High-Sucrose Diet Accelerates Arthritis Progression in a Collagen-Induced Rheumatoid Arthritis Model

ScopeHigh dietary sugar and sweeteners are suspected to cause the development of rheumatoid arthritis (RA) symptoms through the induction of proinflammatory cytokine release. However, the mechanisms by which increased dietary sugar affects RA etiology are not yet fully understood. The study uses a mouse model of collagen-induced RA (CIA) to investigate the relationship between excessive sugar consumption and RA risk.Methods and resultsRA-associated pathological features are assessed in the nonimmunized (NI) control group, the CIA-positive control group, and the CIA + high-sucrose diet (CIA+HS, 63% calories from sucrose) group. Compared with the CIA group, the CIA+HS group shows a greater increase in paw thickness and clinical scores, as well as, a higher degree of pannus formation and inflammation in the knee, ankle, and sole tissues. Moreover, the infiltration of immune cells is increased in the CIA+HS group. Although the expression of hepatic lipogenic genes, is not altered, that of toll-like receptor (TLR4) and IL-1 & beta; is considerably elevated in the CIA+HS group.ConclusionsThese findings suggest that excessive sucrose consumption causes hepatic fibrosis and inflammation, contributing to the pathophysiology of RA. High-sucrose diet enhances TLR4, IL-1 & beta;, and TGF-& beta; expression in the liver, also increases TGF-& beta; expression in immune cells, activates mast cells, neutrophils, and osteoclasts in joint tissue, and increases synovitis, pannus, and cartilage degeneration in joint tissue. Therefore, excessive sugar consumption is a risk factor for RA pathogenesis which is mediated by metabolic perturbations and chronic inflammation. image