Bieswal Florence, Ahn Marie-Thérèse, Reusens Brigitte, Holvoet Paul, Raes Martine, Rees William D, Remacle Claude
Laboratory of Cell Biology, University of Louvain, Louvain-la-Neuve, Belgium.
Obesity (Silver Spring). 2006 Aug;14(8):1330-43. doi: 10.1038/oby.2006.151.
To investigate whether catch-up growth after maternal malnutrition would favor the development of obesity in adulthood.
Pregnant rats were submitted to protein or calorie restriction during the course of gestation. During lactation, pups were protein-restricted, normally fed, or overfed [reduced litter size, control (C) diet]. At weaning, rats were transferred to chow or to a hypercaloric diet (HCD) known to induce obesity. Body weight, food intake, blood parameters, glucose tolerance, adipocyte cellularity, and adipose factors contributing to cardiovascular disease development were measured.
Protein and calorie restriction during gestation led to growth retardation at birth. If malnutrition was prolonged throughout lactation, adult body weight was permanently reduced. However, growth-retarded offspring overfed during the suckling period underwent a rapid catch-up growth and became heavier than the normally fed Cs. Offspring of calorie-restricted rats gained more weight than those of dams fed protein-restricted diet. Feeding an HCD postnatally amplified the effect of calorie restriction, and offspring that underwent catch-up growth became more obese than Cs. The HCD was associated with hyperphagia, hyperglycemia, hyperinsulinemia, glucose intolerance, insulin resistance, and adipocyte hypertrophy. The magnitude of effects varied depending on the type and the timing of early malnutrition. The expression of genes encoding factors implicated in cardiovascular disease was also modulated differently by early malnutrition and adult obesity.
Catch-up growth immediately after early malnutrition should be a key point for the programming of obesity.
研究母体营养不良后的追赶生长是否会促进成年期肥胖的发展。
在妊娠期间，对怀孕大鼠进行蛋白质或热量限制。在哺乳期，幼崽被限制蛋白质摄入、正常喂养或过度喂养[减少窝仔数，对照（C）饮食]。断奶时，将大鼠转移到普通饲料或已知会诱导肥胖的高热量饮食（HCD）中。测量体重、食物摄入量、血液参数、葡萄糖耐量、脂肪细胞数量以及有助于心血管疾病发展的脂肪因子。
妊娠期间的蛋白质和热量限制导致出生时生长迟缓。如果在整个哺乳期持续营养不良，成年体重会永久性降低。然而，在哺乳期过度喂养的生长迟缓后代经历了快速的追赶生长，并且比正常喂养的对照组更重。热量限制组大鼠的后代比蛋白质限制饮食组母鼠的后代体重增加更多。产后喂养HCD放大了热量限制的影响，经历追赶生长的后代比对照组更肥胖。HCD与食欲亢进、高血糖、高胰岛素血症、葡萄糖耐量异常、胰岛素抵抗和脂肪细胞肥大有关。影响的程度因早期营养不良的类型和时间而异。早期营养不良和成年肥胖对参与心血管疾病的相关因子编码基因的表达也有不同的调节作用。
早期营养不良后立即出现的追赶生长应该是肥胖编程的一个关键点。
