Quabbe H J, Bratzke H J, Siegers U, Elban K
J Clin Invest. 1972 Sep;51(9):2388-98. doi: 10.1172/JCI107051.
The influence of plasma free fatty acid (FFA) concentration on the secretion of human growth hormone (HGH) was investigated. (a) FFA depression was produced by means of a nicotinic acid (NA) infusion for either 1 or 5 hr in the presence of glucose-induced hyperglycemia. Controls received only saline. (b) FFA depression was also produced by a 90 min NA infusion and then rapid FFA elevation by a lipid-plus-heparin (lipid) infusion. This procedure was compared with a similar NA infusion not followed by lipid. (c) FFA elevation was produced either by a lipid or by a norepinephrine (NE) infusion and then HGH secretion was stimulated by insulin-induced hypoglycemia. Each subject in this group received both the lipid and the NE infusion on seperate days as well as two control tests (insulin alone and NE alone). Depression of FFA resulted in an increase of HGH with a lag period of approximately 2 hr. Maximal HGH rise after 1 hr NA infusion was 7.7+/-1.9 ng/ml and with 5 hr NA infusion 14.3+/-3.6 ng/ml (both significantly higher than during saline infusion, P < 0.025 and < 0.005 respectively) and occurred despite continuous hyperglycemia. Lipid infusion just before the expected HGH increase prevented the HGH response to FFA depression. HGH rise during insulin hypoglycemia (32.2+/-6.5 ng/ml) was significantly inhibited by prior FFA elevation whether achieved by lipid infusion (maximum HGH rise 11.4+/-1.6 ng/ml) or by NE infusion (maximum HGH rise 19.0+/-6.2 ng/ml). The results are suggestive of a negative feedback loop between plasma FFA and HGH secretion, of importance for subacute rather than acute changes in the plasma FFA concentration. FFA lack itself seems to be the signal for HGH release despite the lag period between FFA decrease and HGH increase. Glucose and FFA can at least not fully replace each other in their respective influence on HGH release.
研究了血浆游离脂肪酸(FFA)浓度对人生长激素(HGH)分泌的影响。(a)在葡萄糖诱导的高血糖情况下,通过输注烟酸(NA)1或5小时来降低FFA。对照组仅输注生理盐水。(b)通过输注NA 90分钟来降低FFA,然后通过输注脂质加肝素(脂质)使FFA快速升高。将该程序与未输注脂质的类似NA输注进行比较。(c)通过输注脂质或去甲肾上腺素(NE)使FFA升高,然后通过胰岛素诱导的低血糖刺激HGH分泌。该组中的每个受试者在不同的日子接受脂质和NE输注以及两项对照试验(单独胰岛素和单独NE)。FFA降低导致HGH增加,延迟约2小时。输注NA 1小时后HGH的最大升高为7.7±1.9 ng/ml,输注NA 5小时后为14.3±3.6 ng/ml(两者均显著高于输注生理盐水期间,分别为P<0.025和<0.005),并且尽管持续存在高血糖仍会发生。在预期的HGH增加之前输注脂质可阻止HGH对FFA降低的反应。无论是通过输注脂质(最大HGH升高11.4±1.6 ng/ml)还是通过输注NE(最大HGH升高19.0±6.2 ng/ml)使FFA预先升高,都能显著抑制胰岛素低血糖期间HGH的升高(32.2±6.5 ng/ml)。结果提示血浆FFA与HGH分泌之间存在负反馈回路,这对于血浆FFA浓度的亚急性而非急性变化很重要。尽管FFA降低与HGH增加之间存在延迟,但FFA缺乏本身似乎是HGH释放的信号。葡萄糖和FFA在它们对HGH释放的各自影响中至少不能完全相互替代。