Bautista C J, Montaño S, Ramirez V, Morales A, Nathanielsz P W, Bobadilla N A, Zambrano E
1Departamento de Biología de la Reproducción,Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán",Mexico City,14080,Mexico.
2Departamento de Nutrición Animal,Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán",Mexico City,14080Mexico.
Br J Nutr. 2016 Feb 14;115(3):538-46. doi: 10.1017/S0007114515004547. Epub 2015 Nov 26.
Maternal obesity programmes offspring development. We addressed maternal obesity effects induced by high-fat diets on maternal mammary gland (MG) structure and function and offspring brain, liver and fat outcomes. Mothers were fed control (C, n 5) or obesogenic (MO, n 5) diet from the time they were weaned through pregnancy beginning at 120 d, through lactation. At offspring postnatal day (PND) 20, milk leptin and nutrients were determined. At the end of lactation, maternal liver and MG fatty acid profile were measured. Desaturase (Δ6D and Δ5D) and elongase (ELOVL 5 and ELOVL 2) protein was measured by immunohistochemistry and Western blotting (WB) in the liver and WB in the MG. In mothers, liver, MG and milk fat content were higher in MO than in C. Liver arachidonic acid (AA) and EPA and MG EPA were lower in MO than in C. Liver desaturases were higher in MO. The MG was heavier in MO than in C, with decreased Δ5D expression in MO. Desaturases and elongases were immunolocalised in parenchymal cells of both groups. Milk yield, water, carbohydrate content, EPA and DHA were lower, whereas milk leptin and AA were higher in MO than in C. At PND 21 and 36, brain weight was less and fat depots were greater in MO offspring than in C. MO decreased male absolute brain weight but not female absolute brain weight. In conclusion, maternal obesity induced by an obesogenic diet negatively affects maternal liver and MG function with the production of significant changes in milk composition. Maternal obesity adversely affects offspring metabolism and development.
母体肥胖会影响子代发育。我们研究了高脂饮食诱导的母体肥胖对母体乳腺(MG)结构和功能以及子代脑、肝脏和脂肪的影响。从断奶后开始,母亲们在120天时开始接受对照饮食(C组,n = 5)或致肥胖饮食(MO组,n = 5),直至怀孕和哺乳期结束。在子代出生后第20天(PND 20),测定乳汁中的瘦素和营养成分。在哺乳期结束时,测量母体肝脏和MG的脂肪酸谱。通过免疫组织化学和Western印迹法(WB)测定肝脏中的去饱和酶(Δ6D和Δ5D)和延长酶(ELOVL 5和ELOVL 2)蛋白,并用WB法测定MG中的蛋白。在母亲中,MO组的肝脏、MG和乳脂含量高于C组。MO组肝脏中的花生四烯酸(AA)、二十碳五烯酸(EPA)和MG中的EPA低于C组。MO组肝脏中的去饱和酶较高。MO组的MG比C组更重,MO组中Δ5D的表达降低。两组实质细胞中均有去饱和酶和延长酶的免疫定位。MO组的产奶量、水分、碳水化合物含量、EPA和DHA较低,而乳汁中的瘦素和AA较高。在PND 21和36时,MO组子代的脑重量较轻,脂肪储存量比C组更大。MO降低了雄性子代的绝对脑重量,但未降低雌性子代的绝对脑重量。总之,致肥胖饮食诱导的母体肥胖会对母体肝脏和MG功能产生负面影响,并导致乳汁成分发生显著变化。母体肥胖会对后代的代谢和发育产生不利影响。