The weight gain response to stress during adulthood is conditioned by both sex and prenatal stress exposure.
Food intake and weight gain are known to be affected by stress. However, the type and duration of the stress may have variable effects, with males and females responding differently. We report the short-term and long-term effects of prenatal and adult immobilization stress, as well as the combination of these two stresses, on weight gain and food intake in male and female rats and the role of post-pubertal gonadal hormones in this process. No long-term effect of prenatal stress on food intake or weight gain was found in either sex. However, during the period of adult stress [at postnatal day (P) 90; 10 days duration] stressed male rats gained significantly less weight than controls and previous exposure to prenatal stress attenuated this effect (control: 31.2+/-2.1g; prenatal stress: 24.6+/-3.8g; adult stress: 8.1+/-3.4g; prenatal and adult stress: 18.2+/-3.3g; p<0.0001). There was no change in food intake in response to either prenatal or adult stress. Adult stress increased circulating corticosterone levels during the initial part of the stress period, in both male and female rats with this rise being greater in male rats. No effect on corticosterone levels was observed on the last day of stress in either sex. No effect on weight gain or food intake was observed in female rats. Following adult stress, male rats increased their weight gain, with no change in food intake, such that 1 month later they reached control levels. At the time of sacrifice (P180), there were no differences in weight or circulating metabolic hormone levels between any of the male groups. Although castration alone modulated body weight in both male and female rats, it did not affect their weight gain response to adult stress. These results indicate that the weight gain response to adult stress is sexually dimorphic and that this is not dependent on post-pubertal gonadal steroids. Furthermore, the outcome of this response closely depends on the time at which the change in weight is analyzed, which could help to explain different results reported in the literature. Indeed, weight and metabolic hormone levels were normalized by the end of the study.
García-Cáceres
Cristina
C
Hospital Infantil Universitario Niño Jesús, Universidad Autónoma de Madrid, CIBER Fisiopatología de Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, 28009 Madrid, Spain.
Diz-Chaves
Yolanda
Y
Lagunas
Natalia
N
Calmarza-Font
Isabel
I
Azcoitia
Iñigo
I
Garcia-Segura
Luis M
LM
Frago
Laura M
LM
Argente
Jesús
J
Chowen
Julie A
JA
D000367:Age Factors; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002369:Castration; D003345:Corticosterone / Q000097:blood; D004435:Eating / Q000502:physiology / Q000523:psychology; D005260:Female; D006728:Hormones / Q000097:blood; D008297:Male; D008550:Melatonin / Q000097:blood; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000097:blood / Q000503:physiopathology* / Q000523:psychology; D051381:Rats; D012737:Sex Factors; D012741:Sexual Maturation / Q000502:physiology; D013315:Stress, Psychological / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D015430:Weight Gain / Q000502:physiology*
D001786:Blood Glucose; D006728:Hormones; D008550:Melatonin; D003345:Corticosterone