Figure 6. Schematic of metabolic changes in obese and lean endometrial tumors and impact of metformin treatment.

Metabolic pathways were dysfunctional in obese- versus lean-OCs in KpB mice, reflected by the inability to metabolize glucose, heightened omega-fatty acid oxidation for energy production and indications of impaired SDH/complex II. In the presence of metformin, complex I was inhibited in the OCs from both lean and obese KpB mice. However, when metformin inhibited complex 1 in the complex II impaired ovarian tumors in obese mice, this led to a profound switch in energy production from fatty acid oxidation to glycolysis. Lysolipids were also significantly increased in metformin-treated obese-OCs, leading to further disruption of mitochondrial function.