In:
eLife, eLife Sciences Publications, Ltd, Vol. 6 ( 2017-04-19)
Abstract:
Obesity and the diseases associated with it are among the biggest healthcare problems in developed countries. The word obesity means, simply, the accumulation of too much fat tissue in the body, but this ignores growing evidence that fat tissue is highly complex. Fat tissue is important for “mopping up” and storing excess calories safely, but also sends messages to the brain and other organs to report how full the body’s energy stores are. Understanding how fat tissues perform these roles will aid the development of strategies to treat or prevent obesity. A hormone called leptin acts as a signal of the status of the body’s fat stores. High levels of leptin in the blood tell the brain that the body has plenty of fat stored. On the other hand, if the levels of leptin in the blood become very low it tells the brain to prioritize finding food and shut down any nonessential processes. This helps to prevent the body from starving. It is not clear how the production of leptin is controlled, in part because fat tissues in different parts of the body behave very differently. Individuals who have a particular rare genetic mutation accumulate large amounts of fat tissue in their upper bodies and gradually lose fat tissue in their arms and legs. Despite accumulating a lot of fat tissue in the upper body, these individuals have extremely low levels of leptin in their blood. To investigate this genetic condition, Rocha et al. studied two children with the mutation and their healthy parents. The experiments show that this mutation alters a protein called mitofusin 2, which is found in cell compartments called mitochondria. Mitofusin 2 helps the mitochondria to bind to each other and to other parts of the cell, which is important for the mitochondria to generate the energy needed for vital cell processes. The mitochondria in the fat cells of the children are less closely linked to each other and have an unusual appearance compared to the mitochondria in the parents’ fat cells. Further experiments showed that some genes, including the one that produces leptin, are less active in the children compared to their parents – while other genes that are involved in starvation or stress responses are more active. This work suggests that mitochondria play an important role in regulating the production of leptin. Furthermore, it suggests that leptin or drugs that switch off stress-related genes may have the potential to be used to treat individuals with this particular mutation.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.23813.001
DOI:
10.7554/eLife.23813.002
DOI:
10.7554/eLife.23813.003
DOI:
10.7554/eLife.23813.004
DOI:
10.7554/eLife.23813.005
DOI:
10.7554/eLife.23813.006
DOI:
10.7554/eLife.23813.007
DOI:
10.7554/eLife.23813.008
DOI:
10.7554/eLife.23813.009
DOI:
10.7554/eLife.23813.010
DOI:
10.7554/eLife.23813.011
DOI:
10.7554/eLife.23813.012
DOI:
10.7554/eLife.23813.013
DOI:
10.7554/eLife.23813.014
DOI:
10.7554/eLife.23813.015
DOI:
10.7554/eLife.23813.016
DOI:
10.7554/eLife.23813.017
DOI:
10.7554/eLife.23813.018
DOI:
10.7554/eLife.23813.019
DOI:
10.7554/eLife.23813.020
DOI:
10.7554/eLife.23813.021
DOI:
10.7554/eLife.23813.022
DOI:
10.7554/eLife.23813.023
DOI:
10.7554/eLife.23813.024
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2017
detail.hit.zdb_id:
2687154-3
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