Tsuduki Tsuyoshi, Yamamoto Kazushi, E Shuang, Hatakeyama Yu, Sakamoto Yu
Laboratory of Food and Biomolecular Science, Graduate School of Agriculture, Tohoku University, Sendai 981-8555, Japan.
Nutrients. 2015 Jul 17;7(7):5916-32. doi: 10.3390/nu7075257.
This study examined how a maternal high-fat diet (HD) during lactation and exposure of offspring to isolation stress influence the susceptibility of offspring to the development of obesity. C57BL/6J mice were fed a commercial diet (CD) during pregnancy and a CD or HD during lactation. Male offspring were weaned at three weeks of age, fed a CD until seven weeks of age, and fed a CD or HD until 11 weeks of age. Offspring were housed alone (isolation stress) or at six per cage (ordinary circumstances). Thus, offspring were assigned to one of eight groups: dams fed a CD or HD during lactation and offspring fed a CD or HD and housed under ordinary circumstances or isolation stress. Serum corticosterone level was significantly elevated by isolation stress. High-fat feeding of offspring reduced their serum corticosterone level, which was significantly elevated by a maternal HD. A maternal HD and isolation stress had combined effects in elevating the serum corticosterone level. These findings suggest that a maternal HD during lactation enhances the stress sensitivity of offspring. White adipose tissue weights were significantly increased by a maternal HD and isolation stress and by their combination. In addition, significant adipocyte hypertrophy was induced by a maternal HD and isolation stress and exacerbated by their combination. Thus, a maternal HD and isolation stress promote visceral fat accumulation and adipocyte hypertrophy, accelerating the progression of obesity through their combined effects. The mechanism may involve enhanced fatty acid synthesis and lipid influx from blood into adipose tissue. These findings demonstrate that a maternal HD during lactation may increase the susceptibility of offspring to the development of stress-induced obesity.
本研究考察了哺乳期母体高脂饮食(HD)以及子代暴露于隔离应激如何影响子代肥胖发生的易感性。C57BL/6J小鼠在孕期喂食普通饮食(CD),在哺乳期喂食CD或HD。雄性子代在3周龄时断奶,7周龄前喂食CD,11周龄前喂食CD或HD。子代单独饲养(隔离应激)或每笼饲养6只(正常情况)。因此,子代被分为八组之一:哺乳期母鼠喂食CD或HD,子代喂食CD或HD,并饲养于正常情况或隔离应激条件下。隔离应激显著提高了血清皮质酮水平。子代高脂喂养降低了其血清皮质酮水平,而母体HD则使其显著升高。母体HD和隔离应激对血清皮质酮水平有联合升高作用。这些发现表明,哺乳期母体HD增强了子代的应激敏感性。母体HD、隔离应激及其联合作用均显著增加了白色脂肪组织重量。此外,母体HD和隔离应激均诱导了显著的脂肪细胞肥大,二者联合作用使其加剧。因此,母体HD和隔离应激通过联合作用促进内脏脂肪堆积和脂肪细胞肥大,加速肥胖进程。其机制可能涉及脂肪酸合成增强以及脂质从血液流入脂肪组织。这些发现表明,哺乳期母体HD可能增加子代发生应激诱导性肥胖的易感性。