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Sökning: L773:1932 7420 OR L773:1550 4131 > (2020-2024)

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  • Lopez-Otin, C, et al. (författare)
  • Meta-hallmarks of aging and cancer
  • 2023
  • Ingår i: Cell metabolism. - : Elsevier BV. - 1932-7420 .- 1550-4131. ; 35:1, s. 12-35
  • Tidskriftsartikel (refereegranskat)
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  • Luukkonen, Panu K., et al. (författare)
  • The PNPLA3 I148M variant increases ketogenesis and decreases hepatic de novo lipogenesis and mitochondrial function in humans
  • 2023
  • Ingår i: Cell Metabolism. - : Elsevier. - 1550-4131 .- 1932-7420. ; 35:11, s. 1887-1896.e5
  • Tidskriftsartikel (refereegranskat)abstract
    • The PNPLA3 I148M variant is the major genetic risk factor for all stages of fatty liver disease, but the underlying pathophysiology remains unclear. We studied the effect of this variant on hepatic metabolism in homozygous carriers and non-carriers under multiple physiological conditions with state-of-the-art stable isotope techniques. After an overnight fast, carriers had higher plasma b-hydroxybutyrate concentrations and lower hepatic de novo lipogenesis (DNL) compared to non-carriers. After a mixed meal, fatty acids were channeled toward ketogenesis in carriers, which was associated with an increase in hepatic mitochondrial redox state. During a ketogenic diet, carriers manifested increased rates of intrahepatic lipolysis, increased plasma b-hydroxybutyrate concentrations, and decreased rates of hepatic mitochondrial citrate synthase flux. These studies demonstrate that homozygous PNPLA3 I148M carriers have hepatic mitochondrial dysfunction leading to reduced DNL and channeling of carbons to ketogenesis. These findings have implications for understanding why the PNPLA3 variant predisposes to progressive liver disease.
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  • Romeo, Stefano, 1976, et al. (författare)
  • Leveraging Human Genetics to Identify Potential New Treatments for Fatty Liver Disease.
  • 2020
  • Ingår i: Cell metabolism. - : Elsevier BV. - 1932-7420 .- 1550-4131. ; 31:1, s. 35-45
  • Tidskriftsartikel (refereegranskat)abstract
    • Fatty liver disease (FLD), including its more severe pathologies, namely steatohepatitis, hepatocarcinoma, and cirrhosis, is the most common cause of chronic liver disease worldwide and is projected to become the leading cause of hepatocellular carcinoma and end-stage liver disease. FLD is heterogeneous with multiple etiologies and diverse histological phenotypes, so therapies will ultimately need to be individualized for relevant targets. Inherited factors contribute to FLD, and most of the genetic variation influencing liver disease development and progression is derived from genes involved in lipid biology, including PNPLA3, TM6SF2, GCKR, MBOAT7, and HSD17B13. From this point of view, we focus in this perspective on how human molecular genetics of FLD have highlighted defects in hepatic lipid handling as a major common mechanism of its pathology and how this insight could be leveraged to treat and prevent its more serious complications.
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  • Resultat 11-20 av 34

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