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Trace glucose and lipid metabolism in high androgen and high-fat diet induced polycystic ovary syndrome rats

DOI: 10.1186/1477-7827-10-5

Keywords: Andronate, Glucose metabolism, Lipid metabolism, High-fat diet, Polycystic ovary syndrome

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Female Sprague-Dawley rats were divided into 3 groups: the control group(C), n = 10; the andronate-treated group (Andronate), n = 10 (treated with andronate, 1 mg/100 g body weight/day for 8 weeks); and the andronate-treated and high-fat diet group (Andronate+HFD), n = 10. The rate of glucose appearance (Ra of glucose), gluconeogenesis (GNG), and the rate of glycerol appearance (Ra of glycerol) were assessed with a stable isotope tracer. The serum sex hormone levels, insulin levels, glucose concentration, and the lipid profile were also measured.Compared with control group, both andronate-treated groups exhibited obesity with higher insulin concentrations (P < 0.05) but similar blood glucose concentrations. Of the two andronate-treated groups, the andronate+HFD group had the most serious insulin resistance (IR). Estrus cycles were completely acyclic, with polycystic ovaries and elevated serum lipid profiles in the andronate+HFD group (P < 0.05). Ra of glucose and GNG increased significantly in the andronate+HFD rats. However, the Ra of glycerol was similar in the three groups.Andronate with HFD rat model showed ovarian and metabolic features of PCOS, significant increase in glucose Ra, GNG, and lipid profiles, as well as normal blood glucose levels. Therefore, aberrant IR, increased glucose Ra, GNG, and lipid metabolism may represent the early-stage of glucose and lipid kinetics disorder, thereby might be used as potential early-stage treatment targets for PCOS.Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in women of reproductive age [1] and is the most frequent cause of hyperandrogenism and anovulation [2]. PCOS is also strongly associated with abdominal obesity, hyperinsulinemia, insulin resistance, and type 2 diabetes [3]. The pathophysiology of PCOS is largely unknown but has been attributed to defects in various organ systems. Uncontrolled ovarian steroidogenesis with a thickened thecal layer that secrets excessive androgen is


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