Hence, future studies should use both outcome measures of hepatic fat/de novo lipogenesis as markers for NAFLD, while simultaneously measuring more specific inflammatory markers ideally related to hepatic fat, e.g., fetuin A, etc. There is some evidence from human and animal studies that suggests a relationship between fructose consumption and increased visceral adipose tissue [51], which is metabolically active and produces numerous inflammatory cytokines, including TNF-α, and IL-6 [52], which may, in turn, induce CRP release in the liver. Here, AHSG is linked to metabolic dysfunction-associated steatotic liver disease.