APN deficiency limited adiposity and mitigated HFD-induced insulin resistance and adipose tissue inflammation in gonadally intact male and female, but not in OVX mice. ![]() Indirect calorimetry was used to determine observed phenotype differences. Therefore, a subsequent HFD experiment was performed utilizing male and female (both gonadally intact and OVX) APN deficient mice (APN −/−) and wildtype littermates to determine if APN is the factor which protects OVX females from the similar degree of metabolic dysfunction as males in the setting of obesity. However, despite a higher body fat percentage and a similar degree of hepatic and skeletal muscle lipid accumulation, female OVX HFD-fed mice exhibited enhanced insulin sensitivity relative to HFD-fed males. In corroboration with previous data, estrogen deficiency (OVX) exacerbated HFD-induced obesity in female mice. Body composition, adipose tissue inflammation, ectopic lipid accumulation as well as glucose metabolism and insulin resistance were assessed. An additional group of HFD ovariectomy (OVX) mice were included to assess estrogen deficiency’s impact on obesity. An initial experiment was performed in which gonadally intact male and female mice were fed either a purified low-fat diet (LFD) or high-fat diet (HFD) (40% kcals from fat) for 16 weeks. We proposed to determine if adiponectin (APN) serves as this protective factor. ![]() However, epidemiological data suggests that males are more prone to developing T2D, and at a lower BMI, compared to females during post-menopausal years suggesting that another factor, other than estrogen, protects females. The general consensus is that estrogen is protective, whereas its deficiency in post-menopause is associated with adiposity and impaired insulin sensitivity. ![]() Epidemiological literature indicates that women are less susceptible to type II diabetes (T2D) than males.
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