Alcohol Consumption And Metabolic Syndrome

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Both alcohol consumption and metabolic syndrome are risk factors for development of fatty liver diseases with similar pathology which ultimately can result in development of liver cancer.3, 4, 24-273, 4, 23-26 Using a two-stage mouse model in which tumor initiation by DEN was followed by a 35% high fat diet, we have previously reported increased tumor incidence, suggestive of a diet-related promotional effect.11 Consistent with these findings, in the current study, we observed increased adenoma incidence and tumor multiplicity in the HF/CAS group relative to chow controls. More importantly, substituting SPI for casein in the diet produced a marked reduction in hepatic lipid accumulation, inflammation and cell proliferation, resulting in lower tumor incidence and multiplicity. SPI feeding prevented liver weight increase and hepatic steatosis in HF-fed mice relative to mice fed casein (Figure 1). In rats, replacing casein with soy in various feeding regimes has also led to significant reductions in hepatic weight and steatosis .17, 28, 29 This was found to be associated with hepatic activation of PPAR-signaling pathways and inhibition of SREBP signaling which might promote fatty acid utilization over fatty acid synthesis.17 Similar mechanisms may be operating in our mouse model, as SPI induces genes involved in fatty acid uptake, fatty acid degradation and oxidative phosphorylation. The employed model demonstrates protective effects of SPI in early tumorigenesis.
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