Multiple sclerosis (MS), an autoimmune chronic inflammatory disorder of the Central Nervous System (CNS), leading to demyelination of CNS neurons, with its pathology being related with various genetic and environmental factors, such as diet and obesity. Obesity has reached the dimensions of a global epidemic. It is due to excessive fat accumulation and hypertrophy of adipocytes and results in insufficient energy expenditure in combination with genetic, social and environmental factors. The aim of this review is to analyze at molecular level, the relationship of obesity, as a chronic inflammatory condition, with the pathophysiology of MS as a chronic autoimmune inflammatory disease. Particular emphasis is placed on the role of cytokines, adiponectin and oxidative stress (OS) in neuronal damage and the pathogenesis of MS, in order to understand the complex links between obesity and MS. Chronic inflammation and OS, which are implicated and promoted in obesity, are interconnected processes, causing a toxic state, which contributes to the development of CNS neuroinflammation and neuronal damage, resulting in neuronal demyelination and the onset of MS. Adipose tissue is a complex endocrine organ, in addition to being a lipid storage organ, that secretes cytokines and adipokines, which are involved in the regulation of hormones, metabolism, inflammation, and whole-body homeostasis. Obesity triggers a chronic low-grade inflammation causing insulin resistance (IR) and leptin resistance, disruption of the blood-brain barrier (BBB) and brain metabolism, infiltration of the CNS by immune cells, production of reactive oxygen species (ROS), and generation of oxidative stress (OS). Therefore, obesity affects MS through common underlying mechanisms and thus seems to be a modifiable risk factor for this disease, whilst compounds with multi-functional characteristics, and antioxidant and anti-inflammatory potential could be an additive tool towards the progression of MS and its promotion through obesity.
Varra et al. (Thu,) studied this question.