“New obesity jab could be available within two years,” the Mail Online reports. The headline comes following news that scientists have identified a protein that may help stimulate the production of brown fat.
Brown fat helps keep mammals warm. In humans, it is mostly found in newborn babies, who are particularly vulnerable to cold. As we age, we do not need brown fat as much, and in adulthood we have mostly white fat. Excess white fat (obesity) can damage your health, whereas brown fat has been linked to protection against obesity and type II diabetes; as such, it has attracted increasing interest and research.
Brown fat also helps to burn calories when the body is exercising (or, less pleasantly, when you are cold enough to shiver). Unlike white fat, it acts like muscle, keeping the body firm and toned.
The study, which involved mice rather than people, found that the new protein helped stimulate the production of brown fat.
The optimism surrounding these findings is based on the hope that researchers could potentially harness the effects of this molecule to develop an obesity treatment in the future.
However, claims that an “obesity jab could be available within two years” seem overly optimistic.
Studies on people are needed before any claims of this kind can be made.
Where did the story come from?
The study was carried out by researchers from Harvard Medical School and the Dana-Farber Cancer Institute, in the U.S., and was funded by grants from the US National Institutes of Health and JPB Foundation.
The study was published in the peer-reviewed science journal Cell.
The Mail Online’s headline that “a new obesity job could be available within two years” is not supported by the publication, although the authors did state that the “therapeutic potential in metabolic diseases is obvious”.
There was a related study, performed by the same research team, in which the effects of the hormone irisin were studied, also in mice. Evidence suggests that irisin can also help stimulate production, by turning white fat into brown fat.
Somewhat confusingly, the Mail Online and the Daily Express seem to have reported on the findings of both studies as if they were a single piece of research.
What kind of research was this?
This was a laboratory study that used mice to identify and investigate the function of hormones released in muscles in response to exercise and cold.
As a result, the authors state there is increasing interest in brown fat – which uses energy to create heat and stops mammals becoming overly cold. In humans, brown fat is mostly found in newborn babies, who are particularly vulnerable to cold (as they have a large surface area to body volume ratio and are unable to shiver). As we age, we do not need as much brown fat to keep us warm, and have mostly white fat. However, brown fat has also been linked to protection against obesity and type II diabetes. Some hope that finding a way to make the body produce more brown fat, or convert white fat into brown fat, may help prevent obesity.
Exercising is a simple way to increase energy expenditure, and helps prevent obesity and associated metabolic disorders. It also increases the circulating levels of certain hormones released from muscle, which are known to mediate some of the beneficial effects of exercise.
The researchers wanted to see if there was the potential to harness some of these hormones to artificially mimic the beneficial effects of exercise, and investigated the role of brown fat in this process.
What did the research involve?
The research involved numerous genetic and protein studies involving mice. They were looking for molecules that were released during exercise and in response to cold, which would give them clues as to how exercise and brown fat activity were generating health benefits. By screening numerous molecules, they sought to identify those that were having the most important effects.
What were the basic results?
- The experiments identified a molecule called meteorin-like (Metrnl), which was present in muscle and fat.
- Circulating levels of Metrnl rose after mice exercised and when they were exposed to the cold.
- Metrnl was found to stimulate energy expenditure and converted regular fat into heat-producing brown fat. Metrnl also improved glucose tolerance – a sign of metabolic health – in mice fed a high-fat diet. It was doing this by interacting with many aspects of the body’s immune system and its temperature regulation systems.
- Blocking Metrnl action stopped these beneficial effects – confirmation that it was heavily involved in this process.
- Metrnl levels increased as a result of repeated bouts of prolonged exercise, but not during short-term muscle activity.
How did the researchers interpret the results?
The researchers concluded that Metrnl’s “therapeutic potential in metabolic diseases is obvious. The recombinant Metrnl protein used here hints at that potential, but other proteins with better pharmacological properties will be required”.
This study identified a molecule that is induced by exercise and exposure to cold. It has been implicated in stimulating brown fat development and improving glucose tolerance – both of which have been linked to a lower risk of obesity and type II diabetes, giving hope that harnessing the effects of this molecule could create obesity treatments.
However, this optimism appears premature, as the research was conducted solely in mice. It will need to be reproduced and validated in humans to see if it is safe and effective at stimulating weight loss or other benefits. These remain unproven at this stage.
Other promised potential “anti-obesity jabs” include leptin and irisin, neither of which have delivered convincing results in human trials. This serves to highlight that when a new compound shows promise in mice, these don’t necessarily translate into effective medicines for humans.
On this basis, the Mail’s headline that a “new obesity jab could be available within two years” appears unjustified.
Analysis by Bazian
Edited by NHS Website
Links to the headlines
Mail Online, 6 June 2014
Daily Express, 6 June 2014
Links to the science
Cell. Published online June 5 2014