Carotenoids in Orange Carrots Mitigate Against Non‐alcoholic Fatty Liver Disease Progression

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BackgroundCarotenoids are naturally occurring compounds found in brightly colored fruits and vegetables. Increased consumption of these dietary sources may alleviate the harmful effects of the high‐fat diet. They can be used as co‐adjuvant against metabolic syndrome (MetS). Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of MetS characterized by the extensive lipid deposition in the liver tissue without significant alcohol intake. Mechanistically, NAFLD results from imbalanced hepatic lipid homeostasis stemming from elevated hepatic triglyceride (TG) uptake, upregulated fatty acid (FA) synthesis, or decreased β‐oxidation.ObjectiveThe purpose of the study was to illustrate the impact of carotenoid‐rich whole foods on obesity‐associated NAFLD progression.MethodsMale C57BL/6J mice (n = 48) were randomized to one of four experimental diets for 15 weeks (n=12 animals/diet): Low‐fat diet (LFD, 10% calories from fat), high‐fat diet (HFD, 60% calories from fat), HFD with 20% white carrot powders (HFD+WC), and HFD with 20% orange carrot powders (HFD+OC). The concentrations of α‐carotene and β‐carotene in carrot powders, diet pellets, serum, liver, and feces were detected by analytical assays. Tissue histology and TG content analysis were used to depict the extent of hepatic steatosis. Western blot and qPCR were utilized to observe trends of fatty synthesis and β‐oxidation.ResultsThe HFD+OC group reduced weight gain significantly compared to the HFD group and efficiently decreased hepatic lipid accumulation based on the histological and TG analysis. We observed minimal down‐regulation of FA synthesis proteins in the HFD+OC group as depicted by Western blot and qPCR. On the other hand, the HFD+OC treatment significantly enhanced β‐oxidation proteins, possibly by promoting master regulators of hepatic lipid metabolism (i.e., p‐AMPK, PGC‐1α, PPARα).ConclusionsCarotenoids in orange carrots may decrease the severity of hepatic steatosis in NAFLD by partial inhibition of fatty acid synthesis and increased activity of β‐oxidation.