British research has found that if you have gestational diabetes, the risk of developing type 2 diabetes in the future will be 10 times higher! Researchers have developed a new antiviral targeted drug therapy for nasopharyngeal carcinoma! Nature: sialylation of IGE is the decisive factor leading to allergic disease. American scientist: Vaccinia virus that inhibits smallpox can be used to make coronavirus pneumonia-19 vaccine! There should be some people around you and me who can eat whatever they want, hardly exercise, but never get fat. Was he born so lucky? Now, in a study published in Cell magazine, scientists have discovered a gene, which is why these naturally lucky people can stay slim forever. The gene can resist the weight gain of lean people with healthy metabolism. The results show that deleting the gene can make flies and mice thinner, and it is found that its expression in the brain may be related to regulating energy consumption.

Is the cancer target gene actually related to slimness?

ALK is actually a well-known cancer-related gene. Protein encoded by ALK gene plays a key role in cell communication and the development and function of nervous system. The mutation of ALK gene is related to non-small cell lung cancer and neuroblastoma.

After analyzing a health research database, an international team of scientists led by Josef Penninger, director of the Institute of Life Sciences at the University of British Columbia and professor of medical genetics, published a study in Cell magazine, pointing out that some mutations in ALK gene are related to the low sensitivity of naturally thin people to weight gain. Transgenic mice lacking ALK gene also showed obvious obesity resistance.

So far, most studies have focused on obesity, and few studies have paid attention to thinness in human or animal models. Penninger pointed out: "Everyone studies obesity and the inheritance of obesity. But we thought,' let's turn the tables and start a new research field.' Let's study thinness. Therefore, the Penninger team did not pay attention to the risk factors of obese individuals, but began to study slim people.

Researchers searched the database for genetic clues related to emaciation, which contained data of 47 102 healthy people aged 20-44 in Estonia. The researchers conducted genome-wide association studies (GWAS), and compared the DNA samples and clinical data of healthy emaciated people (the population is at the lowest level of 6%) with those of normal-weight individuals, in order to find the genetic variation related to emaciation. They analyzed the genetic characteristics of people with body mass index below 18kg/cm2, and the results showed the genetic variation of ALK gene, which was aimed at thin people.

Mice with ALK removed consumed more calories.

They found two specific variants in ALK gene, which are different from known cancer-driven mutations and related to thinness. Then, they tried to eliminate the equivalent genes in fruit flies. The research team found that this greatly reduced the fat content in the blood. Then, they studied the role of ALK in mice and compared it with the animal control group that exhausted ALK gene. The food intake, daily activity and intestinal lipid absorption of the two groups were the same, but the mice without ALK lost weight and improved their glucose tolerance.

In addition, the results of challenging these animals with a high-fat diet showed that mice without ALK escaped weight gain, but normal mice became obese. The research team reported that mice without ALK seemed to consume more calories. Even though the diet and activities of ALK knockout mice are the same as those of normal mice, they still show low body weight and low body fat from childhood and continue to adulthood. Further analysis shows that ALK with high expression in brain may play a role in guiding adipose tissue to burn more energy.

From: Mobile phone.

ALK inhibitors may be used as a therapeutic strategy for obesity in the future.

ALK has been recognized as an anticancer target, and researchers suggest that targeting this gene may be used as a therapeutic strategy for obesity in the future.

Michael Orthofer, the first author of the study and a postdoctoral researcher at the Vienna Institute of Molecular Biology, said in a press release that the gene plays a role outside the digestive system. Orthofer explained: "Our research shows that ALK plays a role in the brain, and the brain regulates metabolism by integrating and controlling energy consumption. 」

Josef Penninger, a senior author, director of the Institute of Life Sciences at the University of British Columbia and professor of medical genetics, pointed out that research may be conducted in the future to determine how ALK regulates human metabolism to promote weight loss. Penninger said in a statement: "If you think about it, we can determine whether we are still slim by turning off ALK and reducing its functions. At present, ALK inhibitors have been used in cancer treatment, and we can inhibit ALK through them. In fact, we will try to do so. 」