Multiple Sclerosis and Obesity: Possible Roles of Adipokines

Figure 1

An integrative view of the possible involvement of some adipokines present in patients with multiple sclerosis (MS) at different disease stages. Obesity during adolescence constitutes a relevant risk factor for the later development of MS. Adult obesity negatively affects evolution of the disease and response to treatment in patients with MS. During relapsing-remitting stages, a decrease in adiponectin has been reported as well as, concomitantly, an increase in resistin, adipsin, and leptin concentrations (in serum or CSF or both). Additionally, A-FABP is increased in patients with SPMS, and resistin is also increased in patients with PPMS. Given that inflammation occurs at a variable intensity from the onset of the disease and that neurodegeneration process starts after disease initiation, in this context the adipokines produced by lipid tissue constitute an additional element in the neuroimmunomodulation complex of organisms with MS (see text for further explanation); thus the adipokines produced constitute an additional element in the neuroimmunomodulation complex of organisms with MS (see text for further explanation). RRMS, Remittent Recurrent Multiple Sclerosis. SPMS, Secondary Progressive Multiple Sclerosis. PPMS, Primary Progressive Multiple Sclerosis. CSF, CerebroSpinal Fluid. Resistin (serum) [32–34]. Adipsin (in CSF) [35]. Leptin (serum and CSF) [35]. Adiponectin (in serum) [32, 36, 37]. Chemerin (serum) [38]. A-FABP, Adipocyte-Fatty Acid-Binding Protein (in serum) [39].