Giblin Linda, Darimont Christian, Leone Patricia, McNamara Louise B, Blancher Florence, Berry Donagh, Castañeda-Gutiérrez Eurídice, Lawlor Peadar G
Teagasc Food Research Centre, Moorepark, Fermoy, Co.Cork, Ireland.
Nestlé Research Centre, Nutrition & Health Research Department, Vers-Chez-les-Blanc, Lausanne, Switzerland.
Reprod Biol Endocrinol. 2015 Mar 8;13:16. doi: 10.1186/s12958-015-0009-0.
Excessive maternal weight gain during pregnancy impacts on offspring health. This study focused on the timing of maternal gestational weight gain, using a porcine model with mothers of normal pre-pregnancy weight.
Trial design ensured the trajectory of maternal gestational weight gain differed across treatments in early, mid and late gestation. Diet composition did not differ. On day 25 gestation, sows were assigned to one of five treatments: Control sows received a standard gestation diet of 2.3 kg/day (30 MJ DE/day) from early to late gestation (day 25-110 gestation). E sows received 4.6 kg food/day in early gestation (day 25-50 gestation). M sows doubled their food intake in mid gestation (day 50-80 gestation). EM sows doubled their food intake during both early and mid gestation (day 25-80 gestation). L sows consumed 3.5 kg food/day in late gestation (day 80-110 gestation). Offspring body weight and food intake levels were measured from birth to adolescence. Markers of lipid metabolism, hypertrophy and inflammation were investigated in subcutaneous adipose tissue of adolescent offspring.
The trajectory of gestational weight gain differed across treatments. However total gestational weight gain did not differ except for EM sows who were the heaviest and fattest mothers at parturition. Offspring birth weight did not differ across treatments. Subcutaneous adipose tissue from EM offspring differed significantly from controls, with elevated mRNA levels of lipogenic (CD36, ACACB and LPL), nutrient transporters (FABP4 and GLUT4), lipolysis (HSL and ATGL), adipocyte size (MEST) and inflammation (PAI-1) indicators. The subcutaneous adipose depot from L offspring exhibited elevated levels of CD36, ACACB, LPL, GLUT4 and FABP4 mRNA transcripts compared to control offspring.
Increasing gestational weight gain in early gestation had the greatest impact on offspring postnatal growth rate. Increasing maternal food allowance in late gestation appeared to shift the offspring adipocyte focus towards accumulation of fat. Mothers who gained the most weight during gestation (EM mothers) gave birth to offspring whose subcutaneous adipose tissue, at adolescence, appeared hyperactive compared to controls. This study concluded that mothers, who gained more than the recommended weight gain in mid and late gestation, put their offspring adipose tissue at risk of dysfunction.
孕期母亲体重过度增加会影响后代健康。本研究以孕前体重正常的母猪为模型，重点关注母亲孕期体重增加的时间点。
试验设计确保了母亲孕期体重增加的轨迹在妊娠早期、中期和晚期的各处理组之间存在差异。饮食组成无差异。在妊娠第25天，母猪被分配到五种处理组之一：对照组母猪从妊娠早期到晚期（妊娠第25 - 110天）每天接受2.3千克标准妊娠日粮（30兆焦消化能/天）。E组母猪在妊娠早期（妊娠第25 - 50天）每天摄入4.6千克食物。M组母猪在妊娠中期（妊娠第50 - 80天）食物摄入量翻倍。EM组母猪在妊娠早期和中期（妊娠第25 - 80天）食物摄入量均翻倍。L组母猪在妊娠晚期（妊娠第80 - 110天）每天消耗3.5千克食物。测量后代从出生到青春期的体重和食物摄入量水平。在青春期后代的皮下脂肪组织中研究脂质代谢、肥大和炎症的标志物。
妊娠体重增加的轨迹在各处理组之间存在差异。然而，除了EM组母猪在分娩时是最重且最胖的母亲外，总妊娠体重增加并无差异。各处理组后代的出生体重无差异。EM组后代的皮下脂肪组织与对照组有显著差异，其脂肪生成（CD36、ACACB和LPL）、营养转运蛋白（FABP4和GLUT4）、脂肪分解（HSL和ATGL）、脂肪细胞大小（MEST）和炎症（PAI - 1）指标的mRNA水平升高。与对照后代相比，L组后代的皮下脂肪库中CD36、ACACB、LPL、GLUT4和FABP4 mRNA转录本水平升高。
妊娠早期体重增加对后代出生后的生长速度影响最大。妊娠晚期增加母亲的食物供应量似乎使后代脂肪细胞的关注点转向脂肪积累。在孕期体重增加最多的母亲（EM组母亲）所生的后代，在青春期时其皮下脂肪组织与对照组相比显得过度活跃。本研究得出结论，在妊娠中期和晚期体重增加超过推荐量的母亲，会使后代的脂肪组织有功能障碍的风险。
