Midea discovers important factors affecting fat storage and metabolism

According to the physicist organization network reported on January 6, in the study of the physiological factors that lead to obesity, scientists in the US Jocelyn Diabetes Center determined that TRIP-Br2 as a co-regulator of cell cycle transcription is involved in fat storage and energy metabolism Played an important role. This discovery may lay the foundation for the development of new treatment methods for obesity. The related research report was published on the online version of the "Natural Medicine" magazine.

Transcription co-regulators can control DNA expression by activating or inhibiting gene expression, while TRIP-Br2 can regulate metabolic genes related to fat storage and energy metabolism. Scientists observed the levels of TRIP-Br2 in mice fed low-fat and high-fat foods and obese mice, and found that the levels of TRIP-Br2 in the adipose tissue of mice that ate high-fat foods and obese mice were higher. In addition, they also found that TRIP-Br2 in the visceral fat area of ​​obese people has been significantly improved. The fat accumulated in the middle of the body can have a greater harmful effect than the fat accumulated in other parts.

To elucidate the physiological effects of TRIP-Br2 in fat storage and metabolism, scientists conducted experiments on genetically-treated KO mice that no longer produce TRIP-Br2. They are fed low-fat and high-fat foods, respectively. The test results show that the weight of mice eating high-fat food did not increase significantly, which was basically the same as the weight of mice eating low-fat food. This is because the increase in heat production and the increase in oxygen consumption caused KO mice to consume more Much energy. In addition, the glucose tolerance and insulin sensitivity of KO mice consuming high-fat foods were improved, and triglycerides were also reduced.

When TRIP-Br2 is inhibited, the expression of hormone-sensitive lipase (HSL) and β3 adrenergic receptor (Adrb3) associated with lipolysis is significantly enhanced. When obese and high-fat foods promote TRIP-Br2 levels, it will also suppress the expression of HSL and Adrb3 receptors, resulting in a sharp reduction in energy consumption and an increase in fat accumulation. "Therefore TRIP-Br2 is very important for fat storage. When this element is missing, animals cannot accumulate fat." Research leader Rossit Kulkani, associate professor of medicine at Harvard Medical School, said.

In addition, TRIP-Br2 can also regulate lipolysis, energy output and oxidative metabolism. Kurkani said: "This is the first time that a cell cycle transcriptional regulator can control these processes. Unlike previous studies, TRIP-Br2 seems to exhibit a different mechanism of action this time."

For the treatment of obesity and related complications including insulin resistance, TRIP-Br2 can be described as a promising treatment base. Researchers are currently exploring ways to reduce TRIP-Br2 in visceral fat in order to enhance the expression of HSL and Adrb3 receptors. And the ability to change these two molecules will open up new ways for us to fight obesity. In addition, the research team is also exploring whether the inhibition of TRIP-Br2 and the obesity resistance caused by it will have a relevant effect on cardiovascular disease and metabolic complications.

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