Foss M C, Saad M J, Paccola G M, Paula F J, Piccinato C E, Moreira A C
Department of Medicine, School of Medicine of Ribeirao Preto, Sao Paulo University, Brazil.
J Clin Endocrinol Metab. 1991 May;72(5):1048-53. doi: 10.1210/jcem-72-5-1048.
The present study was designed to determine the effect of chronic GH excess on forearm muscle glucose uptake and oxidation during the postabsorptive state and after an oral glucose challenge. Nine normal subjects and 10 nondiabetic acromegalic patients (5 of them with normal glucose tolerance) were studied after an overnight fast (12-14 h) and for 3 h after the ingestion of 75 g glucose. Peripheral glucose metabolism was analyzed by the forearm technique to estimate muscle exchange of substrate combined with indirect calorimetry. Decreased forearm glucose uptake was observed in the acromegalic patients compared to that in the normal subjects (380 +/- 84 vs. 709 +/- 56 mumol/100 mL forearm.3 h) with diminished nonoxidative glucose metabolism (262 +/- 81 vs. 572 +/- 53 mumol/100 mL forearm.3 h). The acromegalics with normal glucose tolerance also showed decreased forearm glucose uptake and nonoxidative glucose metabolism compared to normal subjects (271 +/- 124 vs. 709 +/- 56 and 133 +/- 110 vs. 572 +/- 53 mumol/100 mL forearm.3 h, respectively). Muscle glucose oxidation did not differ significantly in normal subjects, the entire group of acromegalic patients, and the acromegalics with normal glucose tolerance (137 +/- 18 vs. 118 +/- 22 vs. 138 +/- 34 mumol/100 mL forearm.3 h, respectively). Serum FFA levels and lipid oxidation rates were similar in the normal subjects and the acromegalic patients, and declined in a similar fashion after glucose ingestion. Insulin levels were significantly higher in acromegalic patients than in normal subjects before and after glucose loading. In conclusion, this study showed that the insulin resistance occurring in the presence of chronic GH excess is accompanied by impaired muscle glucose uptake and nonoxidative glucose metabolism, which are early derangements because they are also observed in acromegalic patients with normal glucose tolerance.
本研究旨在确定慢性生长激素(GH)过量对空腹状态及口服葡萄糖激发后前臂肌肉葡萄糖摄取和氧化的影响。对9名正常受试者和10名非糖尿病性肢端肥大症患者(其中5名糖耐量正常)进行了研究,研究过程包括过夜禁食(12 - 14小时)以及摄入75克葡萄糖后3小时。采用前臂技术分析外周葡萄糖代谢,以评估底物的肌肉交换情况,并结合间接测热法进行研究。与正常受试者相比,肢端肥大症患者的前臂葡萄糖摄取量降低(分别为380±84与709±56μmol/100 mL前臂·3小时),非氧化葡萄糖代谢减少(分别为262±81与572±53μmol/100 mL前臂·3小时)。糖耐量正常的肢端肥大症患者与正常受试者相比,前臂葡萄糖摄取量和非氧化葡萄糖代谢也降低(分别为271±124与709±56,以及133±110与572±53μmol/100 mL前臂·3小时)。正常受试者、整个肢端肥大症患者组以及糖耐量正常的肢端肥大症患者的肌肉葡萄糖氧化无显著差异(分别为137±18、118±22与138±34μmol/100 mL前臂·3小时)。正常受试者和肢端肥大症患者的血清游离脂肪酸(FFA)水平及脂质氧化率相似,且葡萄糖摄入后均以相似方式下降。葡萄糖负荷前后,肢端肥大症患者的胰岛素水平显著高于正常受试者。总之,本研究表明,慢性GH过量时出现的胰岛素抵抗伴有肌肉葡萄糖摄取和非氧化葡萄糖代谢受损,这些是早期紊乱,因为在糖耐量正常的肢端肥大症患者中也观察到了这些情况。