Scientists believe that a “pill which has the same effect as a strenuous workout could keep age-related disease at bay”, reported the Daily Mail today. The paper goes on to declare that a study in mice bred to produce large amounts of a muscle protein that speeds up metabolism, found they were less vulnerable to age-related diseases such as diabetes and hardening of the arteries (atherosclerosis).
According to the newspaper, the researchers maintain that this may be a popular treatment for obesity and related diseases; “You can eat less, but that's unpopular, or you could eat what you want as these animals did and introduce an altered physiology.”
New treatments are usually tested on animals first, but relatively few make it beyond that stage. Until the protein can be tested in humans – several years away at least – the meaning of this research is unclear. For now, people are best advised not to wait for a workout pill, but to keep healthy through physical activity and a good diet, and using established treatments for conditions such as hypertension and obesity.
Dr Allison Gates and colleagues from the US Washington University School of Medicine conducted this research. The study was funded by grants from the National Institute of Health, the Clinical Nutrition Research Unit, the Diabetes Research and Training Centre, and the Digestive Diseases Research Core Centre. The study was published in the peer-reviewed scientific journal: Cell Metabolism .
This was a laboratory study in mice. The researchers were interested in seeing the effect that a higher concentration of a particular protein (called an uncoupled protein - UCP1) in skeletal muscle cells would have on the mice’s survival and diseases.
The researchers bred mice that had a gene mutation affecting the protein (uncoupled mice). The mice’s lifespan and causes of death were compared to normal mice that did not have the protein in their muscles. Both groups of mice were given access to normal food and allowed to live out their natural lives. Using chemical analyses, the researchers compared the proteins in the muscle cells between the two mice groups.
The researchers also investigated what effect the UCP1 protein in muscles had on heart disease. For this, they used mice that had a particular deficiency which meant they developed hyperlipidemia (high cholesterol and other fats in the blood) and atherosclerosis (build up of plaques in the arteries) when fed a high fat diet. These mice are often used to study heart problems, as the disease they develop resembles human vascular disease. The researchers mated some of these mice with the UCP1 mice to compare the effect of the protein in muscles on heart disease.
Mice whose production of UCP1 in muscles could be “turned on” with another chemical were also bred. The researchers compared mice that had the production of UCP1 switched on with mice whose production was not switched on.
The researchers found that the UCP1 mice lived for an average three months longer than normal mice. The longest lifespan was not changed though, with the oldest mice in each group living to around 39 months. They also found that female mice with the UCP1 protein were less likely to have died from lymphoma (cancers of the lymph system) than normal female mice.
Changes in the UCP1 mouse muscles suggested “nutritional deprivation” (i.e. higher levels of certain proteins and lower levels of others). Having the UCP1 protein in muscles seemed to delay the onset of heart disease but did not prevent it. Compared to normal mice, there was less plaque build up in the arteries of UCP1 mice after six weeks on a high fat diet but no difference after 12 weeks on the diet.
The UCP1 mice weighed less than the normal mice and had lower levels of high-density lipoproteins (the fats that carry cholesterol to the liver to be broken down).
The researchers conclude that “respiratory uncoupling”, (i.e. causing the protein UCP1 to concentrate in muscle cells) increased the metabolism in muscles, and this reduced fat deposits and inflammation. The increase in energy consumption had beneficial effects in mice on their survival and the diseases they had. The researchers conclude that “strategies to safely accelerate energy consumption specifically in skeletal muscle could decrease the impact of some common age-related diseases”.
This animal study uses recognised laboratory techniques and reports the methods and results clearly. The research advances knowledge about the effects of mice metabolism on life and how metabolism can be changed at a cellular level.
This discovery of an ability to induce higher metabolic rates in mice (albeit through a genetic mutation) will open up new avenues for future research. In time, this technology may lead to treatments for diseases. Until then, the more established ways of maintaining a healthy metabolism should be the focus. This includes exercising and maintaining a healthy, balanced diet and following other sensible advice to prevent obesity and related diseases.
In the meantime - that is for the next ten years at least - just walk it. An extra 3,000 steps - 30 extra minutes of walking a day - will give your metabolism a boost that will keep your weight constant.