Scientists from the University of Kentucky found the tumor-suppressing Par-4 “supergene” that has been shown to kill cancer cells could help prevent obesity.
The research is published in Frontiers in Oncology and was conducted by Vivek Rangnekar et al.
The team first discovered Par-4 and its role in cell death in prostate tissue in 1993.
Since then, subsequent studies revealed that Par-4 is a tumor suppressor and that increased expression of Par-4 prevents tumor growth.
In the study, the team uncovered a new role for Par-4 as a predictor of future obesity.
They found that lack of Par-4 in mice led to increased fat absorption and fat accumulation in fat-storing cells (adipocytes), which resulted in the development of obesity.
However, genetically restoring the missing Par-4 gene reversed the obesity, making the mice lean again.
Additionally, the study showed that Par-4 loss may serve as a predictor for individuals who could be at risk for developing obesity later in life.
Moreover, the researchers also found that lower expression of Par-4 was linked to obesity in men and women.
They found the risk of developing obesity is much greater in people who have low Par-4 levels compared to those who have high Par-4 levels.
The work reveals a novel function of the tumor suppressor Par-4 in regulating obesity and significantly advances the fields of adipocyte biology, physiology, and metabolism.
Future research is looking into treatment strategies that may be useful to overcome obesity and inhibit obesity-associated cancer, including an ongoing clinical trial using a drug to elevate Par-4 in cancer patients.
If you care about weight loss, please read studies about gamechanger drug that can treat obesity by cutting body weight by 20%, and this weight loss diet may prevent heart disease.
For more information about heart health, please see recent studies about foods that could increase risks of heart disease, and results showing doing exercise this way is best for your heart health.
Copyright © 2022 Knowridge Science Report. All rights reserved.