PUFA modulate immune function and have been associated with the risk of childhood atopy and asthma. We investigated the effect of maternal fat intake in mice on PUFA status, elongase and desaturase gene expression, inflammatory markers and lung function in the offspring. C57BL/6J mice (n 32) were fed either standard chow (C, 20·4 % energy as fat) or a high-fat diet (HFD, 39·9 % energy as fat) for 4 weeks prior to conception and during gestation and lactation. At 21 d of age, offspring were weaned onto either the HFD or C, generating four experimental groups: C/C, C/HF, HF/C and HF/HF. Plasma and liver fatty acid composition were measured by GC and gene expression by quantitative PCR. Lung resistance to methacholine was assessed. Arachidonic acid concentrations in offspring plasma and liver phospholipids were increased by HFD; this effect was greater in the post-natal HFD group. DHA concentration in offspring liver phospholipids was increased in response to HFD and was higher in the post-natal HFD group. Post-natal HFD increased hepatic fatty acid desaturase (FADS) 2 and elongation of very long-chain fatty acid 5 expression in male offspring, whereas maternal HFD elevated expression of FADS1 and FADS2 in female offspring compared with males. Post-natal HFD increased expression of IL-6 and C-C motif chemokine ligand 2 (CCL2) in perivascular adipose tissue. The HFD lowered lung resistance to methacholine. Excessive maternal fat intake during development modifies hepatic PUFA status in offspring through regulation of gene expression of enzymes that are involved in PUFA biosynthesis and modifies the development of the offspring lungs leading to respiratory dysfunction.

中文翻译：

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小鼠的母体高脂肪饮食改变了后代的免疫调节和肺功能

PUFA 调节免疫功能，并与儿童特应性和哮喘的风险相关。我们研究了小鼠母体脂肪摄入对后代 PUFA 状态、延伸酶和去饱和酶基因表达、炎症标志物和肺功能的影响。C57BL/6J 小鼠 (n32) 在受孕前以及妊娠和哺乳期间喂食标准食物（C，20·4 % 能量作为脂肪）或高脂肪饮食（HFD，39·9 % 能量作为脂肪）4 周。在 21 天时，后代断奶到 HFD 或 C，产生四个实验组：C/C、C/HF、HF/C 和 HF/HF。通过GC测量血浆和肝脏脂肪酸组成，通过定量PCR测量基因表达。评估了对乙酰甲胆碱的肺抗性。HFD 会增加后代血浆和肝脏磷脂中的花生四烯酸浓度；这种影响在产后 HFD 组中更大。子代肝磷脂中的 DHA 浓度随着 HFD 的增加而增加，并且在出生后 HFD 组中更高。产后 HFD 增加肝脏脂肪酸去饱和酶 (时尚) 2 和超长链脂肪酸 5 在雄性后代中的表达延长，而母体 HFD 提高了FADS1和FADS2雌性后代与雄性相比。产后 HFD 表达增加IL-6和 CC 基序趋化因子配体 2 (CCL2) 在血管周围的脂肪组织中。HFD 降低了肺对乙酰甲胆碱的抵抗力。在发育过程中过多的母体脂肪摄入会通过调节参与 PUFA 生物合成的酶的基因表达来改变后代的肝脏 PUFA 状态，并改变后代肺部的发育，导致呼吸功能障碍。