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胰岛素治疗对2型糖尿病患者肝脏脂肪含量及肝脏胰岛素敏感性的影响。

Effects of insulin therapy on liver fat content and hepatic insulin sensitivity in patients with type 2 diabetes.

作者信息

Juurinen Leena, Tiikkainen Mirja, Häkkinen Anna-Maija, Hakkarainen Antti, Yki-Järvinen Hannele

机构信息

Department of Medicine, Helsinki University of Technology, Finland.

出版信息

Am J Physiol Endocrinol Metab. 2007 Mar;292(3):E829-35. doi: 10.1152/ajpendo.00133.2006. Epub 2006 Nov 7.

DOI:10.1152/ajpendo.00133.2006
PMID:17090752
Abstract

UNLABELLED

We determined whether insulin therapy changes liver fat content (LFAT) or hepatic insulin sensitivity in type 2 diabetes. Fourteen patients with type 2 diabetes (age 51+/-2 yr, body mass index 33.1+/-1.4 kg/m2) treated with metformin alone received additional basal insulin for 7 mo. Liver fat (proton magnetic resonance spectroscopy), fat distribution (MRI), fat-free and fat mass, and whole body and hepatic insulin sensitivity (6-h euglycemic hyperinsulinemic clamp combined with infusion of [3-(3)H]glucose) were measured. The insulin dose averaged 75+/-10 IU/day (0.69+/-0.08 IU/kg, range 24-132 IU/day). Glycosylated hemoglobin A1c (Hb A1c) decreased from 8.9+/-0.3 to 7.4+/-0.2% (P<0.001). Whole body insulin sensitivity increased from 2.21+/-0.38 to 3.08+/-0.40 mg/kg fat-free mass (FFM).min (P<0.05). This improvement could be attributed to enhanced suppression of hepatic glucose production (HGP) by insulin (HGP 1.04+/-0.28 vs. 0.21+/-0.19 mg/kg FFM.min, P<0.01). The percent suppression of HGP by insulin increased from 72+/-8 to 105+/-11% (P<0.01). LFAT decreased from 17+/-3 to 14+/-3% (P<0.05). The change in LFAT was significantly correlated with that in hepatic insulin sensitivity (r=0.56, P<0.05). Body weight increased by 3.0+/-1.1 kg (P<0.05). Of this, 83% was due to an increase in fat-free mass (P<0.01). Fat distribution and serum adiponectin concentrations remained unchanged while serum free fatty acids decreased significantly.

CONCLUSIONS

insulin therapy improves hepatic insulin sensitivity and slightly but significantly reduces liver fat content, independent of serum adiponectin.

摘要

未标注

我们确定了胰岛素治疗是否会改变2型糖尿病患者的肝脏脂肪含量(LFAT)或肝脏胰岛素敏感性。14例仅接受二甲双胍治疗的2型糖尿病患者(年龄51±2岁,体重指数33.1±1.4kg/m²)额外接受了7个月的基础胰岛素治疗。测量了肝脏脂肪(质子磁共振波谱法)、脂肪分布(磁共振成像)、去脂体重和脂肪量,以及全身和肝脏胰岛素敏感性(6小时正常血糖高胰岛素钳夹试验联合输注[3-(3)H]葡萄糖)。胰岛素剂量平均为75±10IU/天(0.69±0.08IU/kg,范围24 - 132IU/天)。糖化血红蛋白A1c(Hb A1c)从8.9±0.3%降至7.4±0.2%(P<0.001)。全身胰岛素敏感性从2.21±0.38增加至3.08±0.40mg/kg去脂体重(FFM)·分钟(P<0.05)。这种改善可归因于胰岛素对肝脏葡萄糖生成(HGP)的抑制增强(HGP 1.04±0.28对0.21±0.19mg/kg FFM·分钟,P<0.01)。胰岛素对HGP的抑制百分比从72±8%增加至105±11%(P<0.01)。LFAT从17±3%降至14±3%(P<0.05)。LFAT的变化与肝脏胰岛素敏感性的变化显著相关(r = 0.56,P<0.05)。体重增加了3.0±1.1kg(P<0.05)。其中,83%是由于去脂体重增加(P<0.01)。脂肪分布和血清脂联素浓度保持不变,而血清游离脂肪酸显著降低。

结论

胰岛素治疗可改善肝脏胰岛素敏感性,并轻微但显著降低肝脏脂肪含量,与血清脂联素无关。

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