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The commenter indicated that this conclusion was based on the limited weight gain or lack of weight gain found in animals given these steroids compared to control animals not exposed to the steroids. Based on this information, and after examining weight gain that was observed in this study, and considering the potential mechanism that contributes to these responses (e.g., enhanced insulin sensitivity), this commenter proposed the recommendations to further explore whether similar benefits are obtained with these drugs in humans. Discussion In this pilot clinical trial, we reported the effects of four different long-acting recombinant androgens on a subset of 17S ribosomal RNA (rRNA)-expressed pancreatocytes. We found that the 17S rRNA-transfected androgen-treated rats did not experience a significant weight gain, and neither did the control group of 17S rRNA-transfected rats. However, the androgen-treated rats remained lean as adults: their average weight was about the same as the control group. Further, we found that the androgen-treated animals were not less sensitive to hypoglycemic or insulin resistance than the controls. In contrast, the androgen-treated animals exhibited a significantly greater response to insulin resistance than the controls. In addition, no significant changes in glucose metabolism were observed when the rats were provided with their usual diet. Our findings reveal the potential of rRNA-insect-derived androgens, when paired with insulin, to improve postprandial glucose metabolism and to reduce insulin resistance. These androgen treatments are of critical importance to optimize the long-term efficiency of insulin action in humans, and further investigation of how these effects may be accomplished in humans is warranted. The effects of these androgen treatments on the metabolic response to a diet, as well as insulin resistance, also warrant further study. This additional research will be most likely helpful in providing improved treatment options for individuals whose conditions have been previously demonstrated to be related to altered androgen responsiveness. The mechanism responsible for the effects on body composition described in this study could involve induction of adipogenesis in response to long-term androgen exposure. This pathway is highly conserved among vertebrates. This pathway involves a series of regulatory events involving various genes, including AR, PPARα, and aromatized testosterone. AR participates in the metabolic activation of adipogenesis by stimulating the expression of aromatase (18). At least one other receptor, PPARα, has been implicated in adipogeneization and is believed to be important for the androgen-induced suppression of adiposity (39). In addition, several signaling pathways involved in adipocytogenesis can be activated by AR and PPARα (30, 41 Similar articles: