Hormones (2023) 23:15–23

https://doi.org/10.1007/s42000-023-00505-y

REVIEW ARTICLE

The neurohypophyseal hormone oxytocin and eating behaviors:

a narrative review
Michele Iovino1 · Tullio Messana2 · Simonetta Marucci3 · Domenico Triggiani1 · Vito Angelo Giagulli1 ·
Edoardo Guastamacchia1 · Giuseppina Piazzolla1 · Giovanni De Pergola4,5 · Giuseppe Lisco1 · Vincenzo Triggiani1

Received: 17 May 2023 / Accepted: 3 November 2023 / Published online: 18 November 2023
© The Author(s) 2023, corrected publication 2024

Abstract
Background The neuropeptide oxytocin (OT) is crucial in several conditions, such as lactation, parturition, mother-infant
interaction, and psychosocial function. Moreover, OT may be involved in the regulation of eating behaviors.
Methods This review briefly summarizes data concerning the role of OT in eating behaviors. Appropriate keywords and
medical subject headings were identified and searched for in PubMed/MEDLINE. References of original articles and reviews
were screened, examined, and selected.
Results Hypothalamic OT-secreting neurons project to different cerebral areas controlling eating behaviors, such as the
amygdala, area postrema, nucleus of the solitary tract, and dorsal motor nucleus of the vagus nerve. Intracerebral/ventricular
OT administration decreases food intake and body weight in wild and genetically obese rats. OT may alter food intake and
the quality of meals, especially carbohydrates and sweets, in humans.
Discussion OT may play a role in the pathophysiology of eating disorders with potential therapeutic perspectives. In obese
patients and those with certain eating disorders, such as bulimia nervosa or binge/compulsive eating, OT may reduce appe-
tite and caloric consumption. Conversely, OT administered to patients with anorexia nervosa may paradoxically stimulate
appetite, possibly by lowering anxiety which usually complicates the management of these patients. Nevertheless, OT admin-
istration (e.g., intranasal route) is not always associated with clinical benefit, probably because intranasally administered OT
fails to achieve therapeutic intracerebral levels of the hormone.
Conclusion OT administration could play a therapeutic role in managing eating disorders and disordered eating. However,
specific studies are needed to clarify this issue with regard to dose-finding and route and administration time.

Keywords Oxytocin · Oxytocin receptor · Food intake · Eating behaviors · Eating disorder · Obesity · Disordered eating

Abbreviations
AP Area postrema
DMV Dorsal motor nucleus of the vagus nerve
* Giuseppe Lisco DVC Dorsal vagal complex
[email protected] GLP-1 Glucagon-like peptide 1
1
Interdisciplinary Department of Medicine, Section MCN Magnocellular neurosecretory neurons
of Internal Medicine, Geriatrics, Endocrinology and Rare NA Noradrenaline
Diseases, University of Bari “Aldo Moro”, School NTS Nucleus of the solitary tract
of Medicine, Bari, Apulia, Italy OT Oxytocin
2
Infantile Neuropsychiatry, IRCCS – Institute of Neurological OTR Oxytocin receptor
Sciences, Bologna, Italy PVN Paraventricular nuclei neurons
3
Università Campus Biomedico, Dip. “Scienze e Tecnologie SON Supraoptic
per l’Uomo e l’ambiente”, Via Alvaro del Portillo, 21 Roma, VMH Ventromedial nucleus of the hypothalamus
Italy
4
National Institute of Gastroenterology IRCCS “Saverio de
Bellis”, Research Hospital, Castellana Grotte, Bari, Italy
5
Department of Biomedical Science and Human Oncology,
University of Bari, School of Medicine, Bari, Apulia, Italy

