Coenzyme Q10 in Metabolic syndrome

Metabolic syndrome (MS) has become a global health issue due to affect a high percentage of people in most of the countries. MS can be defined as the presence of three of the following factors: obesity, high triglyceride and cholesterol levels, low HDL cholesterol, high blood pressure or high fasting plasma glucose. All these factors increase the risk of cardiovascular disease, diabetes type II, some kind of cancers, sleep abnormalities or physical incapacity among other. Several factors have been identified in the aetiology of MS such as dietary patterns, sedentary lifestyle, genetic background, microbiota, socioeconomic status or age. Different treatments have been proposed for the treatment of MS, but, until today, there is no efficient solution. CoQ10 has emerged as a potential way in MS treatment endorsed by several clinical trials have shown improvements in lipid profile, glucose control, insulin homeostasis and hypertension control in MS patients. The molecular mechanism that could explain these improvements would be the antioxidant capacity of CoQ10 inhibiting oxidative stress that it is present in MS. Additionally, the proportion of CoQ10H2 could be also a crucial role in the protection again MS components. Furthermore, CoQ10 administration could be also helpful in the management of mitochondrial dysfunction associated to MS

Targeting Mitochondrial Defects to Increase Longevity in Animal Models of Neurodegenerative Diseases

International audienceBioenergetic homeostasis is a vital process maintaining cellular health and has primary importance in neuronal cells due to their high energy demand markedly at synapses. Mitochondria, the metabolic hubs of the cells, are the organelles responsible for producing energy in the form of ATP by using nutrients and oxygen. Defects in mitochondrial homeostasis result in energy deprivation and can lead to disrupted neuronal functions. Mitochondrial defects adversely contribute to the pathogenesis of neurodegenerative diseases such as Alzheimer's (AD) and Parkinson's disease (PD). Mitochondrial defects not only include reduced ATP levels but also increased reactive oxygen species (ROS) leading to cellular damage. Here, we detail the mechanisms that lead to neuronal pathologies involving mitochondrial defects. Furthermore, we discuss how to target these mitochondrial defects in order to have beneficial effects as novel and complementary therapeutic avenues in neurodegenerative diseases. The critical evaluation of these strategies and their potential outcome can pave the way for finding novel therapies for neurodegenerative pathologies