Publications by authors named "Daniela Mestre"
Lipid metabolism rearrangements in nonalcoholic fatty liver disease (NAFLD) contribute to disease progression. NAFLD has emerged as a major risk for hepatocellular carcinoma (HCC), where metabolic reprogramming is a hallmark. Identification of metabolic drivers might reveal therapeutic targets to improve HCC treatment.
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- * Researchers have identified MCJ (Methylation-Controlled J protein) as a therapeutic target for NASH, a severe form of NAFLD, as it negatively regulates mitochondrial function in the liver.
- * Targeting MCJ using specially formulated siRNA in mice results in less liver fat and fibrosis by improving fatty acid metabolism and reducing liver cell damage, suggesting that inhibiting MCJ could be a new treatment strategy for NAFLD.
Osteopontin (OPN), a multifunctional cytokine that controls liver glycerolipid metabolism, is involved in activation and proliferation of several liver cell types during regeneration, a condition of high metabolic demands. Here we investigated the role of OPN in modulating the liver lipidome during regeneration after partial-hepatectomy (PH) and the impact that atorvastatin treatment has over regeneration in OPN knockout (KO) mice. The results showed that OPN deficiency leads to remodeling of phosphatidylcholine and triacylglycerol (TG) species primarily during the first 24 h after PH, with minimal effects on regeneration.
View Article and Find Full Text PDFBackground & Aims: Very-low-density lipoproteins (VLDLs) export lipids from the liver to peripheral tissues and are the precursors of low-density-lipoproteins. Low levels of hepatic S-adenosylmethionine (SAMe) decrease triglyceride (TG) secretion in VLDLs, contributing to hepatosteatosis in methionine adenosyltransferase 1A knockout mice but nothing is known about the effect of SAMe on the circulating VLDL metabolism. We wanted to investigate whether excess SAMe could disrupt VLDL plasma metabolism and unravel the mechanisms involved.
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- Methionine adenosyltransferase 1A (MAT1A) and glycine N-methyltransferase (GNMT) play crucial roles in the synthesis and degradation of S-adenosylmethionine (SAMe) in the liver; studying Gnmt(-/-) mice revealed that increased SAMe contributes to liver steatosis despite normal lipogenesis and triglyceride release.
- In Gnmt(-/-) mice, there is an observed increase in the conversion of phosphatidylethanolamine (PE) to phosphatidylcholine (PC), leading to higher levels of diglycerides (DG) and triglycerides (TG), which are linked to fatty liver development.