Vol.:(0123456789)
16 Hormones (2023) 23:15–23

Background Overview of physiological aspects

of oxytocin
Hypothalamic nuclei play a role in eating behaviors, stim-
ulating or inhibiting food intake. Appetite is triggered by The stimulation of the cervix uteri and nipples stimulates
nuclei located in the lateral hypothalamus, also known the synthesis of a precursor protein encoded by the OT gene
as the “hunger center,” while it is suppressed by neurons to synthesize OT and its carrier protein neurophysin 1 [8,
located in the ventromedial nucleus of the hypothalamus 9]. These peripheral signals originating from cervix uteri
(VMH) (“satiety center”) [1–5]. and nipple receptors are transmitted to the SON and PVN
Oxytocin (OT), a neurohypophyseal hormone, is syn- OT-ergic neurons via the spinal cord, the dorsal lateral fas-
thesized by hypothalamic magnocellular neurosecre- ciculus, the medial forebrain bundle, and the mammillary
tory neurons (MCN) of the supraoptic (SON) and para- peduncle [10–12]. The glial cells, mainly astrocytes, stimu-
ventricular nuclei neurons (PVN) [6, 7]. It is pivotal in late the morphological plasticity of the OT-ergic neurons
inducing parturition and lactation and in regulating social during lactation and parturition to facilitate the synthesis
behaviors. Also, OT is synthesized in other areas of the and transport of OT [10, 13].
forebrain, such as the amygdala, hippocampus, septum, The neurokinin 3 receptor is associated with the nuclear
striatum, and bed nucleus of the terminal stria and is also chaperone protein importin β1, which induces the internali-
detectable in the cerebrospinal fluid [6, 7]. zation of the OT precursor in the Golgi complex and rough
The role of OT in regulating eating behaviors has yet endoplasmic reticulum [10, 11].
to be understood entirely. In this review, we have sum- Once synthesis has occurred, OT and its carrier protein
marized the neuroanatomical and biochemical OT-ergic neurophysin 1 are conveyed to the neurohypophysis where
pathways synapsing on brain areas involved in regulating they are stored in secretory vesicles and released into the
eating behaviors in animal models and humans (Fig. 1). systemic circulation [10, 13, 14].
PubMed/MEDLINE was searched for references of origi- The OT receptor (OTR) is a Gq/11 protein-linked recep-
nal articles and reviews. Appropriate keywords and medi- tor, and OT-binding sites have been localized in the brain.
cal subject headings terms were identified and included Efferent pathways arising from the hypothalamic OT-ergic
the following: “oxytocin,” “eating disorders,” “eating neurons project to brain areas containing a high concentra-
behaviors,” “hypothalamus,” “hypothalamic ventromedial tion of OTR, including the olfactory bulb, bed nucleus of
nucleus,” “amygdale,” “area postrema,” “nucleus of the the stria terminalis, nucleus accumbens septi, hypothalamic
solitary tract,” and “dorsal motor nucleus of the vagus suprachiasmatic, arcuate and VM nuclei, amygdala, hip-
nerve.” References were screened according to a hierar- pocampus, septum, the nucleus of the solitary tract (NTS)
chical strategy by title and abstract, and full text. Original of the oblongata medulla, cingulate cortex, and spinal cord
papers and reviews were screened, selected when appropri- [15]. OTR is also expressed in peripheral tissue such as the
ate, and discussed in detail. kidney, heart, thymus, pancreas, and adipose tissue [16].

Fig. 1  Simplified depiction

of the relationship between
Supraoptic and paraventricular nuclei/Neurohypophysis
OT-ergic hypothalamic PVN
and SON neurons and brain Thalamus

sites involved in regulating Amygdala

eating behaviors (blue arrows).
Nucleus of the solitary tract
OT-ergic projections from PVN
synapse within the amygdala Area Postrema
(AMY), area postrema (AP), Dorsal motor nucleus of vagus
nucleus of the solitary tract
(NTS), and dorsal motor
Rapid satiation
nucleus of vagus nerve (DMV)
playing a role in anorexigenic
response, taste aversion, gastric Taste aversion
emptying (red arrows)

