Impact of metabolic disorders on prostate cancer growth: Androgen and insulin resistance perspectives

<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>A high prevalence of cancers in metabolic disorders, like metabolic syndrome (MetS) and type 2 diabetes mellitus (T2<jats:styled-content style="fixed-case">DM</jats:styled-content>), recently has been noted, including prostate cancer (<jats:styled-content style="fixed-case">PC</jats:styled-content>), which is androgen‐sensitive. However, the pathological relationship among testosterone and insulin and insulin‐like growth factor (<jats:styled-content style="fixed-case">IGF</jats:styled-content>)‐1 signaling in relation to MetS and T2<jats:styled-content style="fixed-case">DM</jats:styled-content> with <jats:styled-content style="fixed-case">PC</jats:styled-content> remains unclear.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Papers were reviewed, including those by the authors.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>In MetS or the initial stage of T2<jats:styled-content style="fixed-case">DM</jats:styled-content> accompanying insulin resistance, insulin and <jats:styled-content style="fixed-case">IGF</jats:styled-content>‐1 signaling could be essential for <jats:styled-content style="fixed-case">PC</jats:styled-content> growth. In the advanced stage of T2<jats:styled-content style="fixed-case">DM</jats:styled-content>, the decrease in insulin secretion might work against <jats:styled-content style="fixed-case">PC</jats:styled-content> growth. A decrease in testosterone concentration with T2<jats:styled-content style="fixed-case">DM</jats:styled-content> also might suppress <jats:styled-content style="fixed-case">PC</jats:styled-content> proliferation. Androgen deprivation therapy in patients with <jats:styled-content style="fixed-case">PC</jats:styled-content> might increase the risk of MetS and/or T2<jats:styled-content style="fixed-case">DM</jats:styled-content> and consequently cardiovascular events. Certain drugs for T2<jats:styled-content style="fixed-case">DM</jats:styled-content> treatment, such as metformin and glucagon‐like peptide‐1 analog, potentially might be useful for the treatment of <jats:styled-content style="fixed-case">PC</jats:styled-content>.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>The improvement of insulin resistance appears to be essential for the prevention of <jats:styled-content style="fixed-case">PC</jats:styled-content> growth. Further studies are needed to clarify the complicated pathophysiology of metabolic disorders in <jats:styled-content style="fixed-case">PC</jats:styled-content> growth.</jats:p></jats:sec>