Nature Subsidon: Blowing the air conditioner is not only cool, but also to lose weight!Two doors!

With the improvement of living standards, "obesity/overweight" has become the main problem that plagues most of us. Obesity is related to many non -infectious diseases, including cardiovascular disease, type II diabetes and cancer, have become the main health problems in the world.

"Sweating like rain, burning fat" has become the "golden label" of many obese people as Guiyu.

However, is this "hot -body fever" way of weight loss really healthy?

Recently, Zeng Yuhua's team in Harvard Medical College published a research paper entitled "Brown Adipose Tissue-Derived Mar2 Contributes to Cold-Inflammmation" in "Nature Metabolism". Researchers in the article found that low temperature can generate lipid molecular MARESIN 2 (MAR2) to reduce inflammation caused by the brown adipose tissue (BAT), increasing the sensitivity and glucose tolerance of obesity mice, providing a new method strategy for the treatment of obesity to treat obesity Essence

In the process of obesity, immune cells such as macrophages, neutral granulocytes and lymphocytes will gradually accumulate and interfere with insulin signals in the body in sensitive tissue of insulin, and release inflammatory factor (such as tumor necrosis factors-α (TNF -α), pantin 1β (IL-1β)) produces chronic inflammation and cause metabolic disorders. This is the main way for obesity to damage our health.

In the process of obesity to produce chronic inflammation, our body will also correspond to real estate resistance. The process of "inflammation" is achieved by specific inflammation pro-resolving Mediaators (SPM). SPM is an enzyme substance derived from essential fatty acids. It played a role in inhibiting inflammation reactions and promoting inflammation and regression in the process of tissue inflammation. A large number of studies have shown that chronic inflammation caused by obesity is correlated with SPM synthesis disorders. Lipid molecule Maresin 2 (Mar2) is a type of SPM, and its role in obesity inflammation still needs to be studied.

Studies have shown that low temperature can improve human insulin sensitivity, but its mechanism has not been fully clarified. Cold stimulation can stimulate brown adipose tissue to generate heat. However, its role in the chronic inflammation produced by obesity also needs to be studied.

Fig.1 Cold Exposure Reduces Inflammation and Insulin Resistance and IMPROVES Glucose Tolerance in DIO MICE.

In order to explore chronic inflammation and metabolic disorders caused by whether low temperature can improve obesity. The researchers first raised obese mice (DIO) and normal mice in cold (5 ° C) and heat (30 ° C) for 7 days. It was found that the low temperature significantly reduced the weight of the two groups of male mice, which may be due to the decrease in fat and liver weight. And low temperatures significantly improved the blood sugar and insulin levels increased from high-fat diet, reducing the high TNF-α level (the main inflammatory factor) generated by the high-fat diet induced. These results have the same results in female mice, indicating that there is no gender difference in the improvement of low temperature on obesity inflammation.

Fig.2 Cold Resolves Obesity-INDuced Inflammation in Bat and Liver of Dio Mice.

Immediately after, in order to determine whether it was weight loss, insulin resistance, glucose tolerance and inflammation that affected the low temperature for 7 days. Researchers conducted a short -term low -temperature test. It was found that the low temperature improvement of obesity inflammation and insulin resistance were not affected by weight changes before weight loss.

Further, researchers explored whether low temperature improved obesity inflammation related to specific tissue organs. It was found that the high -fat diet of 14 weeks produced severe inflammation in mice fat tissue and liver. The inflammation in the white adipose tissue is the main site. The inflammation is associated with Gengre1 (F4/80), CCL2, CCR2, ITGAX (CD11C), TNF-α, and II1β high. Although the low temperature improves most of the whole body caused by obesity, it is not effective for epididymal and groin white adipose tissue. In addition, the improvement effect of low temperature is not because of changing the inflammatory response in the white adipose tissue, but other mechanisms.

Fig.3 Cold Increases DHA-DHA-DERIVED Mar2 and Relacted Structural Isomers in Bat and Liver of Dio Mice.

In addition, researchers have found that low temperatures can reduce the process of liver fibrosis by reducing the expression of TLR2 and TGFβ1. This process is achieved by reducing the three -fat levels of rats and other fat synthetic genes. The process of researchers found that the process of lowering liver inflammation reactions was before the accumulation of liver lipids. Fig.4 BAT Secretes Mar2 Isomers in Circulation

Through liquid chromatography, researchers have found that low temperature will increase the MAR2 and its heterogeneous derived of brown adipose tissue and DHA in the liver. Further, the researchers conducted a quantitative analysis of the production of MARESIN channels in the liver. The results showed that the low temperature increased the product of the MAR2 pathway in the brown adipose tissue, which was protected by the liver. What happened instead of liver.

Fig.5 BAT-Specific Loss of Alox12 Increases Inflammation in the Cre/ALOX12-KD OBESE MALE MALE MICE UCP1CRE and CRISPR-C

Finally, the researchers verified the above results in human volunteers. It was found that low -temperature can stimulate activated brown adipose tissue to secrete the product of the MARESIN pathway into the cycle of mice and humans. These results are consistent with the experimental results of mice.

In summary, this study allows us to see a treatment method that can achieve verification of obesity only through physical forms. This strategy is simple and does not have side effects, and has a great application prospect compared to the current commonly used immunosuppressive agents.

Of course, this research also provides strong theoretical support for the majority of "fat people" in the summer!

references:

1.Endle, et al. Agrp Neurons Control Feeding Behavivior At Cortical SynapSapSes Via Peripherald Lysophospholipids. Nat Metab 4, 683–692 (2022).

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