most lipid and glycemic biomarkers moved in an adverse direction (P < 0.01). Quantitative genetic analyses showed that cardiometabolic phenotypes were significantly heritable under both dietary conditions (P < 0.05), and there was significant evidence of G × D interaction for these phenotypes. We observed significant differences in the additive genetic variances for most lipid phenotypes (P < 10(-4) ), indicating that the magnitude of genetic effects varies by diet. Furthermore, genetic correlations between diets differed significantly from 1 with respect to insulin, body weight, and some lipid phenotypes (P < 0.01). This implied that distinct genetic effects are involved in the regulation of these phenotypes under the two dietary conditions. These G × D effects confirm and extend previous observations in baboons (Papio sp.) and suggest that mimicking the typical human nutritional environment can reveal genetic influences that might not be observed in animals consuming standard, plant-based diets.
饮食的营养成分(D)已被证明与遗传易感性(G)相互作用,从而影响各种脂质表型。我们的研究目的是确认 G×D 相互作用,并确定这种相互作用是否扩展到其他心血管代谢风险因素,如血糖测量和体重。研究对象是来自一个多代血统的丛猴(Chlorocebus aethiops sabaeus;n=309),最初以植物性饮食、标准灵长类饮食(18%的热量来自蛋白质,13%来自脂肪,69%来自碳水化合物)喂养,随后用类似于典型美国饮食的饮食(18%的热量来自蛋白质,35%来自脂肪,47%来自碳水化合物)喂养 8 周。我们的结果表明,尽管暴露于挑战饮食并没有导致体重的显著变化,但大多数脂质和血糖生物标志物都朝着不利的方向发展(P<0.01)。定量遗传分析表明,在两种饮食条件下,心血管代谢表型都具有显著的遗传可遗传性(P<0.05),并且这些表型存在显著的 G×D 相互作用证据。我们观察到大多数脂质表型的加性遗传方差有显著差异(P<10(-4)),这表明遗传效应的大小因饮食而异。此外,两种饮食之间的遗传相关性在胰岛素、体重和一些脂质表型方面显著不同于 1(P<0.01)。这意味着在两种饮食条件下,这些表型的调节涉及不同的遗传效应。这些 G×D 效应证实并扩展了之前在狒狒(Papio sp.)中的观察结果,并表明模拟典型的人类营养环境可以揭示在食用标准植物性饮食的动物中可能观察不到的遗传影响。