Oxytocin reduces adipose tissue inflammation in obese mice
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RESEARCH
Open Access
Oxytocin reduces adipose tissue inflammation in obese mice Angela Szeto1, Monia Cecati2, Raisa Ahmed1, Philip M. McCabe1 and Armando J. Mendez2*
Abstract Background: Obesity and adipose tissue expansion is characterized by a chronic state of systemic inflammation that contributes to disease. The neuropeptide, oxytocin, working through its receptor has been shown to attenuate inflammation in sepsis, wound healing, and cardiovascular disease. The current study examined the effects of chronic oxytocin infusions on adipose tissue inflammation in a murine model of obesity, the leptin receptordeficient (db/db) mouse. Methods: The effect of obesity on oxytocin receptor protein and mRNA expression in adipose tissue was evaluated by Western blotting and real-time polymerase chain reaction. Mice were implanted with osmotic minipumps filled with oxytocin or vehicle for 8 weeks. At study endpoint adipose tissue inflammation was assessed by measurement of cytokine and adipokine mRNA tissue levels, adipocyte size and macrophage infiltration via histopathology, and plasma levels of adiponectin and serum amyloid A as markers of systemic inflammation. Results: The expression of adipose tissue oxytocin receptor was increased in obese db/db mice compared to lean controls. In adipose tissue oxytocin infusion reduced adipocyte size, macrophage infiltration, IL-6 and TNFα mRNA expression, and increased the expression of the anti-inflammatory adipokine, adiponectin. In plasma, oxytocin infusion reduced the level of serum amyloid A, a marker of systemic inflammation, and increased circulating adiponectin. Conclusions: In an animal model of obesity and diabetes chronic oxytocin treatment led to a reduction in visceral adipose tissue inflammation and plasma markers of systemic inflammation, which may play a role in disease progression. Keywords: Adipose tissue, Anti-inflammation, Obesity, Oxytocin, Obese mouse model
Background It has been suggested that obesity is characterized by a chronic state of systemic inflammation [1] that contributes to insulin resistance, dyslipidemia, diabetes and cardiovascular disease [2]. Obesity is accompanied by proliferation of adipose tissue [3] which consists of adipocytes, macrophages, fibroblasts, mesenchymal cells, pre-adipocytes, and endothelial cells [4]. Obesity-related * Correspondence: [email protected] 2 Department of Medicine and Diabetes Research Institute, University of Miami Miller School of Medicine, 1450 N.W. 10th Avenue, Miami, FL 33136, USA Full list of author information is available at the end of the article
inflammation is thought to be largely due to increased adipose tissue volume, infiltration of monocytes that differentiate into macrophages and express the classical M1 proinflammatory phenotype, and the subsequent secretion of pro-inflammatory cytokines and adipokines from adipocytes and macrophages [5]. It has been demonstrated that visceral adipose tissue, relative to subcutaneous fat, exhibits a greater inflammatory response as a consequence of obes
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