The possible role of Interleukin-6 as a regulator of insulin sensitivity in patients with neuromyelitis optica spectrum disorder

BMC Neurology

Tarlan Varzandi¹  Abolfazl Omidifar²  Zhila Maghbooli²  Abdorreza Naser Moghadasi²  Nasim Rezaeimanesh²  Mohammad Ali Sahraian² 

[1] ;Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences;

关键词: Neuromyelitis optica spectrum disorder;    Hyperinsulinemia;    Insulin resistance;    Interleukin-6;    Interleukin-17;    NMO-IgG;   

DOI  :  10.1186/s12883-021-02198-5

来源: DOAJ

【 摘 要 】

Abstract Background Neuromyelitis optica spectrum disorder (NMOSD) is associated with inflammatory mediators that may also trigger downstream signaling pathways leading to reduce insulin sensitivity. Methods We aimed to determine the risk association of hyperinsulinemia in NMOSD patients with seropositive AQP4-IgG and the serum levels of interleukin (IL)-6 and IL-17A compared with the control group. Serum levels of metabolic (Insulin, Fasting Blood Sugar (FBS), lipid profile) and inflammatory (IL-6 and IL-17) markers were assessed in 56 NMOSD patients and 100 controls. Results Hyperinsulinemia was more prevalent in NMOSD patients independent of age, sex and body mass index (BMI) (48.2% vs. 26%, p = 0.005) compared to control group. After adjusting age, sex and BMI, there was significant association between lower insulin sensitivity (IS) and NMOSD risk (95% CI: Beta = 0.73, 0.62 to 0.86, p = 0.0001). Circulating levels of IL-6 and IL-17 were higher in NMOSD patients, and only IL-6 had an effect modifier for the association between lower insulin sensitivity and NMOSD risk. Conclusions Our data suggests that inflammatory pathogenesis of NMOSD leads to hyperinsulinemia and increases the risk of insulin resistance.

【 授权许可】

Unknown