Potential Roles of Coenzyme Q10 in Obesity Management
Obesity, a chronic metabolic disease with a high global prevalence, is fundamentally driven by mitochondrial dysfunction, oxidative stress, ferroptosis, and chronic inflammation.
Coenzyme Q10 (CoQ10), a key component of the mitochondrial electron-transport chain and a lipid-soluble antioxidant, has shown multidimensional potential in obesity management, opening new avenues for prevention and treatment.
1. Amelioration of obesity-associated mitochondrial dysfunction
The development of obesity is commonly accompanied by mitochondrial impairment. Under normal conditions, mitochondria oxidize metabolic fuels to generate ATP and participate in thermogenesis; however, nutrient excess in obesity saturates the tricarboxylic-acid cycle and the electron-transport chain, leading to reduced mitochondrial mass, compromised membrane potential, and diminished fatty-acid oxidation—manifestations evident in adipose, muscular, and central-nervous tissues.
CoQ10 serves as the central electron carrier from complexes I and II to complex III, participates in fatty-acid metabolism, and modulates the mitochondrial permeability-transition pore; it therefore can directly rectify obesity-related mitochondrial dysfunction, curbing energy-metabolic disturbances at their source.
2. Disruption of the obesity-related “oxidative-stress–inflammation” cycle
Oxidative stress and inflammation are key accelerators of obesity progression. Mitochondrial dysfunction induced by obesity elevates reactive-oxygen-species (ROS) production while reducing antioxidant levels (e.g., superoxide dismutase, vitamins C and E), creating a pro-oxidant–antioxidant imbalance. Excess ROS then activate inflammatory pathways such as NF-κB, prompting macrophages to release pro-inflammatory cytokines (TNF-α, IL-1β) and establishing a vicious “oxidative-stress–inflammation” cycle.
CoQ10 not only scavenges ROS directly, protecting mitochondria and cellular membranes from oxidative damage, but also regenerates vitamins C and E to enhance endogenous antioxidant capacity. Additionally, it modulates the expression of inflammation-related genes and suppresses the release of pro-inflammatory mediators, thereby breaking this detrimental cycle.
3. Regulation of obesity-related cell death
At the level of cell-death control, obesity can trigger adipocyte apoptosis and ferroptosis. Apoptosis is initiated by mitochondrial release of cytochrome c, while ferroptosis relies on iron-mediated lipid peroxidation; both processes exacerbate adipose-tissue dysfunction.
Studies indicate that CoQ10 up-regulates the anti-apoptotic protein Bcl-2 to inhibit apoptosis and, via the CoQ10–NAD(P)H/FSP1 (ferroptosis-suppressor-protein-1) pathway, blocks phospholipid peroxidation to suppress ferroptosis, thereby preserving adipose-tissue cellular homeostasis.
4. Evidence for CoQ10 intervention in obesity
Current research employs diverse CoQ10 supplementation strategies that vary across experimental models.
Animal studies show that CoQ10 supplementation lowers plasma lipid levels, down-regulates TNF-α expression in adipose tissue, improves hepatic oxidative stress and mitochondrial function, and even reduces white-adipose-tissue mass.
In human trials, combined CoQ10 and selenium supplementation has demonstrated potential for preserving skeletal-muscle mass during weight loss. One study administered 240 µg of selenium daily together with CoQ10 to obese individuals and observed increased muscle mass and decreased fat mass during the weight-loss process, offering a novel approach to maintaining metabolic function while shedding excess weight.
Leveraging its regulatory effects on mitochondrial function, oxidative stress, inflammation, and cell death, and supported by a variety of practical supplementation protocols, CoQ10 offers clear theoretical rationale and preclinical evidence for obesity management. Nevertheless, high-quality clinical trials in uncomplicated obese populations are still needed to establish optimal dosing regimens and to clarify its real-world therapeutic value.
References:
[1] Mantle D, Kozhevnikova S, Larsen S. Coenzyme Q10 and Obesity: An Overview[J]. Antioxidants, 2025, 14(7): 871.
*Special note - This article is for informational purposes only and cannot replace a doctor's treatment diagnosis and advice. It should not be regarded as a recommendation or proof of efficacy of the medical products involved. If it involves disease diagnosis, treatment, and rehabilitation, please be sure to go to a professional medical institution to seek professional advice.
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