In:
eLife, eLife Sciences Publications, Ltd, Vol. 7 ( 2018-02-06)
Abstract:
After we eat, our blood sugar levels increase. To counteract this, the pancreas releases a hormone called insulin. Part of insulin’s effect is to promote the uptake of sugar from the blood into muscle and fat tissue for storage. Under certain conditions, such as obesity, this process can become defective, leading to a condition known as insulin resistance. This condition makes a number of human diseases more likely to develop, including type 2 diabetes. Working out how insulin resistance develops could therefore unveil new treatment strategies for these diseases. Mitochondria – structures that produce most of a cell’s energy supply – appear to play a role in the development of insulin resistance. Mitochondria convert nutrients such as fats and sugars into molecules called ATP that fuel the many processes required for life. However, ATP production can also generate potentially harmful intermediates often referred to as ‘reactive oxygen species’ or ‘oxidants’. Previous studies have suggested that an increase in the amount of oxidants produced in mitochondria can cause insulin resistance. Fazakerley et al. therefore set out to identify the reason for increased oxidants in mitochondria, and did so by analysing the levels of proteins and oxidants found in cells grown in the laboratory, and mouse and human tissue samples. This led them to find that concentrations of a molecule called coenzyme Q (CoQ), an essential component of mitochondria that helps to produce ATP, were lower in mitochondria from insulin-resistant fat and muscle tissue. Further experiments suggested a link between the lower levels of CoQ and the higher levels of oxidants in the mitochondria. Replenishing the mitochondria of the lab-grown cells and insulin-resistant mice with CoQ restored ‘normal’ oxidant levels and prevented the development of insulin resistance. Strategies that aim to increase mitochondria CoQ levels may therefore prevent or reverse insulin resistance. Although CoQ supplements are readily available, swallowing CoQ does not efficiently deliver CoQ to mitochondria in humans, so alternative treatment methods must be found. It is also of interest that statins, common drugs taken by millions of people around the world to lower cholesterol, also lower CoQ and have been reported to increase the risk of developing type 2 diabetes. Further research is therefore needed to investigate whether CoQ might provide the link between statins and type 2 diabetes.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.32111.001
DOI:
10.7554/eLife.32111.002
DOI:
10.7554/eLife.32111.003
DOI:
10.7554/eLife.32111.004
DOI:
10.7554/eLife.32111.005
DOI:
10.7554/eLife.32111.006
DOI:
10.7554/eLife.32111.007
DOI:
10.7554/eLife.32111.008
DOI:
10.7554/eLife.32111.009
DOI:
10.7554/eLife.32111.010
DOI:
10.7554/eLife.32111.011
DOI:
10.7554/eLife.32111.012
DOI:
10.7554/eLife.32111.013
DOI:
10.7554/eLife.32111.014
DOI:
10.7554/eLife.32111.015
DOI:
10.7554/eLife.32111.016
DOI:
10.7554/eLife.32111.017
DOI:
10.7554/eLife.32111.018
DOI:
10.7554/eLife.32111.019
DOI:
10.7554/eLife.32111.020
DOI:
10.7554/eLife.32111.021
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2018
detail.hit.zdb_id:
2687154-3
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