In women, elevated levels of androgens, such as in PCOS, increase the risk of obesity and diabetes. Altered adipose tissue function and eating behavior contribute to this increased risk. In these women, plasma levels of the gut hormone ghrelin are lowered. Ghrelin affects appetite, glucose metabolism, and adipose tissue function, and its deletion improves the metabolic phenotype of male mice. Here, we investigated whether the deletion of ghrelin also improves the metabolic phenotype of hyperandrogenic females. Female wild-type (WT) and ghrelin knock-out (GKO) mice were implanted with a DHT-filled implant, or an empty control implant at 20±1d of age. After ~70d, DHT-treated mice completely lacked estrous cyclicity, indicated by prolonged diestrus. Ghrelin deficiency did not affect cyclicity in control or DHT-treated mice. ~90d post-implantation, plasma DHT levels were elevated 1.5-fold versus controls (P=0.001), indicating a mild hyperandrogenism. We assessed the metabolism of the mice in an indirect calorimetry system. In control mice, food intake was 20.3% lower in GKO than in WT mice (P=0.020), but this effect was ablated in DHT-treated mice. DHT treatment increased body weight, but this was mainly due to increased lean body mass. Nonetheless, DHT mice had 12.3% higher fasting blood glucose levels (P=0.048). Moreover, plasma adiponectin levels were decreased by 48.8% (P<0.001), confirming an effect of DHT on adipose tissue function. However, none of these parameters were affected by ghrelin deficiency. Altogether, we showed that mild hyperandrogenism severely disrupted reproductive function, but only caused a mild metabolic phenotype. This suggests that the reproductive phenotype precedes the metabolic phenotype of DHT treatment, not only temporally, but also by dose. Ghrelin deficiency did not impact the studied phenotypes in this mild hyperandrogenic mouse model. It remains to be determined whether ghrelin deficiency could lead to metabolic improvements under more severe metabolic challenges, like severe hyperandrogenism with or without obesogenic diet.