Gastric emptying
Hormones (2023) 23:15–23 17

Neuroanatomical organization of regions due to acquired experience [17]. In rats, the apomorphine
regulating food intake, appetite, satiety, administration before or 30 min after the ingestion of sac-
and reward charine negatively affected further saccharine intake after
vomiting. This response indicates that the unpleasant gastric
Hypothalamic OT-ergic neurons display widespread projec- effect of apomorphine significantly contributed to taste aver-
tions throughout the brain, mainly to the amygdala, con- sion, ultimately affecting specific food intake such as rapidly
tributing to the satiety process by causing the sensation of absorbed carbohydrates [30].
fullness [17]. Other brain areas typically regulating eating The amygdala determines satiation by oropharyngeal and
behaviors receive afferent projections from hypothalamic gastric afferents; bilateral amygdala lesions lead to overeat-
OT-ergic neurons, including the area postrema, the NTS, ing. The suppression of food intake is mediated by cholin-
and the dorsal motor nucleus of the vagus nerve [18, 19]. ergic stimulation of the amygdala. Conversely, adrenergic
stimuli enhance appetite and food intake in starving but not
satiated animals. Therefore, the amygdala exerts two differ-
The ventromedial nucleus of the hypothalamus ent influences on eating behaviors. First, the amygdala plays
a facilitating effect in the maintenance of consuming activity
The VMH, the Cajal nucleus, is a pear-shaped structure in induced by NA-ergic activation. Subsequently, the amygdala
the hypothalamic tuberal area. The neurons can synthesize plays an inhibitory role leading to satiety and food intake
OTR and express a high density of OTR on their surfaces cessation. This subsequent behavior is due to cholinergic
[20, 21]. Food intake is inhibited, weight gain restricted, activation, which stops NA-ergic ones [30].
and energy expenditure augmented after the leptin-induced OTRs are expressed on the membrane of the amygdala’s
activation of steroidogenic factor 1 positive neurons in the basolateral and central neurons. OT-ergic projections from
VMH [22, 23]. the PVN nuclei to the amygdala have also been described.
Food intake, especially fasting-absorbed carbohydrates, Experiencing gastrointestinal toxicity concomitantly to food
stimulates OT release from OT-secreting neurons [24]. intake is accompanied by OT release in humans and animals.
Moreover, several hormones may stimulate OT release after Therefore, it is believed that OT interaction with cholinergic
the ingestion of a meal, including leptin, cholecystokinin, and adrenergic circuits within the amygdala may have a role
and gastrointestinal incretins. The same is observed after in regulating eating behaviors in terms of food intake, sati-
noradrenergic stimulation of OT-secreting neurons by vagal ety, and taste aversion or predilection [31–33]. Indeed, OT
afferences from the nucleolus of the solitary tract (NTS) administration in the basolateral amygdala effectively sup-
[25]. presses the consumption of palatable saccharin solutions in
It has been hypothesized that OT may be involved in reg- rats. A moderate restriction of food intake was observed after
ulating food intake and energy expenditure directly or by the administration of OT and was attenuated by pretreatment
potentiating central and peripheral anorexigenic stimuli [26]. with an OTR antagonist (L-368,899) [34]. In experimental
Although the VMH has a high density of OTR, it con- conditions, assessing the role of OT in mediating the acqui-
tains a few OT-ergic projections, suggesting that it could sition and retrieval of conditioned taste aversion in mice that
be a local target of OT [21]. To support this hypothesis, OT underwent lithium-induced acute gastric toxicity, OT was
antagonism or silencing of the OT-induced signaling path- found to contribute to causing taste aversion significantly.
way in the VMH predisposes to a much-extended food intake At the same time, OT antagonism partially alleviated it but
in terms of energy intake, delayed satiation, and intake of did not wholly retrieve taste aversion [35].
more carbohydrates while reducing energy expenditure
[27–29].
The area postrema

Extrahypothalamic structures involved Lesions of the medullary circumventricular organ in the area
in the regulation of eating behaviors postrema (AP) reduce food intake and induce weight loss
[36, 37]. As a chemo-sensitive organ, AP modulates the con-
The amygdala ditioned avoidance response (CAR) to toxins, such as car-
bonate lithium. The acquisition of CAR and conditioned pal-
Innate appetite and food aversion are modulated by specific atability to oral sucrose was assessed in rats with lesions of
brain structures, mainly in the limbic system. The basolateral the AP. The abolishment of OT-ergic inputs from the hypo-
and central nuclei of the amygdala regulate the appetite in thalamic PVN induced restricted ingestion and increased
terms of the amount of ingested food and innate aversions aversive responses to intraoral infusion of sucrose following
and control qualitative predisposition toward specific food an intraperitoneal injection of carbonate lithium [38].
18 Hormones (2023) 23:15–23

