■脂肪因子和炎性细胞因子(ADIC)在2型糖尿病(T2DM)中发挥重要作用。本研究旨在比较不同降糖药物对初诊T2DM患者ADIC水平的影响。并进一步研究这些变化对代谢指标的影响,β细胞功能和胰岛素抵抗(IR)。
■来自中国25个中心的四百一十六例新诊断的T2DM患者随机接受了48周的艾塞那肽干预,胰岛素或吡格列酮。人体测量和实验室数据,β细胞功能和IR指标,和AIDC的水平,包括白细胞介素-1β(IL-1β),干扰素-γ(IFN-γ),瘦素,在基线和研究结束时检测到成纤维细胞生长因子21(FGF21)。
■总共,281名参与者(68%为男性,年龄:50.3±9.4岁)完成研究。经过48周的治疗,艾塞那肽治疗后IL-1β和IFN-γ显著降低(分别为P<0.001和P=0.001),但随着胰岛素的增加而增加(分别为P=0.009和P=0.026)。然而,吡格列酮治疗对ADIC无影响.任何治疗均未检测到瘦素或FGF21的显著变化。调整基线值和体重变化后,腰部和HbA1c,在ΔIL-1β中发现了组间差异(艾塞那肽与胰岛素:P=0.048;艾塞那肽与吡格列酮:分别为P=0.003)和ΔIFN-γ(艾塞那肽与胰岛素:P=0.049;艾塞那肽与吡格列酮:分别P<0.001)。多元线性回归分析显示,Δ体重与ΔIL-1β相关(β=0.753;95%CI,0.137~1.369;P=0.017)。调整治疗效果后,Δ重量也与ΔFGF21相关(β=1.097;95CI,0.250-1.944;P=0.012);此外,ΔHOMA-IR也与Δleptin相关(β=0.078;95CI,0.008-0.147;P=0.029)。然而,调整治疗效果后,ΔHOMA-IR与ΔIL-1β没有显着相关(P=0.513)。
■艾塞那肽治疗导致炎性细胞因子水平(IL-1β和IFN-γ)的显著变化,但不是脂肪因子(瘦素和FGF21),在新诊断的T2DM患者中。艾塞那肽介导的体重和IR的改善可能与炎性细胞因子水平的降低有关。
UNASSIGNED: Adipokines and inflammatory cytokines (ADICs) play important roles in type 2 diabetes mellitus (T2DM). This study aimed to compare the changes of ADIC levels (ΔADICs) in patients with newly diagnosed T2DM treated with different antihyperglycemic agents, and further investigate the impact of these changes on metabolic indices, β-cell function and insulin resistance (IR).
UNASSIGNED: Four hundred and sixteen patients with newly diagnosed T2DM from 25 centers in China randomly received 48-week intervention with exenatide, insulin or pioglitazone. Anthropometric and laboratory data, indices of β-cell function and IR, and levels of AIDCs, including interleukin-1 beta (IL-1β), interferon-gamma (IFN-γ), leptin, and fibroblast growth factor 21 (FGF21) were detected at baseline and the end of the study.
UNASSIGNED: In total, 281 participants (68 % male, age: 50.3 ± 9.4 years) completed the study. After 48- week treatment, IL-1β and IFN-γ were significantly decreased with exenatide treatment (P < 0.001 and P = 0.001, respectively), but increased with insulin (P = 0.009 and P = 0.026, respectively). However, pioglitazone treatment had no impact on ADICs. No significant change in leptin or FGF21 was detected with any of the treatments. After adjustment for baseline values and changes of body weight, waist and HbA1c, the between-group differences were found in ΔIL-1β (exenatide vs. insulin: P = 0.048; and exenatide vs. pioglitazone: P = 0.003, respectively) and ΔIFN-γ (exenatide vs. insulin: P = 0.049; and exenatide vs. pioglitazone: P < 0.001, respectively). Multiple linear regression analysis indicated that Δweight was associated with ΔIL-1β (β = 0.753; 95 % CI, 0.137-1.369; P = 0.017). After adjusting for treatment effects, Δweight was also be correlated with ΔFGF21 (β = 1.097; 95%CI, 0.250-1.944; P = 0.012); furthermore, ΔHOMA-IR was correlated with Δleptin (β = 0.078; 95%CI, 0.008-0.147; P = 0.029) as well. However, ΔHOMA-IR was not significantly associated with ΔIL-1β after adjusting for treatment effects (P = 0.513).
UNASSIGNED: Exenatide treatment led to significant changes of inflammatory cytokines levels (IL-1β and IFN-γ), but not adipokines (leptin and FGF21), in newly diagnosed T2DM patients. The exenatide-mediated improvement in weight and IR may be associated with a decrease in inflammatory cytokine levels.