ArticleEuropean journal of nutrition2018
Attenuation of liver cancer development by oral glycerol supplementation in the rat.
Article in European journal of nutrition, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Mitochondria-Associated Pathways in Cancer and Precancerous Conditions: Mechanistic Insights.International journal of molecular sciences · 2025Review
- Genetically Predicted Gut Microbiota and Host Metabolites Mediate the Causal Link Between Dietary Factors and Acute Myeloid Leukemia.Food science & nutrition · 2025Article
- Nuclear magnetic resonance-based lipid metabolite profiles for differentiation of patients with liver cirrhosis with and without hepatocellular carcinoma.Journal of cancer research and clinical oncology · 2025Article
- Integration of clinical phenoms and metabolomics facilitates precision medicine for lung cancer.Cell biology and toxicology · 2024Article
- Three-Dimensional Graphene Enhances Neural Stem Cell Proliferation Through Metabolic Regulation.Frontiers in bioengineering and biotechnology · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
purposeGlycerol usage is increasing in food industry for human and animal nutrition. This study analyzed the impact of glycerol metabolism when orally supplemented during the early stage of rat liver carcinogenesis.
methodsWistar rats were subjected to a 2-phase model of hepatocarcinogenesis (initiated-promoted, IP group). IP animals also received glycerol by gavage (200 mg/kg body weight, IPGly group).
resultsGlycerol treatment reduced the volume of preneoplastic lesions by decreasing the proliferative status of liver foci, increasing the expression of p53 and p21 proteins and reducing the expression of cyclin D1 and cyclin-dependent kinase 1. Besides, apoptosis was enhanced in IPGly animals, given by an increment of Bax/Bcl-2 ratio, Bad and PUMA mitochondrial expression, a concomitant increase in cytochrome c release and caspase-3 activation. Furthermore, hepatic levels of glycerol phosphate and markers of oxidative stress were increased in IPGly rats. Oxidative stress intermediates act as intracellular messengers, inducing p53 activation and changes in JNK and Erk signaling pathways, with JNK activation and Erk inhibition.
conclusionThe present work provides novel data concerning the preventive actions of glycerol during the development of liver cancer and represents an economically feasible intervention to treat high-risk individuals.
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