Japan discovers gene that prevents people from eating fat

According to reports, a Japanese research team recently reported in the online edition of the British journal Nature Communications that the gene called "ARIA" is related to obesity. If the expression of this gene is suppressed, even if you consume high-fat foods, you will not easily become fat.

Researchers at Kyoto Prefectural Medical University and other institutions have found that this gene has the function of hindering fat burning. When experimental mice whose expression of this gene was suppressed were fed for 14 consecutive weeks and normal experimental mice, it was found that the subcutaneous and visceral fat mass of the former was only 1/3 to 1/2 of that of the latter. When experimental mice whose expression of the "ARIA" gene was suppressed ate ordinary food, their blood sugar levels did not increase, indicating that suppressing the gene could prevent the development of diabetes.

Research leader Koji Ikeda said that if new drugs can be developed that inhibit the effect of this gene, it is possible to find new treatments for obesity.

Scientists are enjoying research on the "obesity gene". In July this year, a report published in the American Journal of Clinical Examination stated that the "obesity gene" called FTO can increase the level of "hunger hormone" in the body and make people more interested in high-calorie foods, making them easy to gain weight.

A few days later, Nagoya University's special lecturer, Mr. Asai, and a joint research team from the United States and Britain also announced the discovery of important genetic genes that suppress obesity, and said it would be of great significance to preventing obesity.

This genetic gene acts on the "MRAP2" gene in the hypothalamus of the brain. The experimenters manipulated the "MRAP2" gene to destroy the corresponding gene functions of mice, so that mice with the gene destroyed and normal mice only ate their favorite foods for 150 days after one month of birth.

The results showed that mice with genetically damaged mice could eat about 10% more and weigh twice that of normal mice, reaching 50 grams. The amount of fat burned and exercise was almost the same as that of normal mice. Even with the same amount of feed, mice whose genes had been damaged were fatter. Asai, a special teacher, said: "This discovery will be expected to develop new drugs to prevent obesity, and can also be applied to the breeding industry to fatten livestock using less feed."

Gender-specific genetic research has also yielded new findings. In May this year, scientists discovered an obesity gene exclusive to women and men. It can be concluded that both of these exclusive genes have been mutated and damaged and are controlled by sex hormones, so they act on women and men respectively. Studies have shown that women-specific genes can promote the growth of adipose tissue, and women with this gene are twice as likely to become fat as the average person. Moreover, almost one-third of women have this "obesity gene". Men with male-specific genes are more likely to become addicted to high-calorie junk food.

The discovery of various genes provides the possibility of implementing targeted genetic intervention therapies in the future, which gives hope to those who have been losing weight for a long time but have failed repeatedly. Despite this, genetic research is still in its infancy, and people cannot blame all the causes of obesity on genes. Simply changing genes cannot fully achieve the effect of body shaping.

As the saying goes: Life lies in exercise. Only by exercising more and paying attention to your diet is the "panacea" to ensure a good body and maintain a good figure.