母亲西方饮食可能增加后代肥胖风险，即使肥胖抵抗男性后代
2016年12月1日，美国生理学会官方期刊《美国生理学杂志：调节、整合与比较生理学》正式发表斯克里普斯研究所、圣迭戈加利福尼亚大学、阿拉巴马大学伯明翰分校、新泽西东橙退伍军人事务医疗中心、罗格斯大学新泽西医学院的研究报告，发现怀孕时期的饮食构成可能影响后代是否肥胖。
该研究使用两种品系的大鼠，一种通过高脂饮食喂养容易肥胖，另一种对高脂饮食具有肥胖抵抗。每组大鼠喂食总脂肪、饱和脂肪、碳水化合物和蛋白质水平相同的饮食作为典型的西方饮食，同时喂养低脂肪高谷粒饮食作为对照。
结果发现，在怀孕前几周，怀孕期间和哺乳期给予西方饮食的雌性大鼠生产的后代在青春期早期以及成年后更容易出现肥胖。即使母亲本身保持健康的体重，身体脂肪和胰岛素状态，也会发生这种情况。
既往研究表明，超重的母亲更可能有超重的后代，新发现表明，饮食本身可以产生一个独立的体重增益的差异。西方饮食似乎启动了代谢程序，持续整个大鼠的生活。虽然这些大鼠在青春期和成年早期不胖，但他们仍然表现出较低的基础代谢率以及较高的食物摄取，导致成年中期的肥胖症恢复。
该研究还发现了西方饮食对肥胖易感和肥胖抵抗的影响的一个有趣的差异：饮食削弱肥胖易感线的繁殖能力。能够繁殖的雌鼠显著减少，并且那些繁殖的雌鼠具有更少的后代。
该研究还确定了几种分子，如胰岛素和激素，称为瘦素和脂联素，从出生起在西方饮食和遗传上易受伤害的后代水平升高。该激素谱可以用作检测肥胖风险的早期生物标志物。
研究结果提示，应该提高对健康的产前和产后饮食的重要性的认识，不仅仅是针对那些已经超重的女性。研究还表明，父亲的饮食，也可能通过控制基因如何表达的表观遗传机制，影响肥胖风险的后代。
下一步将研究西方饮食的哪些方面触发这些影响和负责后代的分子变化。
Am J Physiol Regul Integr Comp Physiol. 2016 Dec 1;311(6):R1045-R1059.
Maternal Western diet increases adiposity even in male offspring of obesity-resistant rat dams: early endocrine risk markers.
Frihauf JB, Fekete EM, Nagy TR, Levin BE, Zorrilla EP.
The Scripps Research Institute, La Jolla, California; University of California, San Diego, La Jolla, California; University of Alabama at Birmingham, Birmingham, Alabama; VA Medical Center, East Orange, New Jersey; Rutgers, New Jersey Medical School, Newark, New Jersey.
Maternal overnutrition or associated complications putatively mediate the obesogenic effects of perinatal high-fat diet on developing offspring. Here, we tested the hypothesis that a Western diet developmental environment increases adiposity not only in male offspring from obesity-prone (DIO) mothers, but also in those from obesity-resistant (DR) dams, implicating a deleterious role for the Western diet per se. Selectively bred DIO and DR female rats were fed chow (17% kcal fat) or Western diet (32%) for 54 days before mating and, thereafter, through weaning. As intended, despite chow-like caloric intake, Western diet increased prepregnancy weight gain and circulating leptin levels in DIO, but not DR, dams. Yet, in both genotypes, maternal Western diet increased the weight and adiposity of preweanlings, as early as in DR offspring, and increased plasma leptin, insulin, and adiponectin of weanlings. Although body weight normalized with chow feeding during adolescence, young adult Western diet offspring subsequently showed decreased energy expenditure and, in DR offspring, decreased lipid utilization as a fuel substrate. By mid-adulthood, maternal Western diet DR offspring ate more chow, weighed more, and were fatter than controls. Thus, maternal Western diet covertly programmed increased adiposity in childhood and adulthood, disrupted relations of energy regulatory hormones with body fat, and decreased energy expenditure in offspring of lean, genetically obesity-resistant mothers. Maternal Western diet exposure alone, without maternal obesity or overnutrition, can promote offspring weight gain.
KEYWORDS: diet-induced obesity; endocrine hormone; energy expenditure; environmental programming; heritable obesity
PMID: 27654396
DOI: 10.1152/ajpregu.00023.2016
