Fat belly or fat butt? Science tells you the answer

Recently, the latest issue of cell metabolism published a new research result from the University of Oxford in the United Kingdom. They found that differences in the activity of the WNT/β-catenin signaling pathway in different parts of the human body affect the distribution of body fat, and this difference in fat distribution may lead to different risks of diabetes and cardiovascular disease.

The researchers pointed out that common genetic mutations in the WNT signaling pathway are generally related to bone content and fat distribution, which is often closely related to the risk of diabetes and cardiovascular disease. Previous studies have found that rare mutations in the WNT co-receptor molecules LRP5 and LRP6 are also associated with bone and heart metabolic disorders. Researchers studied the role of LRP5 in human adipose tissue and found that people with gain-of-function mutations in LRP5 had higher bone content and lower fat accumulation. In contrast, the LRP5 allele associated with low bone mineral density was associated with increased abdominal fat. Through in vitro experiments, it was found that abdominal fat precursor cells have higher LRP5 expression than hip fat precursor cells, and moderate knockdown of LRP5 in abdominal and hip fat precursor cells can cause dose-dependent damage to the β-catenin signaling pathway, but will produce different results: hip fat production decreases and abdominal fat production increases.

To sum up, this article focuses on how differences in WNT/β-catenin signaling pathway activity at different locations regulate human fat distribution by affecting adipose precursor cells, and also proves that LRP5 can be used as a potential pharmacological target for the treatment of cardiac metabolic disorders.