In:
eLife, eLife Sciences Publications, Ltd, Vol. 8 ( 2019-04-15)
Kurzfassung:
Obesity has nearly tripled worldwide since the 1970s. A major health concern related to obesity is that excess fat can spill into organs such as the liver. This can lead to fatty liver disease or even liver cancer. Therefore, it is important to fully understand the mechanisms that lead to fat accumulation in the liver in order to develop new treatments. Our bodies are designed to even out the highs and lows of an unpredictable diet by storing and releasing calories. When we are well-fed, liver cells switch on genes involved in making fat. When we have not eaten for a while, they switch them off and turn on genes involved in burning fat. Each switch involves thousands of genes, controlled by proteins called transcription factors. Some work as activators, turning genes on, whilst others work as repressors, turning genes off. For example, the transcription factor PPAR alpha is a well-known activator that helps to regulate fat burning. However, we know much less about the repressors that stop cells burning fat when there is plenty of food available. To find out more, Sommars et al. studied the repressor BCL6 in mouse liver cells. The results revealed that BCL6 interacts with hundreds of the same genes as PPAR alpha. When the mice were eating, BCL6 turns off the genes involved in fat burning, but when they were starved PPAR alpha activated those genes. However, when BCL6 was experimentally removed, many fat-burning genes were permanently switched on. So, even when mice were fed a high-fat diet, they burned off fat in their livers. Understanding the role of genetic switches like PPAR alpha and BCL6 is crucial for understanding how and why our bodies store energy. This could help us to create treatments that enhance the liver's ability to burn excess fat.
Materialart:
Online-Ressource
ISSN:
2050-084X
DOI:
10.7554/eLife.43922.001
DOI:
10.7554/eLife.43922.002
DOI:
10.7554/eLife.43922.003
DOI:
10.7554/eLife.43922.004
DOI:
10.7554/eLife.43922.005
DOI:
10.7554/eLife.43922.006
DOI:
10.7554/eLife.43922.007
DOI:
10.7554/eLife.43922.008
DOI:
10.7554/eLife.43922.009
DOI:
10.7554/eLife.43922.010
DOI:
10.7554/eLife.43922.011
DOI:
10.7554/eLife.43922.012
DOI:
10.7554/eLife.43922.013
DOI:
10.7554/eLife.43922.014
DOI:
10.7554/eLife.43922.015
DOI:
10.7554/eLife.43922.016
DOI:
10.7554/eLife.43922.017
DOI:
10.7554/eLife.43922.018
DOI:
10.7554/eLife.43922.019
DOI:
10.7554/eLife.43922.020
DOI:
10.7554/eLife.43922.021
DOI:
10.7554/eLife.43922.022
DOI:
10.7554/eLife.43922.023
DOI:
10.7554/eLife.43922.024
DOI:
10.7554/eLife.43922.025
Sprache:
Englisch
Verlag:
eLife Sciences Publications, Ltd
Publikationsdatum:
2019
ZDB Id:
2687154-3
