In:
eLife, eLife Sciences Publications, Ltd, Vol. 8 ( 2019-10-17)
Kurzfassung:
Non-alcoholic fatty liver disease, or NAFLD for short, is a medical condition that develops when the liver accumulates excess fat. It can lead to complications such as diabetes and liver scarring. In humans, mutations that inactivate a protein called MBOAT7 increase the risk of fat accumulating in the liver. Genetic studies suggest that low levels of MBOAT7 in a human’s liver cells increase the severity of NAFLD. Yet the links between MBOAT7, NAFLD and obesity are not well understood. Helsley et al. used data from humans and from obese mice that had been fed a high-fat diet to investigate the relationship between NAFLD and MBOAT7. This revealed that people who are obese have lower levels of MBOAT7 in their livers. Next, obese mice were genetically manipulated to produce less MBOAT7, which led them to develop more severe NAFLD. Helsley et al. then grew human liver cells in the laboratory and lowered their levels of MBOAT7, which led to excess fat accumulating in the cells. This increase in fat accumulation was, at least in part, due to how these cells metabolize fats when MBOAT7 is reduced: they start making more new fats and consume fewer lipids to produce energy. These findings provide a link between obesity and liver damage in both humans and mice, and show how a decrease in MBOAT7 levels causes changes in fat metabolism that could lead to NAFLD. The results could drive new approaches to treating liver damage in patients with mutations in the gene that codes for MBOAT7.
Materialart:
Online-Ressource
ISSN:
2050-084X
DOI:
10.7554/eLife.49882.001
DOI:
10.7554/eLife.49882.002
DOI:
10.7554/eLife.49882.003
DOI:
10.7554/eLife.49882.004
DOI:
10.7554/eLife.49882.005
DOI:
10.7554/eLife.49882.006
DOI:
10.7554/eLife.49882.007
DOI:
10.7554/eLife.49882.008
DOI:
10.7554/eLife.49882.009
DOI:
10.7554/eLife.49882.010
DOI:
10.7554/eLife.49882.011
DOI:
10.7554/eLife.49882.012
DOI:
10.7554/eLife.49882.013
DOI:
10.7554/eLife.49882.014
DOI:
10.7554/eLife.49882.015
DOI:
10.7554/eLife.49882.016
DOI:
10.7554/eLife.49882.017
DOI:
10.7554/eLife.49882.018
DOI:
10.7554/eLife.49882.019
DOI:
10.7554/eLife.49882.020
DOI:
10.7554/eLife.49882.021
DOI:
10.7554/eLife.49882.022
DOI:
10.7554/eLife.49882.023
DOI:
10.7554/eLife.49882.024
DOI:
10.7554/eLife.49882.025
DOI:
10.7554/eLife.49882.026
DOI:
10.7554/eLife.49882.027
DOI:
10.7554/eLife.49882.028
Sprache:
Englisch
Verlag:
eLife Sciences Publications, Ltd
Publikationsdatum:
2019
ZDB Id:
2687154-3
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