Abstract：
:Obesity is associated with colon cancer pathogenesis, but the underlying mechanism is actively debated. Here, we confirm that diet-induced obesity promotes tumor growth in two murine colon cancer models and show that this effect is reversed by an orally administered controlled-release mitochondrial protonophore (CRMP) that acts as a liver-specific uncoupler of oxidative phosphorylation. This agent lowered circulating insulin, and the reduction of tumor growth was abrogated by an insulin infusion raising plasma insulin to the level of high-fat-fed mice. We also demonstrate that hyperinsulinemia increases glucose uptake and oxidation in vivo in tumors and that CRMP reverses these effects. This study provides evidence that perturbations of whole-organism energy balance or hepatic energy metabolism can influence neoplastic growth. Furthermore, the data show that glucose uptake and utilization by cancers in vivo are not necessarily constitutively high but rather may vary according to the hormonal milieu.
journal_name
Cell Repjournal_title
Cell reportsauthors
Wang Y,Nasiri AR,Damsky WE,Perry CJ,Zhang XM,Rabin-Court A,Pollak MN,Shulman GI,Perry RJdoi
10.1016/j.celrep.2018.06.008subject
Has Abstractpub_date
2018-07-03 00:00:00pages
47-55issue
1issn
2211-1247pii
S2211-1247(18)30903-3journal_volume
24pub_type
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