When we try to stay healthy by getting rid of excess weight, our bodies rebel. Nutrition experts have struggled to answer this question, and now a new study offers new insights. Recent studies have shown that despite our weight loss efforts, we tend to regain the weight soon after our dieting program ends. Some studies have also suggested that our bodies’ stubborn insistence on storing excess fat may be due to deeply ingrained biological mechanisms. Now, scientists from Monash University in Melbourne, Australia, have discovered another key player in the complex mechanism of weight maintenance: a protein called carnitine acetyltransferase (Crat). Prof. Zane Andrews and his team worked with rats and noticed that the Crat protein, which is found in humans, seems to play a decisive role in regulating the storage of fat in the body. They found that this protein is particularly sensitive in the context of repeated dieting (or “yo-yo dieting”), which seems to make the body “hoard” a period of fasting, a dangerous state of scarcity. The authors of the study explain that one of the problems with dieting is that, from an evolutionary perspective, it triggers signals in our bodies that we are experiencing a period of food shortage. So when a period of controlled fasting is over, our bodies are accustomed to storing as much fat as possible so that this can be converted into energy when we might experience a “famine” again. This is especially true during repeated fasts; it triggers our body’s “alarm system”. In their experiments, the researchers found that a particular protein, Crat, is key to “telling” the body whether to continue storing fat. The protein, which is found in the brain cells of rats, processes hunger and then helps regulate calorie intake and consumption. However, when the researchers turned off the gene that encodes the protein in some of the animals, they noticed that the mechanism for weight gain was immediately affected. When these rats were exposed to repeated dieting, they stored fat much faster than those with the active Crat gene. This led Prof. Andrews and his colleagues to hypothesize that if we could find a way to isolate the protein’s activity from the body, then we could prevent the body from seeing dieting as a signal of impending hunger, thus countering the usual rebound response. “Manipulating this protein provides an opportunity to trick the brain instead of losing weight by increasing appetite and storing fat instead,” explains Prof. Andrews. Furthermore, if a treatment for Crat can be developed, it could be used not only to treat obesity, but also to combat other metabolic diseases associated with it – including type 2 diabetes. By regulating this protein, we could ensure that diet-induced weight loss is not compromised, rather than sneaking back in.