Obesity is one of the main risk factors for developing type II diabetes. Previous studies have shown that mice lacking a protein known as SH2B1 throughout their body are obese and develop diabetes.
However, researchers from the University of Michigan have now shown that replacing SH2B1 only in the brain of these mice rescues them from obesity, indicating that targeting SH2B1 in the brain might be a new avenue of research for the development of treatments for obesity and type II diabetes.
In the study, which appears online on January 18 in advance of publication in the February print issue of the Journal of Clinical Investigation, Liangyou Rui and colleagues show that SH2B1 is expressed in many tissues related to obesity, including the brain, liver, pancreas, and fat tissue.
Replacing SH2B1 in only the brain of mice lacking SH2B1 prevented the mice from becoming obese. It also prevented the mice from developing obesity after being fed a high-fat diet, indicating that SH2B1 in the brain is required to regulate body weight and fat content.
This study therefore implicates SH2B1 in the brain as a potential target for the treatment of obesity and type II diabetes, two of the most pressing health problems in the developed world today.
Reference: Neuronal SH2B1 is essential for controlling energy and glucose homeostasis (https://www.the-jci.org/article.php?id=29417)
Materials provided by Journal Of Clinical Investigation. Note: Content may be edited for style and length.
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