AI Article Synopsis
- - Non-alcoholic fatty liver disease (NAFLD) is a common issue in people who are obese, and a key player in this process is Adenine nucleotide translocase (ANT), which helps transport ADP and ATP in liver cells.
- - Researchers found that knocking out the Ant2 gene in mouse livers increased their ability to burn energy without harming liver health, leading to leaner mice that were more resistant to fatty liver and obesity, even when fed a high-fat diet.
- - The study suggests that inhibiting ANT could be a potential strategy for treating NAFLD and obesity, as seen with the positive effects of a low-dose specific inhibitor, carboxyatractyloside.
Article Abstract
Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disorder in obese individuals. Adenine nucleotide translocase (ANT) exchanges ADP/ATP through the mitochondrial inner membrane, and Ant2 is the predominant isoform expressed in the liver. Here we demonstrate that targeted disruption of Ant2 in mouse liver enhances uncoupled respiration without damaging mitochondrial integrity and liver functions. Interestingly, liver specific Ant2 knockout mice are leaner and resistant to hepatic steatosis, obesity and insulin resistance under a lipogenic diet. Protection against fatty liver is partially recapitulated by the systemic administration of low-dose carboxyatractyloside, a specific inhibitor of ANT. Targeted manipulation of hepatic mitochondrial metabolism, particularly through inhibition of ANT, may represent an alternative approach in NAFLD and obesity treatment.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5316896 | PMC |
| http://dx.doi.org/10.1038/ncomms14477 | DOI Listing |
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