Inhibitory role of oxytocin on TNFα expression assessed in vitro and in vivo
S Garrido-Urbani1, N Deblon2, A L Poher2
1Department of Pathology and Immunology, Medical Faculty, University Medical Center, University of Geneva, Geneva, Switzerland.
Aim:
Oxytocin administration to diet-induced obese (DIO) rodents, monkeys and humans decreases body weight and fat mass with concomitant improvements in glucose metabolism. Moreover, several studies show an immunomodulatory role of oxytocin in a number of settings (such as atherosclerosis, injury, sepsis). This study aims to shed some light on the effects of oxytocin on macrophage polarization and cytokine production, as well as its possible impact on these parameters in adipose tissue in DIO mice with impaired glucose metabolism.
Methods:
Mouse bone marrow cells were differentiated into macrophages and treated with oxytocin. Macrophage proliferation, cytokine secretion and macrophage populations were determined. For experiments in vivo, DIO mice were treated with oxytocin for 2 weeks. Body weight and composition and glucose tolerance were subsequently followed. At the end of treatment, adipose tissue macrophage populations, plasma cytokine levels and cytokine expression in adipose tissue were determined.
Results:
In bone marrow-derived macrophages, oxytocin induced an anti-inflammatory phenotype (decreased M1/M2 ratio). In M1-derived macrophages, oxytocin decreased TNFα secretion, with no effects on the other cytokines tested nor any effect on cytokine secretion by M2-derived macrophages. Oxytocin treatment in DIO mice in vivo led to decreased body weight accompanied by an improvement in glucose tolerance, with no changes in plasma cytokine levels. In adipose tissue, oxytocin decreased Tnfα expression without modifying the M1/M2 macrophage ratio.
Conclusion:
Oxytocin treatment decreases TNFα production both in vitro (in bone marrow-derived macrophages) and in vivo (in epididymal adipose tissue) in DIO mice. This effect may also be contributory to the observed improvement in glucose metabolism.
Insights
Oxytocin treatment reduced body weight and improved glucose tolerance in diet-induced obese mice. It also decreased TNFα production in macrophages and adipose tissue, suggesting a role in metabolic health.
Area of Science:
- Immunology
- Metabolic Science
- Endocrinology
Background:
- Oxytocin administration reduces body weight and fat mass in diet-induced obese (DIO) models and humans.
- Oxytocin exhibits immunomodulatory effects in various conditions, including atherosclerosis, injury, and sepsis.
- The impact of oxytocin on macrophage polarization and cytokine production in adipose tissue of DIO mice remains unclear.
Purpose of the Study:
- To investigate the effects of oxytocin on macrophage polarization and cytokine production.
- To determine the impact of oxytocin on adipose tissue macrophage populations and cytokine expression in DIO mice.
- To assess the influence of oxytocin on body weight, composition, and glucose metabolism in DIO mice.
Main Methods:
- Mouse bone marrow-derived macrophages were treated with oxytocin to assess proliferation, cytokine secretion, and polarization.
- Diet-induced obese mice received oxytocin treatment for two weeks to evaluate body weight, composition, and glucose tolerance.
- Adipose tissue macrophage populations, plasma cytokine levels, and adipose tissue cytokine expression were analyzed post-treatment.
Main Results:
- Oxytocin induced an anti-inflammatory phenotype in bone marrow-derived macrophages, decreasing the M1/M2 ratio and TNFα secretion.
- In DIO mice, oxytocin treatment led to reduced body weight and improved glucose tolerance, without altering plasma cytokine levels.
- Oxytocin decreased TNFα expression in adipose tissue but did not alter the M1/M2 macrophage ratio in vivo.
Conclusions:
- Oxytocin treatment effectively reduces TNFα production in both macrophages and adipose tissue of DIO mice.
- These anti-inflammatory effects of oxytocin may contribute to the observed improvements in glucose metabolism.
- Oxytocin holds potential as a therapeutic agent for managing metabolic dysfunction associated with obesity.
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