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Over the past century, obesity and metabolic syndrome (Mets) have developed into a global epidemic, and many studies have emphasized the immune system regulation of metabolic diseases
In the past century, obesity and metabolic syndrome Metabolic Syndrome (Mets) has developed into a global epidemic, and a number of studies have emphasized the immune system regulation of metabolic diseases
Researchers at Science Science University of Utah School of Health have discovered a specific type of bacteria in the intestines that can prevent mice from becoming obese, indicating that these same microorganisms may also control human weight
Studies have shown that healthy mice have a large number of Clostridium bacteria-a type of 20 to 30 types of bacteria-but those mice with compromised immune systems will lose these microbes in their intestines as they age
Clostridium inhibits intestinal fat absorption
Clostridium inhibits intestinal fat absorption Clostridium inhibits intestinal fat absorption Clostridium inhibits intestinal fat absorptionResearchers have discovered that Clostridium prevents weight gain by blocking the ability of the intestine to absorb fat
Current research has found that one or more molecules produced by Clostridium prevent the absorption of fat in the intestine
Diabetes has discovered a molecular pathway that guides the proper development of T cell-dependent IgA targeting microflora
Defects in intestinal T cell signaling can lead to age-related obesity
Intestinal T cell signaling is defective can lead to obesity, age-related intestinal intestinal T T cell signaling is defective obesity can lead to age-related cell signaling is defective can cause age-related obesityIn the past, almost no mice with compromised immune systems were found to be prone to obesity.
The obesity observed in immunocompromised mice stems from the body's defense system failing to properly recognize bacteria
According to previous studies, obese people also lack Clostridium, which is consistent with the situation in these mice
prevention
Article reference: Charisse Petersen, Rickesha Bell, Kendra A.
Article reference: Charisse Petersen, Rickesha Bell, Kendra A.
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