It is certainly frustrating when we try to stay fit and healthy by getting rid of excess weight, and our bodies rebel against us. “Why do we regain weight after dieting?” is the question that nutrition specialists have been striving to answer, and a new study now offers fresh insights.
Recent studies have shown that despite our weight loss efforts, we tend to gain those pounds right back soon after our dieting program comes to an end.
Some studies also suggest that the reason why our bodies stubbornly insist on storing excess fat could be due to deep-rooted biological mechanisms.
Now, scientists from Monash University in Melbourne, Australia, have discovered yet another key player in the complex mechanism of weight maintenance: a protein called carnitine acetyltransferase (Crat).
Prof. Zane Andrews and team worked with mice and noticed that the Crat protein — which is also found in the human body — seemed to play a decisive role in regulating the storage of fat in the body.
They found that this protein was especially responsive in the context of repeated dieting — or “yo-yo dieting” — which appears to condition the body to “stock up” for the periods of fasting that register as a dangerous situation of resource scarcity.
The team’s findings were published earlier this week in the journal Cell Reports.
One problem with dieting, the study authors explain, is that from an evolutionary point of view, it triggers signals in our bodies to say that we’re experiencing a period of food shortage.
Therefore, when a period of controlled fasting comes to an end, our bodies are conditioned to store as much fat as possible, so that this can be turned into energy later — when we might experience “famine” once more.
This is particularly the case when it comes to yo-yo dieting; it triggers our bodies’ “alarm system.”
The researchers noticed in their experiments with mice that one particular protein, Crat, was key in “telling” the body whether or not keep storing fat in yo-yo dieting conditions.
This protein was found in mice’s brain cells that process the sensation of hunger, and then help to regulate calorie intake and consumption.
However, when the researchers switched off the gene that encodes this protein in some of the animals, they noticed that the weight gain mechanism was immediately impacted.
These mice, when exposed to yo-yo diets, used up their store of fat much faster than their counterparts with an active Crat gene.
This led Prof. Andrews and his colleagues to hypothesize that if we could find a way of switching off the protein’s activity in humans, then we could prevent the body from perceiving dieting as a sign of impending starvation, thus countering the usual rebound response.
“Manipulating this protein offers the opportunity to trick the brain and not replace the lost weight through increased appetite and storage of fat,” Prof. Andrews explains.
Moreover, if a therapy targeting Crat can be developed, it would be useful not just in treating obesity, but also in fighting other metabolic conditions associated with it — including type 2 diabetes.
“By regulating this protein we can ensure that diet-induced weight loss stays off rather than sneaking back on.”
Prof. Zane Andrews