article · Cellular Physiology and Biochemistry
Vitamin B12 deficiency is known to correlate with increased body mass index and dyslipidaemia, but its direct impact on liver lipid metabolism requires clearer biological evidence. Laboratory experiments on human liver cells cultured under low vitamin B12 conditions revealed substantial alterations in lipid processing compared to controls. Cells grown in low vitamin B12 accumulated significantly more lipid droplets and exhibited increased total intracellular triglycerides. Measurements demonstrated an upregulation of genes controlling the biosynthesis of fatty acids, triglycerides, and cholesterol. Concurrently, cellular concentrations of saturated, monounsaturated, trans, and individual fatty acids rose markedly. The low-vitamin environment also suppressed fatty acid oxidation and damaged mitochondrial respiration and functional integrity. These findings confirm that vitamin B12 deficiency promotes hepatic fat accumulation by accelerating fatty acid synthesis while reducing lipid clearance through oxidation.
Obesity and related metabolic disorders are increasing worldwide. Understanding how micronutrients like vitamin B12 influence fat accumulation in the liver clarifies the underlying cellular mechanisms of dyslipidaemia. By demonstrating that vitamin B12 deficiency directly impairs mitochondrial function and stimulates lipid synthesis in liver cells, this research provides a mechanistic foundation for addressing metabolic liver disease through nutritional and metabolic strategies.
This work represents early-stage basic research conducted on cultured human cell lines. The findings could potentially assist academic and pharmaceutical researchers seeking metabolic targets or biomarkers for lipid disorders and fatty liver conditions. However, the abstract does not indicate any current application pathway, diagnostic tool, or clinical therapeutic ready for commercial development.
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BACKGROUND/AIMS: Rise in global incidence of obesity impacts metabolic health. Evidence from human and animal models show association of vitamin B12 (B12) deficiency with elevated BMI and lipids. Human adipocytes demonstrated dysregulation of lipogenesis by low B12 via hypomethylation and altered microRNAs. It is known de novo hepatic lipogenesis plays a key role towards dyslipidaemia, however, whether low B12 affects hepatic metabolism of lipids is not explored. METHODS: HepG2 was cultured in B12-deficient EMEM medium and seeded in different B12 media: 500nM(control), 1000pM(1nM), 100pM and 25pM(low) B12. Lipid droplets were examined by Oil Red O (ORO) staining using microscopy and then quantified by elution assay. Gene expression were assessed with real-time quantitative polymerase chain reaction (qRT-PCR) and intracellular triglycerides were quantified using commercial kit (Abcam, UK) and radiochemical assay. Fatty acid composition was measured by gas chromatography and mitochondrial function by seahorse XF24 flux assay. RESULTS: HepG2 cells in low B12 had more lipid droplets that were intensely stained with ORO compared with control. The total intracellular triglyceride and incorporation of radio-labelled-fatty acid in triglyceride synthesis were increased. Expression of genes regulating fatty acid, triglyceride and cholesterol biosynthesis were upregulated. Absolute concentrations of total fatty acids, saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), trans-fatty acids and individual even-chain and odd-chain fatty acids were significantly increased. Also, low B12 impaired fatty acid oxidation and mitochondrial functional integrity in HepG2 compared with control. CONCLUSION: Our data provide novel evidence that low B12 increases fatty acid synthesis and levels of individual fatty acids, and decreases fatty acid oxidation and mitochondrial respiration, thus resulting in dysregulation of lipid metabolism in HepG2. This highlights the potential significance of de novo lipogenesis and warrants possible epigenetic mechanisms of low B12.
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DOI: 10.33594/000000368
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