2025/06/13

Your Health Supporter: Hyaluronic acid & Biotin

Your Health Supporter: Hyaluronic acid & Biotin

Hyaluronic acid and biotin play essential roles in maintaining cellular health and energy balance.

Hyaluronic acid helps retain moisture in the body and supports the integrity of skin tissues, joints, and the extracellular matrix. Its exceptional water-binding capacity enhances skin elasticity and barrier function while protecting cells from oxidative stress. Recent studies have also highlighted its role in supporting mitochondrial function and energy production.

Biotin is a water-soluble vitamin essential for energy metabolism and protein synthesis. It optimizes the metabolism of carbohydrates, fats, and proteins in the body. In particular, biotin plays a key role in maintaining the health of hair, skin, and nails while supporting mitochondrial function and oxidative stress regulation.

Hyaluronic Acid & Mitochondrial Health

1. Mitochondrial Protection

During energy production, mitochondria naturally generate reactive oxygen species(ROS), which, in excess, can damage mitochondrial DNA and impair function. Hyaluronic acid acts as a protective barrier around cells, helping to reduce oxidative stress and preserve mitochondrial integrity and stable ATP production.

2. Mitochondrial Biogenesis Support

The body has the ability to generate new mitochondria as needed. Hyaluronic acid activates cellular signaling pathways that support the maintenance of mitochondrial function and assist in the process of mitochondrial biogenesis.

3. Activation of Mitophagy

To maintain healthy cellular function, damaged mitochondria must be promptly removed. Hyaluronic acid promotes mitophagy—the selective degradation of dysfunctional mitochondria—helping to preserve mitochondrial quality, improve energy efficiency, and delay cellular aging.

 

Biotin & Mitochondrial Health

1. Activation of Mitochondrial Enzymes

Biotin acts as a coenzyme for key metabolic enzymes within the mitochondria, facilitating carbohydrate, fat, and protein metabolism. Adequate biotin levels are necessary for efficient energy production and nutrient utilization. Biotin deficiency can lead to reduced mitochondrial energy output and increased fatigue.

2. Stabilization of Mitochondrial Membrane Potential

Mitochondria must maintain a stable membrane potential to efficiently produce ATP. Biotin supports this membrane potential, optimizing ATP production and helping to suppress excess ROS generation, thereby reducing cellular stress.

3. Regulation of Protein Acetylation

In the absence of sufficient biotin, mitochondrial proteins can become abnormally acetylated, leading to impaired energy metabolism and heightened sensitivity to oxidative stress. Biotin helps normalize this process, playing a critical role in maintaining mitochondrial function and cellular energy balance.

Hyaluronic acid acts as a protective and regenerative shield for mitochondria, while biotin serves as a key enabler of efficient energy production within them.

Together, they help build and power the cellular “energy factories,” offering a foundational strategy for supporting mitochondrial function, cellular vitality, and overall health.

 

References

  1. Grishko, V., Xu, M., Ho, R., Mates, A., Watson, S., Kim, J. T., ... & Pearsall, A. W. (2009). Effects of hyaluronic acid on mitochondrial function and mitochondria-driven apoptosis following oxidative stress in human chondrocytes. Journal of Biological Chemistry, 284(14), 9132-9139.

  2. Zhang, F., Wang, S., Gao, M., Li, B., He, Z., Tang, T., ... & Zhou, Z. (2022). Hyaluronic acid ameliorates intervertebral disc degeneration via promoting mitophagy activation. Frontiers in Bioengineering and Biotechnology, 10, 1057429.

  3. Depeint, F., Bruce, W. R., Shangari, N., Mehta, R., & O’Brien, P. J. (2006). Mitochondrial function and toxicity: role of the B vitamin family on mitochondrial energy metabolism. Chemico-biological interactions, 163(1-2), 94-112.

  4. Lohr, K. M., Frost, B., Scherzer, C., & Feany, M. B. (2020). Biotin rescues mitochondrial dysfunction and neurotoxicity in a tauopathy model. Proceedings of the National Academy of Sciences, 117(52), 33608-33618.

 

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