The role of cytokines in diabetic retinopathy (DR) and effects of fenofibrate on cytokines were explored by observing changes in serum IL-1β, TNF-α, VEGF, and Lp-PLA2 in different stages of DR and the intervention effect of oral fenofibrate on cytokines.In total, 190 patients with type 2 DR were enrolled and divided into 3 groups: diabetic without retinopathy (NDR) group (n = 30), nonproliferative diabetic retinopathy (NPDR) group (n = 80), and proliferative diabetic retinopathy (PDR) group (n = 80). According to whether or not to accept fenofibrate treatment, NPDR and PDR groups were further divided into the NPDR control (NPDR1) group (n = 40) and the NPDR treatment (NPDR2) group (n = 40), and the proliferative diabetic retinopathy control (PDR1, n = 40) group and the proliferative diabetic retinopathy treatment (PDR2) group (n = 40). At 12 weeks after fenofibrate treatment, serum IL-1β, TNF-α, VEGF, and Lp-PLA2 levels were detected.In PDR and NPDR patients, levels of serum cytokines such as IL-1β (120.56 ± 27.32 pg/mL vs 112.34 ± 19.45 pg/mL vs 82.9 ± 13.8 pg/mL), TNF-α (125.86 ± 25.57 pg/mL vs 109.48 ± 20.15 pg/mL vs 80.7 ± 12.8 pg/mL), VEGF (166.65 ± 37.74 pg/mL vs 148.54 ± 36.27 pg/mL vs 88.97 ± 24.86 pg/mL), and Lp-PLA2 (172.34 ± 45.22 μg/L vs 154.66 ± 40.98 μg/L vs 125.88 ± 38.87 μg/L) were significantly higher than in diabetes patients without retinopathy. After fenofibrate treatment, serum IL-1β, TNF-α, VEGF, and Lp-PLA2 significantly decreased in NPDR and PDR patients.Serum IL-1β, TNF-α, VEGF, and Lp-PLA2 play an important role in occurrence and development of diabetic retinopathy. Fenofibrate can reduce cytokine levels in DR patients and improve inflammatory response.

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Complex forms of diabetes are the ultimate common pathway involving multiple genetic variations and multiple environmental factors. Type 2 diabetes (T2DM) is classified as complex diabetes. Varying degrees of insulin deficiency and tissue insulin resistance are two key links to T2DM. The islet β cell dysfunction plays a crucial role in the pathogenesis of T2DM. The decompensation of the islet β cell to insulin resistance is a common mechanism leading to the pathogenesis of T2DM. Available data show that genetic factors mainly affect cell function. At present, a number of susceptibility genes related to T2DM have been reported at home and abroad. In this study, the diabetes-related genes in the case of early-onset diabetes with a significant family history were examined, and our results showed the presence of the intron mutations of catalase (CAT) gene and hepatocyte nuclear factor 1β (HNF1β) gene. The patient enrolled in this study was observed and analyzed, thus, increasing further understanding of the genes associated with diabetes and exploring the pathogenesis of diabetes from the molecular level. This is significant for guiding the prevention, treatment, and prognosis evaluation of diabetes.