Myocardial Glucose Uptake in Patients with NIDDM and Stable Coronary Artery Disease
Myocardial Glucose Uptake in Patients with NIDDM and Stable Coronary Artery Disease
复制标题
NIDDM 和稳定型冠状动脉疾病患者的心肌葡萄糖摄取
作者：
M. Mäki;P. Nuutila;H. Laine;L. Voipio‐Pulkki;M. Haaparanta;O. Solin;J. Knuuti
全身胰岛素抵抗是NIDDM患者的特征，但尚不清楚胰岛素是否也具有刺激这些患者心肌葡萄糖摄取（MGU）的能力受损。本研究旨在评估在标准化代谢条件下，通过2-[18 F]氟-2-脱氧-D-葡萄糖（[18 F]FDG）和正电子发射断层扫描（PET）测量的NIDDM和稳定性冠状动脉疾病（CAD）患者的MGU。8例NIDDM患者、11例非糖尿病CAD患者和9例健康对照受试者入组研究。用~（18）F FDG和PET定量测定正常心肌区的MGU，用葡萄糖-胰岛素钳夹技术测定全身葡萄糖代谢（血清胰岛素≤ 430 pmol/l）。PET研究期间，所有组的血糖和血清胰岛素浓度相当。与健康对照组（40 ± 17 pmol · min-1 · kg-1体重，P < 0.05）相比，NIDDM患者的全身葡萄糖摄取量（22 ± 9 pmol·min-1·kg-1体重[平均值±标准差]）低45%。在CAD患者中，全身葡萄糖摄取为30 ± 9 pmol · min-1 · kg-1体重（其他组之间为NS）。所有三组正常节段的MGU相似（NIDDM患者为69 ± 28 pmol · min-1 · 100 g-1，CAD患者为72 ± 17 pmol · min-1 · 100 g-1，76 ± 10 pmol. min−1 · 100 g−1（健康对照组，NS）。未发现全身葡萄糖摄取与MGU之间存在相关性。正如在稳定的血糖正常高胰岛素血症条件下通过[18 F]FDG PET所研究的，尽管存在外周胰岛素抵抗，但NIDDM和CAD患者的MGU并未降低。提示NIDDM患者MGU无明显缺陷。
Whole body insulin resistance characterizes patients with NIDDM, but it is not known whether insulin also has impaired ability to stimulate myocardial glucose uptake (MGU) in these patients. This study was designed to evaluate MGU as measured by 2-[l8F]flu-oro-2-deoxy-D-glucose ([18F]FDG) and positron emission tomography (PET) in patients with NIDDM and stable coronary artery disease (CAD) under standardized metabolic conditions. Eight patients with NIDDM, 11 nondiabetic patients with CAD, and 9 healthy control subjects were enrolled in the study. MGU was quanti-tated in the normal myocardial regions with [18F]FDG and PET and the whole body glucose disposal by glucose-insulin clamp technique (serum insulin, ∼430 pmol/l). Plasma glucose and serum insulin concentrations were comparable in all groups during PET studies. The whole body glucose uptake was 45% lower in NIDDM patients (22 ± 9 pmol · min−1 · kg−1 body wt [mean ± SD]), compared with healthy control subjects (40 ± 17 pmol · min−1 · kg−1 body wt, P < 0.05). In CAD patients, whole body glucose uptake was 30 ± 9 pmol · min−1 · kg−1 body wt (NS between the other groups). MGU was similar in the normal segments in all three groups (69 ± 28 pmol · min−1 · 100 g−1 in NIDDM patients, 72 ± 17 pmol · min−1 · 100 g−1 in CAD patients, and 76 ± 10 pmol. min−1 · 100 g−1 in healthy control subjects, NS). No correlation was found between whole body glucose uptake and MGU. As studied by [18F]FDG PET under stable normoglycemic hyperinsulinemic conditions, MGU is not reduced in patients with NIDDM and CAD in spite of peripheral insulin resistance. These findings suggest that there is no significant defect in MGU in patients with NIDDM.
影响因子：
6.5
作者：
Miles,J;Glasscock,R;Aikens,J;Gerich,J;Haymond,M
通讯作者：
Haymond,M
影响因子：
15.9
作者：
DELPRATO, S;BONADONNA, RC;DEFRONZO, RA
通讯作者：
DEFRONZO, RA