What can we learn from fat mice?
Well, maybe quite a bit.
Researchers from the Washington University School of Medicine in St. Louis have found a way to disable a gene in the cells of mice, preventing them from becoming obese even after being fed a high-fat diet.
Scientists successfully blocked critical inflammatory cells called macrophages, which can locate and destroy particles such as bacteria, viruses, fungi, parasites, and pathogens. Because chronic low-grade inflammation is commonly found in conjunction with obesity, researchers tested the mice to see if reducing inflammation could help control weight gain and obesity. The results of the study were published in The Journal of Clinical Investigation just last month.
Wilma and Roswell Messing Professor of Pathology & Immunology and principal investigator of the study, Steven L. Teitelbaum, MD, asserts that their research has developed a “proof of concept that it is possible to regulate weight gain by modulating the activity of the inflammatory cells,” adding that, “It might work in several ways, but we believe that it might be able to control obesity and its complications by managing inflammation better.”
Couple that with the findings of research from Touro College in New York that reveal obese individuals burn fewer calories than those who aren’t obese. The same is true with mice.
So what did they learn other than fat mice (and people) have low metabolism?
According to Wei Zou, MD, Ph.D., a co-author of the study and assistant professor of pathology and immunology, they found that obese mice maintained the same level of calorie-burning as mice that were not obese. They did this by deleting the ASXL2 gene in the macrophages of the obese mice in the first set of experiments. When tested in a second set, the same result was found after injecting the mice with nanoparticles that interfere with the gene’s activity.
Regardless of being fed high-fat diets, the treated mice burned 45% more calories than the obese mice with an active gene in macrophages. They aren’t quite sure how it prevented obesity in mice. Dr. Teitelbaum explained that despite the mice consuming diets high in fat, they didn’t get fatty livers. He believes that confining the macrophages’ inflammatory effects allows them to burn more fat, resulting in the mice being healthier and leaner.
Co-author and instructor in pathology, Nidhi Rohatgi thinks that it likely has something to do with getting white fat cells, which store fat, to behave like brown fat cells that help to burn stored fat.
Although the study’s approach is nowhere near to becoming actual therapy at this point, researchers are hopeful that it has the potential to help obese people burn fat at rates similar to proportions seen in lean people.
This could eventually mean good news for the more than 80 million Americans who
have fatty liver disease and suffer from obesity.