Feng Xiaomeng, Gao Xia, Jia Yumei, Xu Yuan
Department of Endocrinology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, People's Republic of China.
Diabetes Ther. 2017 Apr;8(2):433-444. doi: 10.1007/s13300-017-0257-4. Epub 2017 Mar 30.
Peroxisome proliferator-activated receptor-α (PPAR-α) agonists can regulate metabolism and protect the cardiovascular system. This study investigated the effects of PPAR-α agonist fenofibrate on insulin resistance in patients with impaired glucose tolerance (IGT).
This research evaluated cross-sectional and interventional studies. 191 subjects with IGT were divided into a hypertriglyceridemia group (HTG group, n = 118) and a normal triglyceride (TG) group (NTG group, n = 73). 79 subjects with normal glucose tolerance were recruited as a control group. The HTG group was treated with fenofibrate (200 mg/day) for 12 weeks. The homeostatic model assessment index 2 (HOMA2) and the McAuley index (McA) were calculated.
HOMA2 for β-cell function (HOMA2-%B) was 93.47 ± 26.28, 68.47 ± 21.29, and 79.92 ± 23.15 in HTG, NTG, and control groups, respectively. HOMA2 for insulin sensitivity (HOMA2-%S) was 48.40 (39.70, 68.70), 110.20 (62.55, 141.95), and 101.20 (79.90, 140.10) in HTG, NTG, and control groups, respectively. HOMA2 for insulin resistance (HOMA2-IR) was 2.09 (1.46, 2.52), 0.92 (0.70, 1.61), and 0.99 (0.71, 1.25) in HTG, NTG, and control groups, respectively. McA was 5.05 ± 0.76, 7.99 ± 1.79, and 8.34 ± 1.55 in HTG, NTG, and control groups, respectively. The HTG group had higher HOMA2-%B and HOMA2-IR, and lower HOMA2-%S and McA than NTG and control groups (P < 0.001 for all). Fenofibrate decreased HOMA2-%B and HOMA2-IR and increased HOMA2-%S and McA in the HTG group (HOMA2-%B: from 93.47 ± 26.28 to 89.34 ± 23.53, P = 0.018; HOMA2-%S: from 48.40 (39.70, 68.70) to 56.75 (44.88, 72.53), P < 0.001; HOMA2-IR: from 2.07 (1.46, 2.52) to 1.76 (1.38, 2.30), P < 0.001; McA: from 5.05 ± 0.76 to 9.34 ± 0.88, P < 0.001).
PPAR-α agonists improve parameters of glucoregulation in IGT patients with hypertriglyceridemia.
过氧化物酶体增殖物激活受体-α(PPAR-α)激动剂可调节代谢并保护心血管系统。本研究调查了PPAR-α激动剂非诺贝特对糖耐量受损(IGT)患者胰岛素抵抗的影响。
本研究评估了横断面研究和干预性研究。191例IGT患者被分为高甘油三酯血症组(HTG组,n = 118)和正常甘油三酯(TG)组(NTG组,n = 73)。招募79例糖耐量正常的受试者作为对照组。HTG组接受非诺贝特治疗(200mg/天),为期12周。计算稳态模型评估指数2(HOMA2)和麦考利指数(McA)。
HTG组、NTG组和对照组的β细胞功能HOMA2(HOMA2-%B)分别为93.47±26.28、68.47±21.29和79.92±23.15。HTG组、NTG组和对照组的胰岛素敏感性HOMA2(HOMA2-%S)分别为48.40(39.70,68.70)、110.20(62.55,141.95)和101.20(79.90,140.10)。HTG组、NTG组和对照组的胰岛素抵抗HOMA2(HOMA2-IR)分别为2.09(1.46,2.52)、0.92(0.70,1.61)和0.99(0.71,1.25)。HTG组、NTG组和对照组的McA分别为5.05±0.76、7.99±1.79和8.34±1.55。HTG组的HOMA2-%B和HOMA2-IR高于NTG组和对照组,而HOMA2-%S和McA低于NTG组和对照组(所有P均<0.001)。非诺贝特使HTG组的HOMA2-%B和HOMA2-IR降低,HOMA2-%S和McA升高(HOMA2-%B:从93.47±26.28降至89.34±23.53,P = 0.018;HOMA2-%S:从48.40(39.70,68.70)升至56.75(44.88,72.53),P<0.001;HOMA2-IR:从2.07(1.46,2.52)降至1.76(1.38,2.30),P<0.001;McA:从5.05±0.76升至9.34±0.88,P<0.001)。
PPAR-α激动剂可改善高甘油三酯血症的IGT患者的血糖调节参数。