Estrogen effects on oxytocinergic pathways that regulate food intake

Dusti K. Sloan, Diana S. Spencer, Kathleen Curtis

Research output: Contribution to journalArticle

3 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)128-137
Number of pages10
JournalHormones and Behavior
Volume105
DOIs
StatePublished - 1 Sep 2018

Fingerprint

Oxytocin
Estrogens
Eating
Weights and Measures
Messenger RNA
Solitary Nucleus
estradiol-17-benzoate
Paraventricular Hypothalamic Nucleus
Neuropeptides
Hypothalamus
Neurotransmitter Agents
Oils
Immunohistochemistry

Keywords

  • Body weight
  • Intracerebroventricular injection
  • Microstructural analysis
  • Nucleus of the solitary tract
  • Oxytocin antagonist
  • Paraventricular nucleus

Cite this

Sloan, Dusti K. ; Spencer, Diana S. ; Curtis, Kathleen. / Estrogen effects on oxytocinergic pathways that regulate food intake. In: Hormones and Behavior. 2018 ; Vol. 105. pp. 128-137.
@article{50a227f3d3b64b07b147146320b42a41,
title = "Estrogen effects on oxytocinergic pathways that regulate food intake",
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.",
keywords = "Body weight, Intracerebroventricular injection, Microstructural analysis, Nucleus of the solitary tract, Oxytocin antagonist, Paraventricular nucleus",
author = "Sloan, {Dusti K.} and Spencer, {Diana S.} and Kathleen Curtis",
year = "2018",
month = "9",
day = "1",
doi = "10.1016/j.yhbeh.2018.08.007",
language = "English",
volume = "105",
pages = "128--137",
journal = "Hormones and Behavior",
issn = "0018-506X",
publisher = "Academic Press Inc.",

}

Estrogen effects on oxytocinergic pathways that regulate food intake. / Sloan, Dusti K.; Spencer, Diana S.; Curtis, Kathleen.

In: Hormones and Behavior, Vol. 105, 01.09.2018, p. 128-137.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Estrogen effects on oxytocinergic pathways that regulate food intake

AU - Sloan, Dusti K.

AU - Spencer, Diana S.

AU - Curtis, Kathleen

PY - 2018/9/1

Y1 - 2018/9/1

N2 - 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.

AB - 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.

KW - Body weight

KW - Intracerebroventricular injection

KW - Microstructural analysis

KW - Nucleus of the solitary tract

KW - Oxytocin antagonist

KW - Paraventricular nucleus

UR - http://www.scopus.com/inward/record.url?scp=85051940334&partnerID=8YFLogxK

U2 - 10.1016/j.yhbeh.2018.08.007

DO - 10.1016/j.yhbeh.2018.08.007

M3 - Article

C2 - 30118729

AN - SCOPUS:85051940334

VL - 105

SP - 128

EP - 137

JO - Hormones and Behavior

JF - Hormones and Behavior

SN - 0018-506X

ER -