AI Article Synopsis

  • Metabolic associated fatty liver disease (MAFLD) is a condition where too much fat builds up in the liver, which can lead to serious issues like liver damage and even cancer.
  • Scientists are studying how this disease affects not just the liver, but also the brain, by looking at changes in brain chemistry in mice that are fed different diets.
  • They found that MAFLD can make certain chemicals in the brain higher and can even reduce the overall size of the brain, which might hurt brain cells and how they work.

Article Abstract

Metabolic associated fatty liver disease (MAFLD), commonly known as non-alcoholic fatty liver disease, represents a continuum of events characterized by excessive hepatic fat accumulation which can progress to nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and in some severe cases hepatocellular carcinoma. MAFLD might be considered as a multisystem disease that affects not only the liver but involves wider implications, relating to several organs and systems, the brain included. The present study aims to investigate changes associated with MAFLD-induced alteration of thalamic metabolism in vivo. DIAMOND (Diet-induced animal model of non-alcoholic fatty liver disease) mice were fed a chow diet and tap water (NC NW) or fat Western Diet (WD SW) for up to 28 weeks. At the baseline and weeks 4, 8, 20, 28 the thalamic neurochemical profile and total cerebral brain volume were evaluated longitudinally in both diet groups using H-MRS. To confirm the disease progression, at each time point, a subgroup of animals was sacrificed, the livers excised and placed in formalin. Liver histology was assessed and reviewed by an expert liver pathologist. MAFLD development significantly increases the thalamic levels of total N-acetylaspartate, total creatine, total choline, and taurine. Furthermore, in the WD SW group a reduction in total cerebral brain volume has been observed (p < 0.05 vs NC NW). Our results suggest that thalamic energy metabolism is affected by MAFLD progression. This metabolic imbalance, that is quantifiable by H-MRS in vivo, might cause structural damage to brain cells and dysfunctions of neurotransmitter release.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8786899PMC
http://dx.doi.org/10.1038/s41598-022-05228-5DOI Listing

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