Unlimited food

Who wouldn't want to eat unlimited and still stay slim and fit? This is exactly what genetically modified mice did, as part of a study carried out at the Weizmann Institute of Science and recently published in the scientific journal Cell Reports. The mice did not get fat, even when they ate more than usual, they were in better shape than normal mice, and their heart function improved.

Who wouldn't want to eat unlimited and still stay slim and fit? This is exactly what genetically modified mice did, in part From research which was carried out at the Weizmann Institute of Science and was recently published in the scientific journal Cell reports. The mice did not get fat, even when they ate more than usual, they were in better shape than normal mice, and their heart function improved.

"The mice remained lean even though they ate fatty food, probably thanks to the increased metabolism in their muscle cells. The metabolism led to increased energy consumption and an increase in heat production throughout the body," he says Prof. Eitan Gross, from the Department of Biological Control at the Weizmann Institute of Science. The metabolic level of the mice in the study resembled, in many respects, the levels reached by the body during strenuous physical activity, but the mice reached these levels even when they did not move from their position. They experienced an improvement in blood sugar metabolism and high levels of lactic acid in the muscle cells, and developed a large number of muscle fibers that consume large amounts of oxygen. These fibers are usually activated during long-term physical activity. The mice passed the exercise test on a treadmill more successfully than the mice in the control group, and their hearts functioned more efficiently.

The genetic research of the mice focused on a gene called MTCH2 - or "Mitch", as it is affectionately called in the laboratory - which Prof. Gross discovered more than a decade ago. In the past, Prof. Gross's group discovered that in certain body systems the Mitch protein suppresses the function of tiny intracellular organelles called mitochondria, which produce the energy for the entire cell (Mitch is found in the membranes of these organelles). In the new study - which was led by (then) research student Dr. Liat Bouzglou-Azriel, in collaboration with other members of Prof. Gross's group - the scientists found that when this suppressive factor is absent, that is, when the Mitch protein is missing, and the mice do not gain weight despite eating large amounts Large amounts of high-fat food, the mitochondria grew at least fivefold, and their activity greatly increased, indicating an increased metabolism.

This phenomenon may sound blessed, but in fact it is possible that it is the cell's coping with stress. It is known that during severe stress Mitch participates in cell suicide: when signals reach it regarding the existence of such stress, Mitch contributes to the appearance of holes in the mitochondria and their disintegration, resulting in the death of the cell. However, now that the increased metabolism in Mitch-deficient mice has been discovered, it is possible that these signals are not suicide signals at all, but actually call-to-action signals. "It seems that the cell is not in a hurry to die," says Prof. Gross. "His first reaction to Aka is, first of all, increasing the metabolism to deal with the threat and survive it. Only later may the cell die, for example, if the strain goes on and on."

It is possible that in light of these findings it will be necessary to re-evaluate the role of mitochondria in the cell. It seems that these organelles not only produce energy, but also play a decisive role in determining the fate of the cell. In addition, it is possible that the findings will help in future developments of new ways to treat obesity and diabetes, since it is known that there is a tendency to obesity in people with certain mutations in Mitch. Also, this gene is often associated with diabetes and other metabolic diseases, and the new research indicates that, in the future, it may be possible to alleviate these diseases by temporarily silencing Mitch. "No one is guaranteeing that people will be able to take a pill instead of exercising, but maybe we can develop ways to control Mitch's activity to balance the metabolism," says Prof. Gross.

Dr. Yehudit Salzman, Dr. Liat Shekhnai, Elad Bashet, Dr. Inbal Michilovitsi, Dr. Alona Server and Prof. Eldad Tzhor from the Department of Biological Control participated in the study; Dr. Yael Kuperman and Dr. Michael Tzuri from the Department of Veterinary Resources; and Dr. Smeder Levin Zidman from the Department of Chemical Research Infrastructures - all from the Weizmann Institute of Science. In addition, Dr. Michal Haran from the Kaplan Medical Center and Dr. Cecil Vernochet from the "Pfizer" company in the United States participated.