Abstract
Expansion of intra-abdominal adipose tissue and the accompanying inflammatory response has been put forward as a unifying link between obesity and the development of chronic diseases. However, an apparent sexual dimorphism exists between obesity and chronic disease risk due to differences in the distribution and abundance of adipose tissue. A range of experimental protocols have been employed to demonstrate the role of estrogen in regulating health benefits; however, most studies are confounded by significant differences in body weight and adiposity. Therefore, the purpose of this study was to compare weight-matched obese male and female mice to determine if the sex-dependent health benefits remain when body weight is similar. The development of obesity in female mice receiving a high-fat diet was delayed; however, subsequent comparisons of weight-matched obese mice revealed greater adiposity in obese female mice. Despite excess adiposity and enlarged adipocyte size, obese females remained more glucose tolerant than weight-matched male mice, and this benefit was associated with increased expression of adiponectin and reductions in immune cell infiltration and oxidative stress in adipose tissue. Therefore, the protective benefits of estrogen persist in the obese state and appear to improve the metabolic phenotype of adipose tissue and the individual.
Highlights
Obesity is widely regarded as an independent risk factor for a range of chronic diseases including type 2 diabetes and cardiovascular disease [1, 2]
Expansion of intra-abdominal adipose tissue is associated with increased infiltration and activation of immune cells, and these events are a significant contributor to the systemic inflammation that occurs with obesity [6, 7]
Despite having similar body weights, the adiposity of the female high-fat diet (HFD) mice was greater than the male HFD group as both gonadal and subcutaneous adipose tissue masses were significantly increased (Table 1)
Summary
Obesity is widely regarded as an independent risk factor for a range of chronic diseases including type 2 diabetes and cardiovascular disease [1, 2]. Low-grade systemic inflammation has been put forward as a unifying link between obesity and the onset of these obesity-associated diseases [3,4,5]. Expansion of intra-abdominal adipose tissue is associated with increased infiltration and activation of immune cells, and these events are a significant contributor to the systemic inflammation that occurs with obesity [6, 7]. While an exact explanation for the accumulation of immune cells in adipose tissue is unknown, one potential contributing factor is elevated oxidative stress [8, 9]. Decreasing intraabdominal obesity and/or reducing adipose tissue oxidative stress and inflammation will positively influence chronic disease risk.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
