Pharmacologic inhibition of lipogenesis for the treatment of NAFLD

Esler, William P.; Cohen, David E.

doi:10.1016/j.jhep.2023.10.042

Cited by 8 publications

(2 citation statements)

References 106 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, various tumours activate de novo lipogenesis (DNL), which is a process by which cells produce their own fatty acids, and external lipid uptake regardless of the level of circulating lipids [91]. In addition, altered lipid metabolism is often observed in MASLD patients and is associated with changes in lipid biosynthesis and metabolism pathways [92,93]. Hepatic steatosis develops when the accumulation of fatty acids in the liver, through absorption from the bloodstream and DNL, exceeds the capacity of the liver to metabolize these fats through oxidation and to export them as VLDL triglycerides.…”

Section: Lipid Metabolism and Hcc (Figure 3)mentioning

confidence: 99%

“…Hepatic steatosis develops when the accumulation of fatty acids in the liver, through absorption from the bloodstream and DNL, exceeds the capacity of the liver to metabolize these fats through oxidation and to export them as VLDL triglycerides. In particular, de novo FA synthesis is often upregulated in MASLD patients [93,94]. This increase in lipogenesis may provide the necessary substrates for cell membrane formation and energy production in intrahepatic tumour cells.…”

Section: Lipid Metabolism and Hcc (Figure 3)mentioning

confidence: 99%

See 1 more Smart Citation

Molecular Genealogy of Metabolic-associated Hepatocellular Carcinoma

Kodama,

Takehara

2024

Semin Liver Dis

View full text Add to dashboard Cite

This review examines the latest epidemiological and molecular pathogenic findings of metabolic-associated hepatocellular carcinoma (HCC). Its increasing prevalence is a significant concern and reflects the growing burden of obesity and metabolic diseases, including metabolic dysfunction-associated steatotic liver disease, formerly known as nonalcoholic fatty liver disease, and type 2 diabetes. Metabolic-associated HCC has unique molecular abnormality and distinctive gene expression patterns implicating aberrations in bile acid, fatty acid metabolism, oxidative stress, and proinflammatory pathways. Furthermore, a notable frequency of single nucleotide polymorphisms in genes such as patatin-like phospholipase domain-containing 3, transmembrane 6 superfamily member 2, glucokinase regulator, and membrane-bound O-acyltransferase domain-containing 7 has been observed. The tumor immune microenvironment of metabolic-associated HCC is characterized by unique phenotypes of macrophages, neutrophils, and T lymphocytes. Additionally, the pathogenesis of metabolic-associated HCC is influenced by abnormal lipid metabolism, insulin resistance, and dysbiosis. In conclusion, deciphering the intricate interactions among metabolic processes, genetic predispositions, inflammatory responses, immune regulation, and microbial ecology is imperative for the development of novel therapeutic and preventative measures against metabolic-associated HCC.

show abstract

Section: Lipid Metabolism and Hcc (Figure 3)mentioning

confidence: 99%

Section: Lipid Metabolism and Hcc (Figure 3)mentioning

confidence: 99%