Imaki T, Shibasaki T, Masuda A, Hotta M, Yamauchi N, Demura H, Shizume K, Wakabayashi I, Ling N
Endocrinology. 1986 Jun;118(6):2390-4. doi: 10.1210/endo-118-6-2390.
We have examined the effect of glucose and FFA on GH-releasing factor (GHRF)-mediated GH secretion in rats under pentobarbital anesthesia. Hyperglycemia did not affect GH secretion induced by administration of 20, 100, and 200 ng GHRF/100 g body weight. In contrast, GH response to 50 ng GHRF/100 g body weight in lipid heparin-treated rats, which showed high plasma FFA levels, was significantly suppressed compared with the control group (plasma peak GH: control, 1526 +/- 263 ng/ml; lipid-heparin group, 377 +/- 69 ng/ml P less than 0.05, mean +/- SEM). This suppressive effect of FFA on GH secretion was abolished by pretreatment with antisomatostatin serum (ASS) (GH level at 4 min after GHRF administration: ASS-saline group, 1606 +/- 210 ng/ml; ASS-lipid-heparin group, 1531 +/- 174 ng/ml; mean +/- SEM). These results suggest that hyperglycemia does not change the GH response to GHRF and that elevation of plasma FFA suppresses GHRF-induced GH secretion by the stimulation of somatostatin secretion in rats.
我们研究了葡萄糖和游离脂肪酸（FFA）对戊巴比妥麻醉下大鼠生长激素释放因子（GHRF）介导的生长激素（GH）分泌的影响。高血糖并未影响给予20、100和200 ng GHRF/100 g体重所诱导的GH分泌。相比之下，脂质肝素处理的大鼠血浆FFA水平较高，其对50 ng GHRF/100 g体重的GH反应与对照组相比显著受到抑制（血浆GH峰值：对照组，1526±263 ng/ml；脂质肝素组，377±69 ng/ml，P<0.05，均值±标准误）。FFA对GH分泌的这种抑制作用通过用抗生长抑素血清（ASS）预处理而被消除（给予GHRF后4分钟时的GH水平：ASS-生理盐水组，1606±210 ng/ml；ASS-脂质肝素组，1531±174 ng/ml；均值±标准误）。这些结果表明，高血糖不会改变GH对GHRF的反应，并且血浆FFA升高通过刺激大鼠生长抑素分泌来抑制GHRF诱导的GH分泌。
