背景和目的:本研究的目的是探讨不同的疗法如何调节胰岛素抵抗,无论是因果关系还是结果,影响初治T2DM受试者的代谢参数。受试者和方法:总共212名受试者被分配接受严格的日本饮食(n=65),吡格列酮的剂量范围为15-30毫克/天(n=70),或canagliflozin,剂量范围为50-100mg/天(n=77),持续三个月。研究了代谢参数相对于胰岛素抵抗的相关性和变化(Δ)。结果:在这些不同的治疗干预措施中,ΔHOMA-R与ΔFBG和ΔHOMA-B呈显著相关,同时证明与基线HOMA-R呈负相关。然而,其他参数,如ΔHbA1c,ΔBMI,ΔTC,ΔTG,Δnon-HDL-C,或ΔUA根据治疗方案显示不同的模式。根据ΔHOMA-R的中值将参与者分为两组:下半部分(X)和上半部分(Y)。在所有治疗中,与Y组相比,X组始终表现出更明显的FBG降低。而其他参数包括HbA1c,HOMA-B,TC,TG,HDL-C,非HDL-C,TG/HDL-C比值,或UA表现出不同的调节反应,这取决于所施用的治疗。结论:这些发现表明,(1)在这些治疗中观察到胰岛素抵抗的变化,以及(2)这些治疗对胰岛素抵抗的调节,无论是因果关系还是后果性的,结果对血糖参数的不同影响,β细胞功能,特定脂质,体重,或UA。
Bacground and Objectives: The objective of this study is to investigate how different therapies modulating insulin resistance, either causally or consequently, affect metabolic parameters in treatment-naïve subjects with T2DM. Subjects and Methods: A total of 212 subjects were assigned to receive either a tight Japanese diet (n = 65), pioglitazone at doses ranging from 15-30 mg/day (n = 70), or canagliflozin at doses ranging from 50-100 mg/day (n = 77) for a duration of three months. Correlations and changes (Δ) in metabolic parameters relative to insulin resistance were investigated. Results: Across these distinct therapeutic interventions, ΔHOMA-R exhibited significant correlations with ΔFBG and ΔHOMA-B, while demonstrating a negative correlation with baseline HOMA-R. However, other parameters such as ΔHbA1c, ΔBMI, ΔTC, ΔTG, Δnon-HDL-C, or ΔUA displayed varying patterns depending on the treatment regimens. Participants were stratified into two groups based on the median value of ΔHOMA-R: the lower half (X) and upper half (Y). Group X consistently demonstrated more pronounced reductions in FBG compared to Group Y across all treatments, while other parameters including HbA1c, HOMA-B, TC, TG, HDL-C, non-HDL-C, TG/HDL-C ratio, or UA exhibited distinct regulatory responses depending on the treatment administered. Conclusions: These findings suggest that (1) regression to the mean is observed in the changes in insulin resistance across these therapies and (2) the modulation of insulin resistance with these therapies, either causally or consequentially, results in differential effects on glycemic parameters, beta-cell function, specific lipids, body weight, or UA.