Effects of anti-inflammatory therapies on glycemic control in type 2 diabetes mellitus

BackgroundThe overall evidence base of anti-inflammatory therapies in patients with type 2 diabetes mellitus (T2DM) has not been systematically evaluated. The purpose of this study was to assess the effects of anti-inflammatory therapies on glycemic control in patients with T2DM. MethodsPubMed, Embase, Web of Science, and Cochrane Library were searched up to 21 September 2022 for randomized controlled trials (RCTs) with anti-inflammatory therapies targeting the proinflammatory cytokines, cytokine receptors, and inflammation-associated nuclear transcription factors in the pathogenic processes of diabetes, such as interleukin-1 beta (IL-1 beta), interleukin-1 beta receptor (IL-1 beta R), tumor necrosis factor-alpha (TNF-alpha), and nuclear factor-kappa B (NF-kappa B). We synthesized data using mean difference (MD) and 95% confidence interval (CI). Heterogeneity between studies was assessed by I-2 tests. Sensitivity and subgroup analyses were also conducted. ResultsWe included 16 RCTs comprising 3729 subjects in the meta-analyses. Anti-inflammatory therapies can significantly reduce the level of fasting plasma glucose (FPG) (MD = - 10.04; 95% CI: -17.69, - 2.40; P = 0.01), glycated haemoglobin (HbA1c) (MD = - 0.37; 95% CI: - 0.51, - 0.23; P < 0.00001), and C-reactive protein (CRP) (MD = - 1.05; 95% CI: - 1.50, - 0.60; P < 0.00001) compared with control, and therapies targeting IL-1 beta in combination with TNF-alpha have better effects on T2DM than targeting IL-1 beta or TNF-alpha alone. Subgroup analyses suggested that patients with short duration of T2DM may benefit more from anti-inflammatory therapies. ConclusionOur meta-analyses indicate that anti-inflammatory therapies targeting the pathogenic processes of diabetes can significantly reduce the level of FPG, HbA1c, and CRP in patients with T2DM.