ArticleNutrition & metabolism2024
Effects of riboflavin deficiency and high dietary fat on hepatic lipid accumulation: a synergetic action in the development of non-alcoholic fatty liver disease.
Article in Nutrition & metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Trial
- Dietary Green Alfalfa Supplementation Reduces Backfat Thickness and Improves Muscle Water-Holding Capacity in Diqing Tibetan Pigs.Foods (Basel, Switzerland) · 2026Article
- Water-Soluble Vitamins (Riboflavin, Niacin, Pantothenic Acid) in Dogs with Chronic Liver Disease vs. Healthy Controls.Veterinary sciences · 2025Article
- Changes in Liver Metabolome Induced by Pterostilbene and Resveratrol in a Rat Model of Liver Steatosis.Molecular nutrition & food research · 2025Article
- Aspirin Eugenol Ester Ameliorates HFD-Induced NAFLD in Mice via the Modulation of Bile Acid Metabolism.International journal of molecular sciences · 2025Article
- Multi-organ multi-omic and gut microbiome markers of fat and sucrose dietary oversupply in cardiometabolic disease.iScience · 2025Article
- Exploring the Link Between Vitamin B Levels and Metabolic Syndrome Risk: Insights from a Case-Control Study in Kazakhstan.Journal of clinical medicine · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
backgroundNon-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in the liver. Riboflavin, one of water soluble vitamins, plays a role in lipid metabolism and antioxidant function. However, the effects of riboflavin deficiency on NAFLD development have not yet to be fully explored.
methodsIn the present study, an animal model of NAFLD was induced by high fat diet feeding in mice and a cellular model of NAFLD was developed in HepG2 cells by palmitic acid (PA) exposure. The effects of riboflavin deficiency on lipid metabolism and antioxidant function were investigated both in vivo and in vitro. In addition, the possible role of peroxisome proliferator-activated receptor gamma (PPARγ) was studied in HepG2 cells using gene silencing technique.
resultsThe results showed that riboflavin deficiency led to hepatic lipid accumulation in mice fed high fat diet. The expressions of fatty acid synthase (FAS) and carnitine palmitoyltransferase 1 (CPT1) were up-regulated, whereas that of adipose triglyceride lipase (ATGL) down-regulated. Similar changes in response to riboflavin deficiency were demonstrated in HepG2 cells treated with PA. Factorial analysis revealed a significant interaction between riboflavin deficiency and high dietary fat or PA load in the development of NAFLD. Hepatic PPARγ expression was significantly upregulated in mice fed riboflavin deficient and high fat diet or in HepG2 cells treated with riboflavin deficiency and PA load. Knockdown of PPARγ gene resulted in a significant reduction of lipid accumulation in HepG2 cells exposed to riboflavin deficiency and PA load.
conclusionsThere is a synergetic action between riboflavin deficiency and high dietary fat on the development of NAFLD, in which PPARγ may play an important role.
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