Effects of ovariectomy, estrogen treatment and CI-628 on food intake and body weight in female rats treated neonatally with gonadal hormones

Donohoe, Thomas P.; Stevens, Robin

doi:10.1016/0031-9384(83)90196-8

Cited by 26 publications

(14 citation statements)

References 26 publications

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“…Animal studies allow for experimental manipulation of prenatal testosterone levels, and results show that increasing levels of prenatal testosterone in female rat fetuses leads to masculinized eating patterns in adulthood; including reduced meal number but increased meal size (Madrid et al, 1993; Wade, 1972), and increased weight (Demissie et al, 2008; Donohoe and Stevens, 1983). This effect is not observed when administering testosterone to male rodents prenatally (Wade, 1972), which is interesting as our findings only show significant associations in females when analyzing each gender individually.…”

Section: Discussionmentioning

confidence: 99%

2D:4D Ratio in children at familial high‐risk for eating disorders: The role of prenatal testosterone exposure

Kothari¹,

Gafton

Treasure³

et al. 2013

American J Hum Biol

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ObjectivesMarkers of prenatal hormone exposure have been associated with the development of eating disorder (ED) behaviors. Our aim was to determine whether 2D:4D ratio, a marker for in utero testosterone exposure, is associated with risk for ED in a large population-based cohort: the Avon Longitudinal Study of Parents and Children (ALSPAC).MethodsThis is the first study to investigate prenatal testosterone exposure in children at high-risk for ED, using 2D:4D as a marker. We compared children whose mothers reported a lifetime ED (anorexia, bulimia, or both; N = 446) to children whose mothers did not (n = 5,367).ResultsDaughters of women with lifetime bulimia nervosa (BN) had lower 2D:4D ratio (B: −0.01, 95% CI: −0.02 to −0.002, P = 0.02), indicating higher prenatal testosterone exposure, than daughters of mothers unaffected by ED. No differences were observed in the male children of women with an ED.ConclusionsFindings suggest that children at high-risk for BN may be exposed to higher levels of testosterone in utero. Fetal exposure to androgen excess is thought to be causal in the development of polycystic ovary syndrome (PCOS), a disorder which is highly comorbid with binge eating and BN. Future research should investigate the potential role of testosterone exposure in utero as a risk factor for BN and binge eating. Am. J. Hum. Biol. 26:176–182, 2014. © 2013 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

2D:4D Ratio in children at familial high‐risk for eating disorders: The role of prenatal testosterone exposure

Kothari¹,

Gafton

Treasure³

et al. 2013

American J Hum Biol

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“…Previous studies 6,7 have demonstrated that ovariectomy stimulates food intake, and estradiol replacement inhibits the effect. On the other hand, estrogen is reported to regulate the growth of fat and fat-free tissues, possibly by affecting protein synthesis 8,9 and energy expenditure.…”

Section: Introductionmentioning

confidence: 97%

Estrogen receptor ß is involved in the anorectic action of estrogen

Akishita

et al. 2002

Int J Obes

144

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OBJECTIVE: Estrogen has been implicated in feeding behavior and adiposity. This study was undertaken to elucidate the mechanism underlying the anti-obesity and anorectic action of estrogen and the role of estrogen receptor (ER) in the central nervous system. METHODS AND RESULTS: Ovariectomy in 8-week-old female Wistar rats induced hyperphagia along with an increase in body weight and abdominal fat accumulation compared to control sham-operated rats. These changes were fully reversed by subcutaneous replacement of estradiol and were abrogated by pair-feeding. Then, the effects of intracerebroventricular infusion of estradiol, alone or in combination with antisense oligodeoxynucleotides (ODN), for ER in ovariectomized rats were examined. The estradiol group showed 10 -20% lower daily food intake, and after the 2-week infusion period a 14% reduction in body weight with a similar reduction in abdominal fat compared to the vehicle group. The inhibitory effect of estradiol on food intake and body weight was blocked by co-administration of ER-ß antisense ODN, whereas ER-a antisense ODN did not show any influence. CONCLUSION: These results indicate that ER-ß in the central nervous system is involved in the anorectic action of estrogen.

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“…Estradiol has been shown to have anorexic effects when given in the same time frame as the current experiments [29, 35, 36]. Body weight changes are expressed as a percentage of original body weight for each animal.…”

Section: Methodsmentioning

confidence: 99%

Estrogen Increases Angiotensin II-Induced c-Fos Expression in the Vasopressinergic Neurons of the Paraventricular Nucleus in the Female Rat

Kisley¹,

Sakai

Flanagan‐Cato

et al. 2000

Neuroendocrinology

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Previous studies in female rats have shown that estrogen treatment attenuates angiotensin II (AngII)-induced water intake. The mechanism underlying this attenuation may be decreased responsiveness to AngII, as revealed by a reduction in AngII binding to the angiotensin type 1 (AT₁) receptor in the subfornical organ (SFO). It has not been determined whether these changes in receptor binding translate into changes in neuronal activity that, in turn, may influence behavior. Therefore, an estrogen-modulated change in neuronal pathways relevant to AngII-induced water intake was tested in ovariectomized (OVX) female rats using immunohistochemistry for the immediate early gene c-Fos as a marker for neuronal activation. Third cerebroventricular injection of AngII (6 ng) induced intense c-Fos immunoreactivity in forebrain regions associated with fluid intake, including the organum vasculosum of the lamina terminalis, the median preoptic nucleus, the SFO, the supraoptic nucleus and the paraventricular nucleus (PVN). Forty-eight-hour estradiol (10 µg) administration to OVX female rats increased AngII-induced c-Fos labeling in the lateral magnocellular neurons of the PVN by 30% as compared to vehicle-treated controls. Double labeling neurons in the PVN with c-Fos and either vasopressin or oxytocin antisera revealed that estrogen increased AngII-induced c-Fos expression by 28%, specifically in vasopressinergic neurons. Such changes in neuronal activation may explain the estrogen modulation of AngII-induced water intake that has been previously reported; it may be due to increased water retention to maintain plasma osmolality or to induction of a pressor response.

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Effects of ovariectomy, estrogen treatment and CI-628 on food intake and body weight in female rats treated neonatally with gonadal hormones

Cited by 26 publications

References 26 publications

2D:4D Ratio in children at familial high‐risk for eating disorders: The role of prenatal testosterone exposure

2D:4D Ratio in children at familial high‐risk for eating disorders: The role of prenatal testosterone exposure

Estrogen receptor ß is involved in the anorectic action of estrogen

Estrogen Increases Angiotensin II-Induced c-Fos Expression in the Vasopressinergic Neurons of the Paraventricular Nucleus in the Female Rat

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