Muhlhausler Beverly Sara, Miljkovic Dijana, Fong Laura, Xian Cory J, Duthoit Emmanuelle, Gibson Robert A
School of Agriculture Food and Wine, FOODplus Research Centre, The University of Adelaide Adelaide, SA, Australia.
Front Genet. 2011 Jul 21;2:48. doi: 10.3389/fgene.2011.00048. eCollection 2011.
Adipogenesis and lipogenesis are highly sensitive to the nutritional environment in utero and in early postnatal life. Omega-3 long chain polyunsaturated fatty acids (LCPUFA) inhibit adipogenesis and lipogenesis in adult rats, however it is not known whether supplementing the maternal diet with omega-3 LCPUFA results in reduced fat deposition in the offspring. Female Albino Wistar rats were fed either a standard chow (Control, n = 10) or chow designed to provide ∼15 mg/kg/day of omega-3 LCPUFA, chiefly as docosahexaenoic acid (DHA), throughout pregnancy and lactation (Omega-3, n = 11) and all pups were weaned onto a commercial rat chow. Blood and tissues were collected from pups at 3 and 6 weeks of age and weights of visceral and subcutaneous fat depots recorded. The expression of adipogenic and lipogenic genes in the subcutaneous and visceral fat depots were determined using quantitative real time reverse transcription-PCR. Birth weight and postnatal growth were not different between groups. At 6 weeks of age, total percentage body fat was significantly increased in both male (5.09 ± 0.32% vs. 4.56 ± 0.2%, P < 0.04) and female (5.15 ± 0.37% vs. 3.89 ± 0.36%, P < 0.04) offspring of omega-3 dams compared to controls. The omega-3 LCPUFA content of erythrocyte phospholipids (as a% of total fatty acids) was higher in omega-3 offspring (6.7 ± 0.2% vs. 5.6 ± 0.2%, P < 0.001). There was no effect of maternal omega-3 LCPUFA supplementation on the expression of adipogenic or lipogenic genes in the offspring in either the visceral or subcutaneous fat depots. We have therefore established that an omega-3 rich environment during pregnancy and lactation in a rodent model increases fat accumulation in both male and female offspring, particularly in subcutaneous depots, but that this effect is not mediated via upregulation adipogenic/lipogenic gene transcription. These data suggest that maternal n-3 LCPUFA supplementation during pregnancy/lactation may not be an effective strategy for reducing fat deposition in the offspring.
脂肪生成和脂质生成对子宫内及出生后早期的营养环境高度敏感。ω-3长链多不饱和脂肪酸（LCPUFA）可抑制成年大鼠的脂肪生成和脂质生成，然而，孕期母体饮食补充ω-3 LCPUFA是否会减少后代的脂肪沉积尚不清楚。雌性白化Wistar大鼠在整个孕期和哺乳期分别喂食标准饲料（对照组，n = 10）或旨在提供约15 mg/kg/天ω-3 LCPUFA（主要为二十二碳六烯酸，DHA）的饲料（ω-3组，n = 11），所有幼崽断奶后喂食市售大鼠饲料。在幼崽3周和6周龄时采集血液和组织，记录内脏和皮下脂肪库的重量。使用定量实时逆转录PCR测定皮下和内脏脂肪库中脂肪生成和脂质生成基因的表达。各组间出生体重和出生后生长情况无差异。在6周龄时，与对照组相比，ω-3组母鼠的雄性（5.09±0.32%对4.56±0.2%，P < 0.04）和雌性（5.15±0.37%对3.89±0.36%，P < 0.04）后代的总体脂百分比显著增加。ω-3组后代红细胞磷脂中的ω-3 LCPUFA含量（占总脂肪酸的百分比）更高（6.7±0.2%对5.6±0.2%，P < 0.001）。孕期母体补充ω-3 LCPUFA对后代内脏或皮下脂肪库中脂肪生成或脂质生成基因的表达没有影响。因此，我们确定，在啮齿动物模型中，孕期和哺乳期富含ω-3的环境会增加雄性和雌性后代的脂肪积累，尤其是皮下脂肪库，但这种影响并非通过上调脂肪生成/脂质生成基因转录介导。这些数据表明，孕期/哺乳期母体补充n-3 LCPUFA可能不是减少后代脂肪沉积的有效策略。
