As people age, their muscles naturally weaken, a process called sarcopenia, which can lead to frailty and loss of independence. However, recent research from the National University of Singapore published in Nature Metabolism suggests that trigonelline, a compound found in plant-based foods such as coffee, fenugreek seeds, and garden peas, may slow down this muscle decline. Studies indicate that lower levels of trigonelline in the blood are associated with weaker muscles and slower walking speeds in older adults.
Trigonelline a precursor for cellur metabolism and energy production coenzyme
Researchers investigated the potential impact of trigonelline on muscle health by conducting experiments on human muscle cells, mice, and C. elegans. They found that trigonelline serves as a precursor for NAD+ (nicotinamide adenine dinucleotide), a vital coenzyme crucial for cellular metabolism and energy production. NAD+ decline with age contributes to mitochondrial dysfunction and muscle deterioration.
Vincenzo Sorrentino from NUS Medicine’s Healthy Longevity Translational Research Program said that the discovery of trigonelline as a new precursor to NAD+ metabolism enhances our knowledge in this field. According to Sorrentino This finding has the potential to pave the way for interventions using NAD+-producing vitamins for promoting healthy longevity and addressing age-related diseases.
Trigonelline treatment increases NAD+ levels and enhances mitochondrial function in aged muscle cells from humans and mice. Administering trigonelline to elderly mice for 12 weeks improves grip strength and shields against muscle fatigue.
Trigonelline has antiaging effects
Similar to niacin (vitamin B3), trigonelline, shows potential in enhancing lifespan and muscle integrity in C. elegans worms. Its conversion to NAD+ is crucial for these anti-aging effects, as confirmed by worms lacking this ability. Unlike niacin, trigonelline requires additional metabolic steps before contributing to NAD+ production. Enzymes remove its methyl group, converting it to nicotinic acid, which then enters the NAD+ synthesis pathway via the Preiss-Handler pathway.
Certain tissues, such as the liver, efficiently convert trigonelline to NAD+, while others like skeletal muscle show less effectiveness in this conversion. This discrepancy in NAD+ boost from trigonelline could explain why aged mice didn’t experience significant muscle mass increase despite improved muscle strength and endurance.