Imano E, Kanda T, Nakatani Y, Motomura M, Arai K, Matsuhisa M, Yamasaki Y, Hori M
Department of Gastroenterology and Metabolic Disease, Osaka Prefectural General Hospital, Japan.
J Hepatol. 1999 Sep;31(3):469-73. doi: 10.1016/s0168-8278(99)80039-7.
BACKGROUND/AIM: Patients with liver cirrhosis are insulin-resistant and frequently glucose-intolerant. Although peripheral glucose uptake has been shown to be impaired in liver cirrhosis, little is known about the significance of splanchnic (hepatic) glucose uptake after oral glucose load.
METHODS/RESULTS: We performed an oral glucose tolerance test and euglycemic hyperinsulinemic clamp with oral glucose load for eight patients with liver cirrhosis and eight patients with chronic active hepatitis. The patients with liver cirrhosis had higher plasma glucose levels 2 h after glucose load than those with chronic active hepatitis (228+/-22 mg/dl vs. 102+/-9 mg/dl, p<0.01). Using the euglycemic hyperinsulinemic clamp with oral glucose load, we simultaneously measured peripheral and splanchnic glucose uptake. Peripheral glucose uptake in liver cirrhosis was 6.1+/-0.7 mg x kg(-1) x min(-1), which was lower than that in healthy volunteers (10.5+/-0.9 mg x kg(-1) x min(-1), p<0.05) and in chronic active hepatitis (8.4+/-0.3 mg x kg(-1) x min(-1), p<0.05). Furthermore, splanchnic glucose uptake in liver cirrhosis was much lower (20.1+/-3.4%) than in healthy volunteers (36.0+/-4.0%, p<0.05) and in chronic active hepatitis (37.2+/-3.1%, p<0.05).
These results suggest that glucose intolerance in patients with liver cirrhosis is caused by a defect of the glucose uptake of both splanchnic and peripheral tissues.
背景/目的：肝硬化患者存在胰岛素抵抗且常伴有糖耐量异常。尽管已有研究表明肝硬化患者外周葡萄糖摄取受损，但口服葡萄糖负荷后内脏（肝脏）葡萄糖摄取的意义仍知之甚少。
方法/结果：我们对8例肝硬化患者和8例慢性活动性肝炎患者进行了口服葡萄糖耐量试验以及口服葡萄糖负荷后的正常血糖高胰岛素钳夹试验。肝硬化患者在葡萄糖负荷后2小时的血糖水平高于慢性活动性肝炎患者（228±22mg/dl对102±9mg/dl，p<0.01）。通过口服葡萄糖负荷后的正常血糖高胰岛素钳夹试验，我们同时测量了外周和内脏葡萄糖摄取。肝硬化患者的外周葡萄糖摄取为6.1±0.7mg·kg⁻¹·min⁻¹，低于健康志愿者（10.5±0.9mg·kg⁻¹·min⁻¹，p<0.05）和慢性活动性肝炎患者（8.4±0.3mg·kg⁻¹·min⁻¹，p<0.05）。此外，肝硬化患者的内脏葡萄糖摄取远低于健康志愿者（36.0±4.0%，p<0.05）和慢性活动性肝炎患者（37.2±3.1%，p<0.05）（20.1±3.4%）。
这些结果表明，肝硬化患者的糖耐量异常是由内脏和外周组织葡萄糖摄取缺陷所致。
