Introduction

Readily available, highly calorific foods (Briefel and Johnson 2004), together with an increasingly sedentary lifestyle (Winkleby and Cubbin 2004), are causing progressive detriments in human health (Mokdad et al. 1999, Katzmarzyk and Ardern 2004, Rigby et al. 2004). In the USA alone, overweight or obesity afflicts approximately one in three adult women and contributes to a rapidly increasing incidence of type 2 diabetes (NHANES 2006). The current epidemiological evidence suggests that such an escalating prevalence of obesity and diabetes will continue for the foreseeable future (Zimmet 1999, Zimmet et al. 2003). Such a prediction is of particular concern for women's reproductive health because obesity and diabetes contribute markedly to anovulatory infertility (Norman and Clark 1998, Norman et al. 2004), the most frequent cause of infertility in women (Abbott et al. 2004).

Metabolic dysfunction has considerable consequences for polycystic ovary syndrome (PCOS), a highly prevalent metabolic and infertility disorder of reproductive-aged women that is exacerbated by obesity (Ehrmann et al. 1995, Franks 1995, Dunaif 1997, Escobar-Morreale et al. 2004, Carmina et al. 2005). The syndrome has a highly heterogeneous presentation that can include androgen excess, amenorrhea, insulin resistance, and obesity, among other general health disorders (Abbott et al. 2002a, Dumesic et al. 2005). The most recent PCOS consensus diagnosis (The Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group 2004), however, requires the presence of only two out of three specific androgenic and reproductive criteria: (1) hyperandrogenism, as determined biochemically from circulating total or unbound testosterone levels or clinical signs of hyperandrogenism, (2) intermittent or absent menstrual cycles, and (3) polycystic ovaries, as visualized by ultrasound.