| خلاصه مقاله | Background and Aim:
Multiple Sclerosis (MS) is primarily defined by the targeted and coordinated inflammatory breakdown of myelin, resulting in axon loss. A growing of researchs indicates that metabolic alterations, including obesity and elevated BMI, are important risk factors for MS. Adipokines are hormones, such as Adiponectin and Leptin, that are generated by adipose tissue. Leptin can activate various immune cell types and generate inflammatory conditions. adiponectin's reduction results in a rise in highly inflammatory conditions. This study attempted to investigate whether adipokines are associated with MS .and whether they as biomarkers for the desease.
Methods:
We conducted open-dated searches of PubMed, EMBASE, google scholar, medlinebase and scopus, using the terms ‘Multiple sclerosis’ or ‘MS’ AND ‘adipokine OR ‘leptin OR ‘adiponectin.
Results:
Adipokines have an impact on MS and are crucial in the inflammatory conditions. According to study by Matarese et al., MS patients have higher levels of leptin in both serum and CSF. These levels are adversely correlated with the percentage of Treg and with the CSF's production of IFN-𝛾. Along with leptin, which lead to a proinflammatory state, MS patients also have lower adiponectin level. The significance of consistent physical activity, especially exercise training, is being emphasized more and more for those with MS. Based on available data, exercise training has been shown to reduce adipose tissue and, increased levels of adiponectin and decreased level of leptin being linked to a decreased risk of relapse. These adipokines are thought to be biomarkers that aid in predicting the inflammatory conditions associated with MS disease.
Conclusion:
Adipokine-secreting adipose tissues have a significant influence in the risk of MS development, as does an increase in BMI and obesity. Leptin and adiponectin can influence immune cells and secretory cytokines that lead to inflammatory conditions. This state may be advantageous for MS and lead to increased immune system stimulation in this autoimmune illness. |