Nov, 2020 - By SMI
According to previous research, the PHD3 enzyme plays an important role in regulating fat metabolism in certain cancers.
Fat metabolism is a biological metabolic process that breaks down ingested fats into fatty acids and glycerol after which into simpler compounds that can be used with the aid of cells of the body. These compounds ultimately get processed and broken down to produce energy to the body cells. Sugar is the energy source for most cells, however, when nutrients are scarce, cells will break down fat. Now, the research team from Harvard University has found that the lack of a particular enzyme leads to increased fat metabolism and exercise endurance in mice.
People exercise for many reasons, however, the most common reasons are to burn fat and increase physical performance. The researchers are interested in developing the treatments for obesity and want to understand metabolic functions, as well as physiological effects of exercise. During this research, the researchers examined the functions of an enzyme named PHD3 (prolyl hydroxylase 3). According to previous research, PHD3 plays an important role in regulating fat metabolism in certain cancers. The researchers examined isolated mouse cells (sugar-rich) and observed how PHD3 altered the Acetyl-CoA carboxylase 2 (ACC2) enzyme to exert a break in fat metabolism.
The team then examined isolated mouse cells (low-sugar) and found that the AMPK enzyme cancels out the chemical modifications to ACC2. The team then put the animals on fasting to re-form the low-sugar environment, which resulted in the ACC2 modifications, and increased the chemical modifications AMPK. Moreover, the researchers removed the PHD3 and put them on an exercise. The team found a dramatic improvement in some fitness measures in PHD3-deficient mice. PHD3-deficient mice ran around 40% more and 50% farther on the treadmill compared to the control group, and had higher VO2 max, a marker of aerobic endurance. The research was published in the Cell Metabolism journal.
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