Abstract
Several diseases including microbial infection, rheumatoid arthritis, multiple sclerosis, and cancer have been linked to fatigue. They all have in common an upregulation of cytokines, including interleukin (IL)-1β and tumor necrosis factor-α (TNF-α), which may interfere with clock gene functions (1). Increasing evidence associates type 2 diabetes with inflammatory processes characterized by elevated production of proinflammatory cytokines and infiltration of immune cells. Reducing IL-1 activity in prediabetes and diabetes improves insulin secretion, glycemic control, and markers of systemic inflammation (2–4). Given this background, we hypothesized that fatigue levels may be increased in type 2 diabetes and may be improved by IL-1β antagonism. Within a placebo-controlled, double-blind study of IL-1β antagonism with a monoclonal anti–IL-1β …
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
