Binding and structural properties of oxytocin receptors in isolated rat epididymal adipocytes

Boland, Donna; Goren, H. Joseph

doi:10.1016/0167-0115(87)90045-0

Cited by 23 publications

(10 citation statements)

References 23 publications

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“…Anti-obesity effects have also been observed to continue after the discontinuation of OT treatment in animals (Blevins et al, 2015;Blevins et al, 2016;Maejima et al, 2011), consistent with proposed positive feedforward mechanisms of central OT (Moos et al, 1984;Neumann et al, 1994). Reported effects on weight loss (Zhang et al, 2013) may also occur via OT's impact on adipocytes, which express OT receptors (Boland and Goren, 1987). Importantly, it appears that OT specifically targets adipose tissue as OT treatment leaves lean mass unchanged (Altirriba et al, 2014).…”

Section: Oxytocin and Mets Risk Factorssupporting

confidence: 54%

Oxytocin system dysfunction as a common mechanism underlying metabolic syndrome and psychiatric symptoms in schizophrenia and bipolar disorders

Quintana

Dieset

Elvsåshagen

et al. 2017

Frontiers in Neuroendocrinology

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There is growing interest in using intranasal oxytocin (OT) to treat social dysfunction in schizophrenia and bipolar disorders (i.e., psychotic disorders). While OT treatment results have been mixed, emerging evidence suggests that OT system dysfunction may also play a role in the etiology of metabolic syndrome (MetS), which appears in one-third of individuals with psychotic disorders and associated with increased mortality. Here we examine the evidence for a potential role of the OT system in the shared risk for MetS and psychotic disorders, and its prospects for ameliorating MetS. Using several studies to demonstrate the overlapping neurobiological profiles of metabolic risk factors and psychiatric symptoms, we show that OT system dysfunction may be one common mechanism underlying MetS and psychotic disorders. Given the critical need to better understand metabolic dysregulation in these disorders, future OT trials assessing behavioural and cognitive outcomes should additionally include metabolic risk factor parameters.

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Section: Oxytocin and Mets Risk Factorssupporting

confidence: 54%

Oxytocin system dysfunction as a common mechanism underlying metabolic syndrome and psychiatric symptoms in schizophrenia and bipolar disorders

Quintana

Dieset

Elvsåshagen

et al. 2017

Frontiers in Neuroendocrinology

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“…Additional results obtained using a pair-feeding paradigm or the use of low oxytocin doses (which did not alter food intake) allowed concluding that at least part of the body weight-lowering effect of oxytocin was independent from changes in food intake ( 38 , 39 ). It is noteworthy at that point that the OXTR is highly expressed in adipose tissue [at a similar level as in most of the classical oxytocin target tissues ( 43 , 44 )] and is upregulated in some mice models of obesity ( 44 , 45 ). This could explain the occurrence of oxytocin effects on adipose tissue, as well as the difference between the effects of the oxytocin treatment in lean and obese animals.…”

Section: Oxytocin Treatment In Animal Models Of Obesity and Diabetes:mentioning

confidence: 99%

Chronic Oxytocin Administration as a Treatment Against Impaired Leptin Signaling or Leptin Resistance in Obesity

2015

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This review summarizes the existing literature on the effects of oxytocin administration in the treatment of obesity in different animal models and in humans, focusing on the central control of food intake, the oxytocin effects on adipose tissue, and the relationships between oxytocin and leptin. Oxytocin is a hypothalamic nonapeptide synthesized mainly in the paraventricular and supraoptic nuclei projecting to the pituitary, where it reaches the peripheral circulation, as well as to other brain regions. Moreover, leptin modulates oxytocin levels and activates oxytocin neurons in the hypothalamic paraventricular nucleus, which innervates the nucleus of the solitary tract, partly responsible for the brain-elicited oxytocin effects. Taking into account that oxytocin is located downstream leptin, it was hypothesized that oxytocin treatment would be effective in decreasing body weight in leptin-resistant DIO animals, as well as in those with leptin or with leptin receptor deficiency. Several groups have demonstrated that in such animal models (rats, mice, and rhesus monkeys), central or peripheral oxytocin administration decreases body weight, mainly due to a decrease in fat mass, demonstrating that an oxytocin treatment is able to partly overcome leptin deficiency or resistance. Moreover, a pilot clinical study demonstrated the efficiency of oxytocin in the treatment of obesity in human subjects, confirming the results obtained in the different animal models. Larger multicenter studies are now needed to determine whether the beneficial effects of oxytocin treatment can apply not only to obese but also to type 2 diabetic patients. These studies should also shed some light on the molecular mechanisms of oxytocin action in humans.

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“…OTR, known to be a member of the heptahelical G protein‐coupled receptor family, is expressed in a variety of cell types, including osteoblasts and adipocytes [15, –17]. Its ligand, oxytocin (OT), belongs to the pituitary hormone family and regulates the function of peripheral target organs.…”

Section: Introductionmentioning

confidence: 99%

Oxytocin Controls Differentiation of Human Mesenchymal Stem Cells and Reverses Osteoporosis

et al. 2008

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Osteoporosis constitutes a major worldwide public health burden characterized by enhanced skeletal fragility. Bone metabolism is the combination of bone resorption by osteoclasts and bone formation by osteoblasts. Whereas increase in bone resorption is considered as the main contributor of bone loss that may lead to osteoporosis, this loss is accompanied by increased bone marrow adiposity. Osteoblasts and adipocytes share the same precursor cell and an inverse relationship exists between the two lineages. Therefore, identifying signaling pathways that stimulate mesenchymal stem cells osteogenesis at the expense of adipogenesis is of major importance for developing new therapeutic treatments. For this purpose, we identified by transcriptomic analysis the oxytocin receptor pathway as a potential regulator of the osteoblast/adipocyte balance of human multipotent adipose-derived stem (hMADS) cells. Both oxytocin (OT) and carbetocin (a stable OT analogue) negatively modulate adipogenesis while promoting osteogenesis in both hMADS cells and human bone marrow mesenchymal stromal cells. Consistent with these observations, ovariectomized (OVX) mice and rats, which become osteoporotic and exhibit disequilibrium of this balance, have significant decreased OT levels compared to sham-operated controls. Subcutaneous OT injection reverses bone loss in OVX mice and reduces marrow adiposity. Clinically, plasma OT levels are significantly lower in postmenopausal women developing osteoporosis than in their healthy counterparts. Taken together, these results suggest that plasma OT levels represent a novel diagnostic marker for osteoporosis and that OT administration holds promise as a potential therapy for this disease.

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Binding and structural properties of oxytocin receptors in isolated rat epididymal adipocytes

Cited by 23 publications

References 23 publications

Oxytocin system dysfunction as a common mechanism underlying metabolic syndrome and psychiatric symptoms in schizophrenia and bipolar disorders

Oxytocin system dysfunction as a common mechanism underlying metabolic syndrome and psychiatric symptoms in schizophrenia and bipolar disorders

Chronic Oxytocin Administration as a Treatment Against Impaired Leptin Signaling or Leptin Resistance in Obesity

Oxytocin Controls Differentiation of Human Mesenchymal Stem Cells and Reverses Osteoporosis

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