Liggins Institute, University of Auckland, Auckland, New Zealand.
Sci Rep. 2017 Jul 27;7(1):6663. doi: 10.1038/s41598-017-07108-9.
The developmental origins of health and disease hypothesis proposes that an adverse early life environment, including in utero exposure to a maternal obesogenic environment, can lead to an increased long-term risk of obesity and related metabolic complications in offspring. We assessed whether maternal supplementation with conjugated linoleic acid (CLA) could prevent some of these adverse effects in offspring exposed to a maternal high fat diet. Sprague-Dawley dams consumed either a: control (CD), control with CLA (CLA), high fat (HF) or high fat with CLA (HFCLA) diet 10 days prior to mating and throughout pregnancy/lactation. Male offspring were weaned onto a standard chow diet. Body composition was quantified by DXA and oral glucose tolerance tests conducted on adult offspring. Gene/protein expression and histological analysis were conducted in adipose tissue. Offspring from HF dams had increased body weight, body fat deposition, impaired insulin sensitivity and adipocyte hypertrophy; all of which were rescued in HFCLA offspring. Molecular and histological analyses of the adipose tissue suggest that disturbances in adipogenesis may mediate the metabolic dysfunction observed in HF offspring. Therefore, CLA supplementation to a maternal obesogenic diet may be a promising strategy to prevent adverse programming outcomes.
健康与疾病的起源假说提出，不良的早期生活环境，包括胎儿期暴露于母体肥胖环境，会导致后代肥胖和相关代谢并发症的长期风险增加。我们评估了母体补充共轭亚油酸（CLA）是否可以预防暴露于高脂肪饮食的后代的一些这些不利影响。在交配前 10 天和整个怀孕期间/哺乳期，Sprague-Dawley 母鼠分别摄入：对照（CD）、CLA 对照（CLA）、高脂肪（HF）或高脂肪加 CLA（HFCLA）饮食。雄性后代断奶后接受标准饲料。通过 DXA 定量分析体成分，并对成年后代进行口服葡萄糖耐量试验。在脂肪组织中进行基因/蛋白质表达和组织学分析。高脂肪组母鼠的后代体重增加、体脂肪沉积增加、胰岛素敏感性受损和脂肪细胞肥大；所有这些都在高脂肪加 CLA 组的后代中得到了挽救。脂肪组织的分子和组织学分析表明，脂肪生成的紊乱可能介导了在高脂肪组后代中观察到的代谢功能障碍。因此，CLA 补充到母体肥胖饮食中可能是预防不良编程结果的一种有前途的策略。
