Background

Bisphenol A (BPA) is an endocrine disruptor and also a suggested obesogen and metabolism-disrupting chemical. Accumulating data indicates that the fatty acid (FA) profile and their ratios in plasma and other metabolic tissues are associated with metabolic disorders. Stearoyl-CoA desaturase 1 (SCD-1) is a key regulator of lipid metabolism and its activity can be estimated by dividing the FA product by its precursor measured in blood or other tissues.

Objective

The primary aim of this study was to investigate the effect of low-dose developmental BPA exposure on tissue-specific FA composition including estimated SCD-1 activity, studied in 5- and 52-week (wk)-old Fischer 344 (F344) rat offspring.

Methods

Pregnant F344 rats were exposed to BPA via their drinking water corresponding to 0: [CTRL], 0.5: [BPA0.5], or 50 µg/kg BW/day: [BPA50], from gestational day 3.5 until postnatal day 22.

Results

BPA0.5 increased SCD-16 (estimated as the 16:1n-7/16:0 ratio) and SCD-18 (estimated as the 18:1n-9/18:0 ratio) indices in inguinal white adipose tissue triglycerides (iWAT-TG) and in plasma cholesterol esters (PL-CE), respectively, in 5-wk-old male offspring. In addition, BPA0.5 altered the FA composition in male offspring, e.g. by decreasing levels of the essential polyunsaturated FA linoleic acid (18:2n-6) in iWAT-and liver-TG. No differences were observed regarding the studied FAs in 52-wk-old offspring, although a slightly increased BW was observed in 52-wk-old female offspring.

Conclusions

Low-dose developmental BPA exposure increased SCD-16 in iWAT-TG and SCD-18 in PL-CE of male offspring, which may reflect higher SCD-1 activity in these tissues. Altered desaturation activity and signs of altered FA composition are novel findings that may indicate insulin resistance in the rat offspring. These aforementioned results, together with the observed increased BW, adds to previously published data demonstrating that BPA can act as a metabolism disrupting chemical.

中文翻译：

---

低剂量发育双酚A暴露会改变Fischer 344大鼠后代的脂肪酸代谢

背景

双酚A（BPA）是一种内分泌干扰物，也是建议的促肥胖和破坏代谢的化学物质。越来越多的数据表明，血浆和其他代谢组织中的脂肪酸（FA）谱及其比例与代谢异常有关。硬脂酰辅酶A去饱和酶1（SCD-1）是脂质代谢的关键调节剂，其活性可以通过将FA产物除以在血液或其他组织中测得的FA产物来估算。

客观的

这项研究的主要目的是研究低剂量发育BPA暴露对组织特异性FA组成的影响，包括估计的SCD-1活性，在5周和52周（周）的Fischer 344（F344）大鼠中进行了研究后代。

方法

从妊娠第3.5天到出生后第22天，怀孕的F344大鼠通过其饮用水分别暴露于BPA ：0：[CTRL]，0.5：[BPA0.5]或50 µg / kg BW /天：[BPA50]。

结果

BPA0.5增加了腹股沟白色脂肪组织甘油三酸酯（iWAT）的SCD-16（估计为16：1n-7 / 16：0比率）和SCD-18（估计为18：1n-9 / 18：0比率）指数。 -TG）和5周龄雄性后代的血浆胆固醇酯（PL-CE）中。另外，BPA0.5改变了雄性后代的FA组成，例如通过降低iWAT和肝脏TG中必需的多不饱和FA亚油酸（18：2n-6）的水平。尽管在52周龄的雌性后代中观察到BW略有增加，但对于52周龄的后代中所研究的FA并未观察到差异。

结论

低剂量发育性BPA暴露会增加雄性后代的iWAT-TG中的SCD-16和PL-CE中的SCD-18，这可能反映了这些组织中更高的SCD-1活性。改变的去饱和活性和改变的FA组成的迹象是新发现，可能表明大鼠后代中的胰岛素抵抗。这些前述结果，加上观察到的体重增加，增加了先前发表的数据，证明了BPA可以充当破坏代谢的化学物质。