Trepp R, Stettler C, Diem P, Christ E R
Division of Endocrinology, Diabetes and Clinical Nutrition Inselspital, University of Bern, Switzerland.
Exp Clin Endocrinol Diabetes. 2010 Oct;118(9):596-601. doi: 10.1055/s-0029-1243605. Epub 2010 Feb 9.
Hypopituitarism with adult-onset growth hormone deficiency (GHD) is associated with increased cardiovascular morbidity and mortality due to premature and progressive atherosclerosis. An underlying cause of atherosclerosis is increased insulin resistance. Elevated fasting and postprandial glucose and lipid levels may contribute to premature atherosclerosis. We studied effects of growth hormone replacement (GHRT) on fasting and postprandial metabolic parameters as well as on insulin sensitivity in patients with adult-onset GHD.
Using a standardized mixed meal, we studied insulin, glucose, non-esterified free fatty acid (NEFA) and triglycerides (TG) concentrations in the fasting state and during a 4 h postprandial period in 15 patients with adult-onset GHD before and after 4 months of GHRT. Identical investigations were performed in healthy matched control subjects.
GHD patients before and after GHRT: GHRT did not result in significant changes in fasting glucose, insulin, NEFA and TG concentrations. In the postprandial period GHRT resulted in a non-significant increase in glucose and a decrease in NEFA levels in the presence of unchanged postprandial insulin and TG concentrations. GHD patients vs. control subjects: GHD patients showed similar fasting glucose, insulin and NEFA concentrations, but TG were increased. In the postprandial period GHD patients exhibited similar glucose and TG, but increased insulin and NEFA concentrations. GHRT patients vs. control subjects: Patients after GHRT had similar fasting glucose, insulin and NEFA, but increased TG concentrations. In the postprandial period patients after GHRT had increased glucose and insulin levels in the presence of similar NEFA and TG concentrations.
While impaired insulin action in patients with GHD translates mainly by an impaired fasting TG metabolism, GHRT induced insulin resistance additionally encompasses postprandial glucose metabolism.
成人起病的生长激素缺乏症（GHD）所致的垂体功能减退与因过早和进行性动脉粥样硬化导致的心血管发病率和死亡率增加相关。动脉粥样硬化的一个潜在原因是胰岛素抵抗增加。空腹和餐后血糖及血脂水平升高可能导致过早的动脉粥样硬化。我们研究了生长激素替代治疗（GHRT）对成人起病的GHD患者空腹和餐后代谢参数以及胰岛素敏感性的影响。
我们使用标准化混合餐，研究了15例成人起病的GHD患者在GHRT治疗4个月前后空腹状态及餐后4小时期间的胰岛素、葡萄糖、非酯化游离脂肪酸（NEFA）和甘油三酯（TG）浓度。在健康匹配对照受试者中进行了相同的研究。
GHD患者GHRT治疗前后：GHRT治疗后空腹血糖、胰岛素、NEFA和TG浓度无显著变化。在餐后期间，GHRT治疗后葡萄糖有非显著增加，NEFA水平降低，而餐后胰岛素和TG浓度未改变。GHD患者与对照受试者比较：GHD患者空腹血糖、胰岛素和NEFA浓度相似，但TG升高。在餐后期间，GHD患者葡萄糖和TG相似，但胰岛素和NEFA浓度升高。GHRT治疗患者与对照受试者比较：GHRT治疗后患者空腹血糖、胰岛素和NEFA相似，但TG浓度升高。在餐后期间，GHRT治疗后患者葡萄糖和胰岛素水平升高，而NEFA和TG浓度相似。
虽然GHD患者胰岛素作用受损主要表现为空腹TG代谢受损，但GHRT诱导的胰岛素抵抗还包括餐后葡萄糖代谢。