OT was found to increase intragastric pressure by vagal and food consumption and, lastly, leading to weight loss.
efferences after its administration in the fourth ventricle, These effects are related to the food reward-suppressing role
specifically acting at the level of AP and NTS [39]. The pep- of GLP-1 agonists operating within the NTS [51].
tide hormone amylin, or islet amyloid peptide, is co-secreted Adrenalectomy reduces food intake significantly, but this
with insulin from the pancreatic β-cells and promotes satiety response is reversed by OTR antagonists and by activating
by decelerating gastric emptying. The precise mechanism by satiety-related responses in the NTS. It has been reported
which amylin reduces food intake is mediated by the activa- that OT-ergic projections from the PVN to NTS are highly
tion of NA-ergic neurons within the AP [40]. Similar effects upregulated after bilateral adrenalectomy, thus positively
are also induced by calcitonin, a potent amylin agonist struc- affecting satiety and consequently reducing meal size in
turally similar to amylin, as belonging to the calcitonin-like primary adrenal insufficiency [52]. Glucocorticoid replace-
gene peptide superfamily. AP lesions affecting OT-ergic ment therapy prompts the opposite effect.
release abolish anorexic effects induced by the peripheral Evidence shows that OT directly injected in the dorsal
administration of amylin and calcitonin [41]. This could be vagal complex (DVC) stimulates gastric secretion via the
an additive mechanism by which OT may reduce food intake vagal pathway [53]. OT levels in the DVC were significantly
and prompt satiety. increased in response to food intake, and OTR signaling
within DVC neurons plays a counter regulator of gastroin-
The nucleus of the solitary tract and the dorsal motor testinal activity by stimulating satiation signals to reduce
nucleus of the vagus nerve food intake [54].

The NTS of the dorsal medulla oblongata plays an essen-

tial role in regulating cardiovascular functions, affects the Oxytocin and eating behaviors: what do we
activity of hypothalamic SON and PVN neurons [42, 43], know?
and reduces food intake and body weight [44]. Signals from
the gastrointestinal tract are conveyed to the brain by vagal OT may have a role in controlling emotion and cognition
afferents synapsing within the medullary dorsal vagal com- [55] and regulating food intake [56]. In normal-weight and
plex, including the NTS and the dorsal motor nucleus of the obese animals, OT administered centrally reduces food
vagus nerve (DMV) [45, 46]. Moreover, descending path- intake and facilitates weight loss [57]. These responses
ways from the hypothalamic SON and PVN to the NTS and were also observed when OT was injected peripherally [58].
DMV are involved in the beginning and termination of food Moreover, a pretreatment with both central and peripheral
intake [47]. (fully permeable to the blood-brain barrier) administration
An experimental injury of the median-caudal region of of OTR antagonists reduced the attenuation of food intake
the NTS induced hypophagia with consequent body weight after OT administration [57, 58].
loss [48]. During the first 6 days following the electrolytic Rats with lesions of the PVN, the leading site of OT
lesion of the NTS, rats reduced their food intake by around secretion, exhibited more food intake and weight gain than
80% compared to the sham controls. From the 7th day, food controls [59]. In this model, the peripheral and central
intake slightly recovered, but the appetite remained signifi- administration of OT reduced, in a dose-dependent manner,
cantly reduced compared to baseline [37]. food intake and increased the time intercurrent of the con-
OT may regulate appetite, food intake, and weight gain by sumption of two consecutive meals [60]. The results suggest
acting at the NTS site. An experiment in rats suggested that that OT could be involved in the induction and prolongation
the administration of OT in the NTS decreased caloric intake of satiety.
by reducing food motivation and seeking [49]. In rats, acute Patients with neuropsychiatric diseases often exhibit
intraventricular administration of OT (5 μg) 30 min before eating disorders, with hyperphagia and increased meal
a meal consumption induced a dose-response reduction in size usually the leading determinant of weight gain. The
food intake up to 72% (3rd ventricle) and 60% (4th ventri- therapeutic potential of OT was analyzed in this cluster of
cle). Chronic exposure to OT prevented excessive weight patients, hypothesizing that OT could have also played a
gain after exposing the rats to overfeeding with a high-fat role in the regulation of psychosocial functions coupled with
diet, with OT-treated animals maintaining a higher leptin eating behaviors. A pivotal study conducted in 16 patients
sensibility than vehicle controls [50]. with an established diagnosis of schizophrenia on a stable
Glucagon-like peptide 1 (GLP-1) inhibits food intake by antipsychotic treatment with overweight or obesity (BMI
acting on neurons within the NTS and abolishes food reward > 27 kg/m2) showed that the intranasal administration of
behaviors and motivation to food intake. Microinjections of OT (24 IU) compared to placebo a few minutes before the
native GLP-1 or the GLP-1 analog exendin-4 into the NTS meal consumption did not affect satiety, meal size, post-meal
suppressed food reward behaviors, thus reducing appetite serum glucose, and insulin levels [61].
Hormones (2023) 23:15–23 19

