Obesity: A Global Public Health Challenge – New Metabolic Pathway Discovered for Weight Regulation Independent of GLP-1 Mechanisms

A metabolite of taurine is known as N-acetyltaurine, which is formed when taurine binds to another molecule called acetate. The level of N-acetyltaurine in the body fluctuates in response to physiological changes (including endurance exercise and diet) that affect taurine and acetate levels. To date, the enzymes involved in N-acetyltaurine metabolism and the potential functions of N-acetyltaurine itself have remained unclear.

PTER is N-acetyltaurine Hydrolase

In this study, scientists discovered that an enzyme called PTER (phosphotriesterase-related), which is associated with BMI, acts as the hydrolase for N-acetyltaurine. It can hydrolyze N-acetyltaurine into taurine and acetate. In mice, PTER is expressed in the kidneys, liver, and brainstem. Knocking out the Pter gene in mice resulted in the complete loss of N-acetyltaurine hydrolytic activity in tissues, leading to a systematic increase in N-acetyltaurine levels in the blood and tissues of the mice.

Metabolic Phenotype of Pter-Knockout Mice

Subsequently, the research showed that when obese wild-type mice (with intact Pter gene) were administered N-acetyltaurine, it also reduced food intake and body weight in a manner dependent on the functional GFRAL receptor. Notably, the PTER pathway is independent of the pathway used by currently marketed GLP-1 receptor agonists.

Effects of N-acetyltaurine Administration on Mice

Perhaps one day, we could promote the formation of N-acetyltaurine through probiotics or dietary interventions to reduce body weight. However, there is still a long way to go to achieve this goal.

References

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