TY - JOUR
T1 - Estrogen effects on oxytocinergic pathways that regulate food intake
AU - Sloan, Dusti K.
AU - Spencer, Diana S.
AU - Curtis, Kathleen S.
N1 - Funding Information:
This work was supported by Oklahoma Center for the Advancement of Science and Technology Health Research Grant HR12-196 (KSC) and a Tulsa Community College Faculty Innovation Grant (DKS, DSS, KSC). Portions of this work were presented at the annual meeting of the Study of Ingestive Behavior (Denver, CO; 2015) and at the joint meeting of the American Physiological Society and The Physiological Society (Dublin, Ireland; 2016). The data presented are part of the doctoral dissertation of Dusti Sloan.
Publisher Copyright:
© 2018 Elsevier Inc.
PY - 2018/9
Y1 - 2018/9
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
SN - 0018-506X
VL - 105
SP - 128
EP - 137
JO - Hormones and Behavior
JF - Hormones and Behavior
ER -