In a randomized clinical trial, administering OT twice The observation of a dimorphic action of OT in these two
daily for 3 months compared to placebo improved social kinds of eating disorders suggests that OT regulates the brain
behavior and reduced appetite in children (3–11 years) with circuits subserving eating behaviors. Therefore, the physi-
Prader-Willy syndrome [62]. ological involvement of OT in eating disorders can support
The encephalic functional magnetic resonance imaging its beneficial therapeutic effect in clinical practice since the
revealed that the intranasal administration of OT in obese administration of OT by intranasal route may bypass the
men attenuated the ventral tegmental area firing to food blood-brain barrier [68] and reach the amygdala and brain-
motivation regions such as the insula, oral somatosensory stem structures involved in the control of eating behaviors
cortex, and amygdala in response to high-calorie visual food such as the AP, NTS, and DMV.
images. The results suggested that OT may exert an ano- However, the current level of evidence does not sug-
rexigenic effect by dampening eating cravings activated by gest a possible positive effect of intranasal OT treatment in
reward anticipation in patients with obesity [28]. eating disorders. This could be attributable to the fact that
In women with stress-induced eating disorders, the over- cerebral exposure to OT, after its intranasal administration,
all exposure to serum cortisol is usually higher than normal. may not be sufficient to elicit desirable effects and probably
This mechanism may contribute to increase the appetite and higher doses, alternative routes, and timing of administration
positively affect food intake. The intranasal administration should be considered [69].
of a 24 IU shot compared to the placebo (saline solution) Hypothalamic injury has a wide range of etiology, includ-
was found to reduce the intake of sweet and fatty snakes ing brain surgery, encephalic trauma, tumors, chemotherapy
by 15 min after administering the neurohypophyseal hor- and radiation, vascular diseases (aneurysms), cerebral infec-
mone. Interestingly, the salivary cortisol levels (assessed to tions, and inflammatory and infiltrative diseases. Depend-
test the level of stress) throughout the observation remained ing on the sites, a hypothalamic injury may hypothetically
unchanged up to 75 min after the administration of OT [63]. result in different clinical consequences [70]. A lesion in
The findings were consistent with the fact that OT affected the middle hypothalamic region produces direct damage to
eating behavior independently of the background stress level some specific centers, such as the arcuate nucleus, which is
by acting with a direct mechanism. responsible for the tonic release of dopamine, suppressing
To better investigate the efficacy, safety, and mechanisms the prolactin secretion from lactotrophic cells in the pitui-
via which OT is involved in reducing appetite, caloric intake, tary and phasic release of the growth hormone releasing
and body weight and affecting energy expenditure, body hormone, resulting in a loss of somatotropic cells pulses
composition, glucose and lipid metabolism, and brain acti- of growth hormone. Moreover, the dorsomedial and ven-
vation and control of behaviors and impulses in response to tromedial nuclei are also located in the middle region of
food images, an 8-week randomized, double-blind, placebo- the hypothalamus and are directly involved in controlling
controlled trial has been designed and is currently ongoing. behaviors and gastrointestinal motility (the former) and
The study will clarify several exciting issues about OT as food intake (the latter). This region may be affected in some
a pharmacologic treatment of obesity [64]. Moreover, dys- endocrine diseases, especially pituitary macro/giant adeno-
function in the OT-ergic mechanisms has also been reported mas with considerable suprasellar extension or in the case
in patients with anorexia nervosa, with specific patterns that of primitive hypothalamic disorders (such as craniopharyn-
include lower circulating levels of OT at fasting and after gioma or infiltrative diseases), and the consequent hypotha-
stimulation, lower nocturnal levels of OT, and higher periph- lamic damage usually results in a progressive deterioration
eral OT concentration after meal ingestion [65]. Derange- of food intake control, aggressive behaviors, and typically
ments of OT homeostasis in AN are close to the opposite mild or moderate hyperprolactinemia. Injuries in the anterior
of those observed in other eating disorders characterized by region of the hypothalamus may harm both the supraoptic
weight excess or propension to gain weight and are revers- and paraventricular nuclei, thus also affecting the OT syn-
ible after rehabilitation programs and weight gain in AN. thesis [71]. The disturbance may also be accompanied by
Although no specific trials have been carried out, OT admin- partial or extensive anterior and posterior pituitary failure,
istration may have a particular and disease-related role in resulting in a unimodal or multimodal hormonal deficiency.
improving food intake in AN. The mechanisms potentially Patients with craniopharyngioma, one of the most common
explaining this sui generis and paradoxical effect could be causes of hypothalamic damage, usually exhibit lower cir-
attributable to the contribution of OT administration in culating levels of OT at baseline and after stimulation [72].
reducing eating-related attention and concerns, attenuat- Several studies have been published seeking to determine
ing cognitive rigidity, improving emotional expression, and whether OT deficiency was associated with changes in social
weakening the attitude of avoiding social situations or con- cognition [73] and eating behaviors in craniopharyngioma
texts emotionally provoking stimuli, lastly improving social survivors. Anecdotal cases suggested that the intranasal
behavior [66, 67]. administration of OT improved emotional tasks and social
20 Hormones (2023) 23:15–23

