Department of Psychology, Michigan State University, East Lansing, MI 48824-1116, USA.
J Abnorm Psychol. 2011 Nov;120(4):948-55. doi: 10.1037/a0023600. Epub 2011 May 16.
Puberty is a critical risk period for binge eating and eating disorders characterized by binge eating. Previous research focused almost entirely on psychosocial risk factors during puberty to the relative exclusion of biological influences. The current study addressed this gap by examining the emergence of binge eating during puberty in a rat model. We predicted that there would be minimal differences in binge eating proneness during pre-early puberty, but significant differences would emerge during puberty. Two independent samples of female Sprague-Dawley rats (n = 30 and n = 36) were followed longitudinally across pre-early puberty, mid-late puberty, and adulthood. Binge eating proneness was defined using the binge eating resistant (BER)/binge eating prone (BEP) model of binge eating that identifies BER and BEP rats in adulthood. Across two samples of rats, binge eating proneness emerged during puberty. Mixed linear models showed little difference in palatable food intake between BER and BEP rats during pre-early puberty, but significant group differences emerged during mid-late puberty and adulthood. Group differences could not be accounted for by changes in nonpalatable food intake or body weight. Similar to patterns in humans, individual differences in binge eating emerge during puberty in female rats. These findings provide strong confirming evidence for the importance of biological risk factors in developmental trajectories of binge eating risk across adolescence.
青春期是暴食和暴食障碍的关键风险期,暴食是其特征之一。以前的研究几乎完全关注青春期的心理社会风险因素,而相对忽视了生物学的影响。本研究通过在大鼠模型中检查青春期期间暴食的出现来弥补这一空白。我们预测,在早期青春期前,暴食倾向差异极小,但在青春期会出现显著差异。两个独立的雌性 Sprague-Dawley 大鼠样本(n = 30 和 n = 36)在早期青春期、中晚期青春期和成年期进行了纵向跟踪。使用暴食抵抗(BER)/暴食倾向(BEP)的暴食模型来定义暴食倾向,该模型可在成年期识别出 BER 和 BEP 大鼠。在两个大鼠样本中,暴食倾向在青春期出现。混合线性模型显示,在早期青春期,BER 和 BEP 大鼠之间在美味食物摄入量上差异不大,但在中晚期青春期和成年期出现了显著的组间差异。体重或非美味食物摄入量的变化无法解释组间差异。与人类的模式相似,女性大鼠在青春期出现暴食的个体差异。这些发现为青春期暴食风险的发展轨迹中生物学风险因素的重要性提供了强有力的确认证据。