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Fasting serum fructose is associated with metabolic dysfunction-associated fatty liver disease: A prospective study.
AIM: The association of sugar-sweetened beverages (SSBs) with metabolic disorders has been well studied. However, whether fasting serum fructose is associated with metabolic dysfunction-associated fatty liver disease (MAFLD) is unknown.
METHODS: Participants were enrolled from 2011 to 2012 in Shanghai. Fasting serum fructose concentration was measured with a validated liquid chromatography-tandem mass spectrometry method.
RESULTS: A total of 954 participants without diabetes were included. They were followed for an average of 3.5 years. A total of 320 (33.5%) participants had MAFLD at baseline. With the increase in fasting serum fructose level by quartile, the MAFLD prevalence was increased by 27.0%, 25.0%, 37.4% and 44.5%, p<0.001. Each SD increase in fasting serum fructose level was associated with a 60% increased risk of MAFLD (OR 1.60, 95% CI 1.36-1.88, p<0.001). Fasting serum fructose levels were more closely associated with 4 components of MAFLD (hepatic steatosis, prediabetes, insulin resistance and low HDL). We built a diagnostic model named the fructose fat index (FFI). The AUROC of the FFI was 0.879 (95% CI 0.850-0.908) in the derivation cohort and 0.827 (0.776-0.878) in the validation cohort. Subsequent prospective studies found that the incidence risk of MAFLD was 2.26 times higher in the high-fructose group than in the low-fructose group among female participants (95% CI 1.46-3.49, p<0.001).
CONCLUSION: Fasting serum fructose concentration, which mostly reflects endogenous fructose, was associated with a higher risk of MAFLD. The FFI derived from fasting serum fructose could be used to predict MAFLD. This article is protected by copyright. All rights reserved.
METHODS: Participants were enrolled from 2011 to 2012 in Shanghai. Fasting serum fructose concentration was measured with a validated liquid chromatography-tandem mass spectrometry method.
RESULTS: A total of 954 participants without diabetes were included. They were followed for an average of 3.5 years. A total of 320 (33.5%) participants had MAFLD at baseline. With the increase in fasting serum fructose level by quartile, the MAFLD prevalence was increased by 27.0%, 25.0%, 37.4% and 44.5%, p<0.001. Each SD increase in fasting serum fructose level was associated with a 60% increased risk of MAFLD (OR 1.60, 95% CI 1.36-1.88, p<0.001). Fasting serum fructose levels were more closely associated with 4 components of MAFLD (hepatic steatosis, prediabetes, insulin resistance and low HDL). We built a diagnostic model named the fructose fat index (FFI). The AUROC of the FFI was 0.879 (95% CI 0.850-0.908) in the derivation cohort and 0.827 (0.776-0.878) in the validation cohort. Subsequent prospective studies found that the incidence risk of MAFLD was 2.26 times higher in the high-fructose group than in the low-fructose group among female participants (95% CI 1.46-3.49, p<0.001).
CONCLUSION: Fasting serum fructose concentration, which mostly reflects endogenous fructose, was associated with a higher risk of MAFLD. The FFI derived from fasting serum fructose could be used to predict MAFLD. This article is protected by copyright. All rights reserved.
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