"Why stress can make you overweight: Hormones turn normal cells into dangerous fat," the Mail Online reports. The headline is prompted by research into the newly discovered role of the Adamts1 hormone in the formation of fat cells.
Findings from the animal and laboratory study suggest the Adamts1 hormone can stimulate the development of fat cells. And in turn, Adamts1 is associated with biological pathways, which seem to be activated by stress and a high calorie diet.
This is exciting and useful research which may pave the way for future study into a safe and effective anti-obesity drug targeting this pathway. However, this experiment alone may not lead to this goal. Additionally, it isn't possible to exclude the involvement of other hormones in this process.
That being said, this study raises awareness about the negative impact of stress on the body, and how it may lead to weight gain; both directly and indirectly, by promoting unhealthy behaviours such as comfort eating and drinking too much alcohol.
Where did the story come from?
The study was carried out by researchers from Stanford University School of Medicine in the US and was funded by the US National Institutes of Health, the Stanford SPARK Translational Research Program, the Glenn Foundation for Medical Research and various other grants.
The study was published in the peer-reviewed medical journal Science Signalling.
The coverage by the Mail Online was generally accurate, highlighting the important fact that this research has not necessarily identified a target for anti-obesity treatment options.
A minor inaccuracy was that the hormone did not influence stem cells to turn into fat cells. These were what are known as "precursor" fat cells – they had already started to become fat cells and the hormone finished the maturation process.
What kind of research was this?
This was a combination of laboratory research, mice and human studies. It aimed to investigate molecular pathways involved in the regulation of fat cells in the body.
Laboratory studies were used to identify new pathways, the theories were initially backed up with experiments on mice. A small human study was then conducted to see if similar mechanisms occurred.
This trial followed a previous human study which found that having a demanding job can trigger weight gain. The researchers wanted to identify if there was a molecular basis for how the stress hormone, cortisol, might be involved in weight gain.
Corticosteroid drugs mimic cortisol as they bind to similar receptors. A side effect of corticosteroids is weight gain, which is why it was of particular interest to the researchers.
Laboratory studies such as this are useful as a first step in the potential development of treatments to prevent or treat obesity.
What did the research involve?
The researchers identified a hormone called Adamts1 which is secreted by fat cells. It appeared to be involved in the regulation of fat cells.
Following this, they wanted to learn more about the role of Adamts1 in that particular cellular pathway and conducted a series of experiments on adipose tissue (fatty tissue) from both humans and mice.
Researchers obtained the mouse cells from 10-week old mice that were given corticosteroids and fed a high fat diet for three months.
Human tissue samples were retrieved from overweight and obese volunteers before and after overfeeding for four weeks.
The study investigated how the expression of Adamts1 changed in both the mouse and human cells with exposure to corticosteroids and diet, and how this affected fat cell regulation.
What were the basic results?
When ADAMTS1 was secreted by fat cells it triggered immature fat cells, called adipocyte precursor cells (APCs) to divide, creating more APCs. When there was less Adamts1, these APCs matured into fat cells.
Adamts1 appears to have two roles; it increases production of APCs but prevents them from maturing.
Corticosteroids reduced the levels of Adamts1, therefore increasing the number of mature fat cells. A similar effect was seen when mice were fed a high fat diet. Interestingly, the number of fat cells increased around their organs (known as visceral fat), while the fat cells under the skin increased in size rather than number.
In the human study, it was not possible to take samples of fat around the organs, but the fat under the skin mirrored the molecular results seen in the mice.
How did the researchers interpret the results?
The researchers concluded: "Our study revealed that Adamts1 -mediated inhibition of APC differentiation [maturation] occurred through an extracellular signalling pathway that translated systemic cues into a molecular switch to favour proliferation [increased number] of APCs over differentiation."
This study investigated the role of a stress-responsive hormone called Adamts1 in the development of fat cells. It found that following exposure to the equivalent of the stress hormone cortisol (corticosteroid) the expression of ADAMTS1 was reduced and in turn the development of fat cells increased.
The researchers hope the results from this study could help scientists understand how fat formation in childhood may influence obesity risk in adulthood.
One of the authors, Dr Brian Feldman commented: "We know that fat is a critical endocrine organ, formed almost exclusively during childhood. The rate of fat formation in childhood has lifelong implications, and understanding how that's controlled and regulated is very important."
Advances in this type of research are exciting and pave the way for future study. Although this experiment alone may not lead to the development of anti-obesity treatments. Additionally, it isn't possible to exclude the involvement of other hormones in this process.
Analysis by Bazian
Edited by NHS Website
Links to the headlines
Mail Online, 25 October 2016
Links to the science
Science Signalling. Published online October 25 2016