Møller N, Schmitz O, Møller J, Butler P C
Medical Department M (Endocrinology and Diabetes), Aarhus Kommunehospital, Denmark.
J Clin Endocrinol Metab. 1992 Aug;75(2):432-6. doi: 10.1210/jcem.75.2.1639944.
When present in inappropriate amounts GH induces substantial insulin resistance and it has furthermore been suggested that modest nocturnal surges of GH may precipitate the emergence of the dawn phenomenon. To characterize the metabolic effects of physiologically relevant, small-scale GH exposure, six type 1 diabetic subjects were studied for 5 h in the postabsorptive state after an iv pulse of either 210 micrograms GH or saline. Identical amounts of insulin were infused on both occasions to maintain a prevailing blood glucose concentration of 125 +/- 12 mg/100 ml. The GH bolus caused an increase in serum GH levels to a peak value of 22 +/- 2 micrograms/L after 10 min, a 70% increase in serum FFA (from 570 +/- 80 to 980 +/- 60 mumol/L) and a 400% increase in blood 3-hydroxybutyrate (3-OHB) (from 100 +/- 15 to 420 +/- 35 mumol/l) concentrations after 180 and 240 min respectively (P less than 0.05). Blood glycerol and forearm uptake of 3-OHB rose in parallel (P less than 0.01). Plasma glucose, isotopically measured glucose turnover and forearm glucose uptake was not affected by GH. Blood lactate concentrations increased (P less than 0.05) and nonoxidative glucose use and lipid oxidation tended to increase with GH. Energy expenditure remained unaffected. These results suggest that under everyday conditions GH acts as an important regulator of fuel fluxes in type 1 diabetic subjects, the main effect being a transient stimulation of lipolysis. Since no significant effect on glucose metabolism was recorded, we do not presently find evidence to support a primary role for small surges of GH in the pathogenesis of the dawn phenomenon.
当生长激素(GH)以不适当的量存在时,会引发显著的胰岛素抵抗,此外,有研究表明,夜间适度的GH激增可能会促使黎明现象的出现。为了明确生理相关的小剂量GH暴露的代谢效应,对6名1型糖尿病患者进行了研究,在静脉注射210微克GH或生理盐水后的吸收后状态下观察5小时。两次实验均输注等量胰岛素,以维持血糖浓度在125±12mg/100ml。静脉注射GH推注后,血清GH水平在10分钟内升至峰值22±2微克/升,血清游离脂肪酸(FFA)在180分钟时增加70%(从570±80微摩尔/升升至980±60微摩尔/升),血液3-羟基丁酸(3-OHB)浓度在240分钟时增加400%(从100±15微摩尔/升升至420±35微摩尔/升)(P<0.05)。血液甘油和前臂对3-OHB的摄取量平行上升(P<0.01)。血浆葡萄糖、同位素测量的葡萄糖周转率和前臂葡萄糖摄取不受GH影响。血乳酸浓度升高(P<0.05),非氧化葡萄糖利用和脂质氧化倾向于随GH增加。能量消耗未受影响。这些结果表明,在日常情况下,GH是1型糖尿病患者燃料通量的重要调节因子,主要作用是短暂刺激脂肪分解。由于未记录到对葡萄糖代谢的显著影响,目前我们没有找到证据支持小剂量GH激增在黎明现象发病机制中的主要作用。