Inverse association between liver fat content and hepatic glucose uptake in patients with type 2 diabetes mellitus
Inverse association between liver fat content and hepatic glucose uptake in patients with type 2 diabetes mellitus
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DOI：
10.1016/j.metabol.2008.05.015
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发表时间：
2008-10-01
影响因子：
9.8
通讯作者：
Nuutila, Pirjo
中科院分区：
文献类型：
--
作者：
Borra, Ronald;Lautamaki, Riikka;Nuutila, Pirjo
本研究的目的是研究（1）2型糖尿病患者肝脂肪含量（LFC）与肝葡萄糖摄取（HGU）之间的相互关系，以及（2）罗格列酮诱导的这些患者LFC变化与HGU摄取之间的关系。应用质子磁共振波谱和[F-18]-标记2-氟-2-脱氧葡萄糖正电子发射断层扫描检测了54例2型糖尿病患者和8例健康人的肝脏脂肪和胰岛素刺激的HGU。在罗格列酮（n = 27）或安慰剂（n = 27）干预16周后，对糖尿病患者重复测量。与健康受试者相比，糖尿病患者的HGU较低（24.5 +/- 14.2 vs 35.6 +/- 9.7 μ mol/[kg min]，P < .01），LFC较高（10.9% +/- 9.2% vs 2.5% +/-1.4%，P < .001）。肝脂肪与HGU呈负相关（r =-0.31，P <0.05）。但更强烈地与全身胰岛素敏感性和脂联素水平有关。罗格列酮治疗使肝脏脂肪减少24.8%（P = 0.01，与安慰剂相比），使HGU增加29.2%（P = 0.013，与安慰剂相比）。高胰岛素血症时非酯化脂肪酸水平的抑制增加（P <0.001）和血糖控制改善（P = 0.034）可以最好地解释LFC的降低，但不能解释HGU的变化。观察到LFC和HGU之间的显著负相关，但变化不相关。这表明罗格列酮对肝脏代谢的有益作用是间接的，部分原因是增加了对非酯化脂肪酸水平的抑制，导致肝脏脂肪减少。(C)2008年爱思唯尔公司All rights reserved.
The objective of this research was to study (1) the mutual relationship between liver fat content (LFC) and hepatic glucose uptake (HGU) in patients with type 2 diabetes mellitus and (2) the relationship between changes in LFC and HGU uptake induced by rosiglitazone in these patients. Liver fat was measured with proton magnetic resonance spectroscopy and insulin-stimulated HGU with [F-18]-labeled 2-fluoro-2-deoxyglucose positron emission tomography in 54 patients with type 2 diabetes mellitus and 8 healthy Subjects. Measurements were repeated in diabetic patients after a 16-week intervention period with rosiglitazone (n = 27) or placebo (n = 27). Patients with diabetes had lower HGU (24.5 +/- 14.2 vs 35.6 +/- 9.7 mu mol/[kg min], P < .01) and higher LFC (10.9% +/- 9.2% vs 2.5% +/- 1.4%, P < .001) compared with healthy subjects. Liver fat was inversely associated with HGU (r = -0.31, P < .05). but more strongly with whole-body insulin sensitivity and adiponectin levels. Rosiglitazone treatment reduced liver fat by 24.8% (P = .01 vs placebo) and increased HGU by 29.2% (P = .013 vs placebo). This decrease in LFC was best explained by the increment in suppression of nonesterified fatty acid levels during hyperinsulinemia (P < .001) and improved glycemic control (P = .034), but not by changes in HGU. A significant inverse relationship between LFC and HGU was observed, but changes were not related. This suggests that the beneficial effects of rosiglitazone on liver metabolism are indirect and can be partly explained by increased suppression of nonesterified fatty acid levels, leading to reduced liver fat. (C) 2008 Elsevier Inc. All rights reserved.