ArticleFrontiers in nutrition2024
High-fat diet mouse model receiving L-glucose supplementations propagates liver injury.
Article in Frontiers in nutrition, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Sex Differences in Body Weight Regulation and Hepatic Insulin Signaling Following Bariatric Surgery and Postoperative Diet in Obese Rats.Obesity surgery · 2026Article
- Electroacupuncture in the treatment of non-alcoholic fatty liver disease: mechanistic insights and therapeutic potential.Frontiers in medicine · 2026Review
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Authors and funding
8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Background and aims: Limited data link manufactured sweeteners impact on metabolic dysfunction-associated steatotic liver disease (MASLD). We aimed to evaluate the effects of manufactured sugars (L-glucose) compared to natural sugars (D-glucose) on phenotype, molecular and metabolic changes in mice models fed with either regular diet (RD) or high fat diet (HFD). Methods: C57BL/6 mice fed 16-weeks with either RD; 70% carbohydrate or HFD; 60% fat, with or without additional glucose (Glu, at 18% w/v) to drinking tap water at weeks 8-16; of either natural (D-Glu) or manufactured (L-Glu) sugars. Liver inflammation (ALT and AST serum levels, liver H&E histologic stains and cell viability profile by p-AKT), liver fibrosis [quantitated Results: D- and L-Glu supplementations propagate hepatocytes ballooning and steatosis in HFD-fed mice and were associated with αSMA down-expressions by 1.5-fold compared to the untreated group while showed an acceleration in liver fibrosis in the RD-fed mice. Lipid profile (Steatosis, ADRP and MDA) significantly increased in HFD-fed mice, both Glu supplementations (mainly the L-Glu) increased serum MDA while decreased ADRP. HOMA-IR score and IR significantly increased in HFD-fed mice, with further elevation in HOMA-IR score following Glu supplementations (mainly L-Glu). The increase in HOMA-IR negatively correlated with IR and Glut2 expressions. D- and L-Glu supplementations showed significant decrease of Glycogenesis (low GYS2/PYGL ratio) and unchanged p-AKT pattern compared to their RD counterparts. Conclusion: Our data indicate an increase in rate of de-novo lipogenesis (DNL) in RD-fed mice (High carbohydrate diet) and liver fibrosis following additional sugar supplementations. In contrast, HFD-fed mice (with pre-existing high lipid profile) supplemented with sugar showed less liver fibrosis, because of reduced de-novo fatty acids synthesis and subsequently, the lipid oxidation pathways become dominated and induce the net results of lipid clearance.
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