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Published on: December 16, 2022
Estrogen effects on oxytocinergic pathways that regulate food intake
Dusti K Sloan1, Diana S Spencer2, Kathleen S Curtis3
1Department of Pharmacology and Physiology, Oklahoma State University-Center for Health Sciences, Tulsa, OK 74107, USA; Department of Science and Mathematics, Tulsa Community College, Tulsa, OK 74133, USA.
Abstract:
Multiple stimulatory and inhibitory neural circuits control eating, and these circuits are influenced by an array of hormonal, neuropeptide, and neurotransmitter signals. For example, estrogen and oxytocin (OT) both are known to decrease food intake, but the mechanisms by which these signal molecules influence eating are not fully understood. These studies investigated the interaction between estrogen and OT in the control of food intake. RT-qPCR studies revealed that 17β-estradiol benzoate (EB)-treated rats showed a two-fold increase in OT mRNA in the paraventricular nucleus of the hypothalamus (PVN) compared to Oil-treated controls. Increased OT mRNA expression may increase OT protein levels, and immunohistochemistry studies showed that EB-treated rats had more intense OT labeling in the nucleus of the solitary tract (NTS), a region known to integrate signals for food intake. Food intake measurements showed that EB treatment reduced food intake, as expected. EB-treated rats lost weight over the course of the experiment, as expected, and EB-treated rats that received the highest dose of OT lost more weight than EB-treated rats that did not receive OT. Finally, OT antagonist administered to EB-treated rats reversed the effect of EB on food intake, suggesting that estrogen effects to decrease food intake may involve the oxytocinergic pathway.
Insights
Estrogen and oxytocin (OT) reduce food intake. Estrogen increases OT mRNA and protein, and blocking OT reverses estrogen
Area of Science:
- Neuroendocrinology
- Neuroscience
Background:
- Neural circuits and signaling molecules regulate eating behavior.
- Estrogen and oxytocin (OT) are known to decrease food intake, but their interaction is not fully understood.
Purpose of the Study:
- To investigate the interaction between estrogen and oxytocin in controlling food intake.
- To elucidate the mechanisms underlying estrogen's effect on appetite.
Main Methods:
- RT-qPCR to measure OT mRNA in the hypothalamus (PVN).
- Immunohistochemistry to assess OT protein levels in the nucleus of the solitary tract (NTS).
- Food intake and body weight measurements in rats following estrogen and OT administration or antagonism.
Main Results:
- 17β-estradiol benzoate (EB) treatment significantly increased OT mRNA in the PVN and OT labeling in the NTS.
- EB treatment reduced food intake and body weight.
- Co-administration of OT enhanced EB's weight-reducing effects, while OT antagonist reversed EB's effect on food intake.
Conclusions:
- Estrogen's appetite-suppressing effects may be mediated through the oxytocinergic pathway.
- Estrogen influences central oxytocin pathways involved in the regulation of energy homeostasis.
- This study highlights a potential neuroendocrine mechanism linking estrogen and oxytocin in appetite control.
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