The Role of Dyslipidemia in Colitis-Associated Colorectal Cancer

Figure 1

Lipid metabolism of cancer. Reprogrammed cancer cells not only acquire lipid species by uptake of exogenous lipids through diffusion and transmembrane channel CD36 but also endogenously synthesize fatty acids. The precursor mass of de novo synthesized fatty acids is initiated by pyruvate of glycolysis metabolites and NADPH of the pentose phosphate pathway. Following several key enzymes involved in lipogenesis, acetyl-CoA is aggregated as 16-carbon saturated palmitate. By the desaturation of SCD-1, the saturated fatty acid is converted into monounsaturated fatty acid, but polyunsaturated lipids are mostly acquired by exogenous supplements. These lipids function as lipid mediators in cellular signaling transduction, build cellular membrane blocks, modify substrates by lipid modification, and are directly utilized to generate ATP molecules by β-oxidation. Excess lipids are also stored in lipid droplets. FASN: fatty acid synthase; ACC: acetyl-CoA carboxylase; ACLY: ATP-citrate lyase; HMG-CoA: 3-hydroxy-3-methylglutaryl-CoA; SFAs: saturated fatty acids; MUFAs: monounsaturated fatty acids; PUFAs: polyunsaturated fatty acids; LDH: lactate dehydrogenase; TCA cycle: tricarboxylic acid cycle; SREBPS: sterol regulatory element-binding proteins; CM: chylomicrons; TGRL: triglyceride-rich lipoprotein lipase.