We are analyzing https://link.springer.com/article/10.1007/s11154-013-9260-x.

Title:
Role of oxytocin signaling in the regulation of body weight | Reviews in Endocrine and Metabolic Disorders
Description:
Obesity and its associated metabolic disorders are growing health concerns in the US and worldwide. In the US alone, more than two-thirds of the adult population is classified as either overweight or obese [1], highlighting the need to develop new, effective treatments for these conditions. Whereas the hormone oxytocin is well known for its peripheral effects on uterine contraction during parturition and milk ejection during lactation, release of oxytocin from somatodendrites and axonal terminals within the central nervous system (CNS) is implicated in both the formation of prosocial behaviors and in the control of energy balance. Recent findings demonstrate that chronic administration of oxytocin reduces food intake and body weight in diet-induced obese (DIO) and genetically obese rodents with impaired or defective leptin signaling. Importantly, chronic systemic administration of oxytocin out to 6 weeks recapitulates the effects of central administration on body weight loss in DIO rodents at doses that do not result in the development of tolerance. Furthermore, these effects are coupled with induction of Fos (a marker of neuronal activation) in hindbrain areas (e.g. dorsal vagal complex (DVC)) linked to the control of meal size and forebrain areas (e.g. hypothalamus, amygdala) linked to the regulation of food intake and body weight. This review assesses the potential central and peripheral targets by which oxytocin may inhibit body weight gain, its regulation by anorexigenic and orexigenic signals, and its potential use as a therapy that can circumvent leptin resistance and reverse the behavioral and metabolic abnormalities associated with DIO and genetically obese models.
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Keywords {🔍}

research, support, google, scholar, pubmed, cas, govt, oxytocin, nonus, nih, extramural, physiol, neurons, nucleus, phs, rats, intake, neurosci, obesity, brain, food, review, receptor, rat, effects, leptin, hypothalamic, peptide, central, endocrinology, comp, study, mice, res, weight, hypothalamus, paraventricular, expression, nonphs, gastric, regul, signaling, doijneurosci, body, blevins, control, hindbrain, comparative, feeding, doien,

Topics {✒️}

tnf-alpha-induced c-fos generation corticotropin-releasing hormone-synthesizing neurons meal-induced c-fos expression month download article/chapter fat-rich diet activates methamphetamine-induced hyperactivity related severe early-onset obesity prolactin-releasing peptide receptor leptin-regulated genes revealed hetero-dimeric complex formations diet-induced obese mice hypothalamic-pituitary-adipose axis diet-induced obese rodents pro-opiomelanocortin gene transfer refeeding-activated glutamatergic neurons pvn-hindbrain pathway involved nicotine-induced cfos expression resting-stage feeding manipulation diet-induced obese rats gut-sensitive feeding processes llewellyn-smith ij leptin-independent melanocortin pathway retrograde tract-tracing studies pvn-hindbrain feeding pathway lesioning oxytocin-receptive neurons region-specific leptin resistance nesfatin-1-regulated oxytocinergic signaling ventral tegmental area high-fat diet c-fos expression diet-induced obese brainstem nutrient sensing putative satiety cells hypothalamic hyperphagia-obesity syndrome pgc-1alpha deficiency prolactin releasing peptide prolactin-releasing peptide centrally administered oxytocin express cck-induced activation diet-induced obesity high energy diets cholecystokinin-induced satiety anorectic peptide regulated cholecystokinin-mediated suppression oxytocin decreases methamphetamine visceral fat mass long-term impairments privacy choices/manage cookies cholecystokinin-induced suppression activates hindbrain glucagon

Questions {❓}

Hypothesis paper Brain talks with fat–evidence for a hypothalamic-pituitary-adipose axis?
The brain oxytocin receptor(s)?

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