behaviors in young survivors of craniopharyngioma with individuals exhibit different responses to OT administra-
low (case report) [74] and detectable basal levels of OT tion before meals, including caloric restriction, less prefer-
(case series) [75]. In one cross-sectional case-control study ence for fatty snake consumption, and unaltered propension
in 34 patients with craniopharyngioma and 73 controls, toward carbohydrates [83].
adverse eating behaviors and eating disorders were more Although OT may be enumerated as another therapeutic
frequently observed among patients with extensive (anterior tool to manage weight gain or induce weight loss [84] and
and posterior) hypothalamic injury than in those with less despite anecdotal evidence suggesting that OT administra-
extensive damage, and controls. Among individuals with tion may improve social behaviors, emotional tasks, and eat-
adverse eating behaviors, lower postprandial levels of OT ing behaviors, trials are needed for deeper insight into the
compared to control were also found [76], as observed in therapeutic role of OT in patients with hypothalamic injury,
patients with obesity [71]. The intranasal administration of such as craniopharyngioma.
OT in combination with the opiate antagonist naltrexone Special studies are surely necessary to verify more pre-
(10 weeks of OT alone + 38 weeks of OT and naltrexone) cisely the therapeutic role of OT in certain disorders char-
was significantly effective in reducing the appetite, caloric acterized by overeating, eating disorders, and disordered
intake, and hyperphagia in a 13-year-old boy with confirmed eating as well.
hypothalamic obesity and hyperphagia post-resection of
craniopharyngioma [77]. These positive results could be
Author contribution M.I. conceived the review. M.I., T.M., G.L., S.M.,
attributable to the numerous metabolic effects of the neu- and V.T. performed database searches and selected appropriate ref-
rohormone, including direct reduction of food intake by erences. M.I., T.M., and G.L. drafted the manuscript. F.M., V.A.G.,
decreasing appetite in homeostatic and reward-driven con- E.G., G.D.P., and V.T. provided minor editing. E.G., G.D.P., and V.T.
ditions (hence, properly insisting on hypothalamic regions provided feedback. All the authors read the text and approved the final
manuscript submission.
involved in the regulation of hunger and satiation), enhance-
ment of lipolysis and energy expenditure, positive affection Funding Open access funding provided by Università degli Studi di
of body composition due to improvement of peripheral insu- Bari Aldo Moro within the CRUI-CARE Agreement.
lin sensitivity, ultimately favoring lean over fat mass build-
ing [78]. Nevertheless, a recently published randomized, Declarations
double-blind, placebo-controlled, crossover pilot study (13 Ethical approval Not applicable.
patients randomized; 10 concluded) did not find any relevant
changes in body weight between the OT arm 16–24 IU at Informed consent Not applicable.
the three main mealtimes and placebo after 8 weeks of treat-
ment [79]. This finding lays the basis for better-designed Conflict of interest The authors declare no competing interests.
multicentric trials to assess the role of OT treatment (alone
Open Access This article is licensed under a Creative Commons Attri-
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One piece of evidence suggests that OT and OTR may regu- the article's Creative Commons licence and your intended use is not
late eating behaviors and food intake. In neuropsychiatric permitted by statutory regulation or exceeds the permitted use, you will
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anorexia nervosa, OT and OTR agonists could potentially
have pharmacological use [80]. In addition, OTR gene poly-
morphisms may also be involved in the pathogenesis of such
disorders [81]. References
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