Body composition and endocrine status of long-term stress-induced binge-eating rats

被引:29
作者
Artiga, A. I. [1 ]
Viana, J. B. [1 ]
Maldonado, C. R. [1 ]
Chandler-Laney, P. C. [1 ]
Oswald, K. D. [1 ]
Boggiano, M. M. [1 ]
机构
[1] Univ Alabama, Behav Neurosci Div, Dept Psychol, Birmingham, AL 35294 USA
关键词
corticosterone; caloric restriction; hyperphagia; weight cycling; dieting; leptin; insulin; food restriction; bulimia; overeating; palatable food; body fat; lean mass; animal model; BULIMIA-NERVOSA; PALATABLE FOOD; DIETARY RESTRAINT; ANOREXIA-NERVOSA; OVERWEIGHT WOMEN; PLASMA LEPTIN; NORMAL-WEIGHT; ANIMAL-MODEL; FEMALE RATS; RESTRICTION;
D O I
10.1016/j.physbeh.2007.04.001
中图分类号
B84 [心理学];
学科分类号
04 ; 0402 ;
摘要
Clinical binge eating runs a protracted course. The etiology of binge eating remains perplexing in part because, in humans, it is difficult to isolate and assess the independent and aggregate impact of various contributing variables. Using rats, we found that footshock stress and a history of caloric restriction (S+R), combine synergistically to induce binge eating. Stress and dieting are also strong antecedents and relapse factors in human eating disorders. Here we report further behavioral and physiological parallels to human binge eating. Like the protracted course of human binge eating, young female Sprague-Dawley rats continued to binge eat after 23 restriction/stress cycles (7 months) and this despite experiencing no significant weight loss during the restriction phases. Stress alone reduced adiposity by 35% (p<0.001) but S+R rats had no significant fat loss. An endocrine profile of normal plasma leptin and insulin levels but marked elevation of plasma corticosterone levels was found only in the bingeeating (S+R) rats (p<0.01), also paralleling endocrine profiles reported in clinical binge-eating studies. These behavioral and physiological similarities between this animal model and clinical binge eating increase its utility in understanding binge eating. Importantly, our findings also highlight the stubborn nature of binge eating: once a critical experience with dieting and stress is experienced, little if any further weight loss or food restriction is necessary to sustain it. (C) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:424 / 431
页数:8
相关论文
共 42 条
[11]   STRESS-INDUCED EATING [J].
GREENO, CG ;
WING, RR .
PSYCHOLOGICAL BULLETIN, 1994, 115 (03) :444-464
[12]  
Hagan MM, 1997, INT J EAT DISORDER, V22, P411, DOI 10.1002/(SICI)1098-108X(199712)22:4<411::AID-EAT6>3.0.CO
[13]  
2-P
[14]   The role of palatable food and hunger as trigger factors in an animal model of stress induced binge eating [J].
Hagan, MM ;
Chandler, PC ;
Wauford, PK ;
Rybak, RJ ;
Oswald, KD .
INTERNATIONAL JOURNAL OF EATING DISORDERS, 2003, 34 (02) :183-197
[15]   Incidence of chaotic eating behaviors in binge-eating disorder: Contributing factors [J].
Hagan, MM ;
Shuman, ES ;
Oswald, KD ;
Corcoran, KJ ;
Profitt, JH ;
Blackburn, K ;
Schwiebert, MW ;
Chandler, PC ;
Birbaum, C .
BEHAVIORAL MEDICINE, 2002, 28 (03) :99-105
[16]   A new animal model of binge eating: Key synergistic role of past caloric restriction and stress [J].
Hagan, MM ;
Wauford, PK ;
Chandler, PC ;
Jarrett, LA ;
Rybak, RJ ;
Blackburn, K .
PHYSIOLOGY & BEHAVIOR, 2002, 77 (01) :45-54
[17]   Variations in maternal care influence vulnerability to stress-induced binge eating in female rats [J].
Hancock, SD ;
Menard, JL ;
Olmstead, MC .
PHYSIOLOGY & BEHAVIOR, 2005, 85 (04) :430-439
[18]   Relationship of plasma leptin to plasma insulin and adiposity in normal weight and overweight women: Effects of dietary fat content and sustained weight loss [J].
Havel, PJ ;
KasimKarakas, S ;
Mueller, W ;
Johnson, PR ;
Gingerich, RL ;
Stern, JS .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1996, 81 (12) :4406-4413
[19]   BINGE EATING AS ESCAPE FROM SELF-AWARENESS [J].
HEATHERTON, TF ;
BAUMEISTER, RF .
PSYCHOLOGICAL BULLETIN, 1991, 110 (01) :86-108
[20]   The rat arcuate nucleus integrates peripheral signals provided by leptin, insulin, and a ghrelin mimetic [J].
Hewson, AK ;
Tung, LYC ;
Connell, DW ;
Tookman, L ;
Dickson, SL .
DIABETES, 2002, 51 (12) :3412-3419