Pituitary secretions related to adrenocorticotropic hormone induce sensitivity of adipose tissue to the insulin-like actions of growth hormone.

Pituitary secretions related to adrenocorticotropic hormone induce sensitivity of adipose tissue to the insulin-like actions of growth hormone.
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与促肾上腺皮质激素相关的垂体分泌物诱导脂肪组织对生长激素的胰岛素样作用的敏感性。

DOI:
10.1159/000124719
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发表时间:
1987
期刊:
影响因子:
4.1
通讯作者:
Goodman,HM
Goodman,HM
中科院分区:
医学2区
文献类型:
--
作者:
Coiro,V;Goodman,HM

文献摘要

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在体外首次接触生长激素 (GH) 时,从 GH 缺乏的大鼠中切除的附睾脂肪会产生类似胰岛素的葡萄糖代谢增加反应。从正常大鼠身上新鲜切除的组织对 GH 的胰岛素样作用具有抵抗力,但在手术应激后立即变得敏感。在应激前服用阿片类拮抗剂纳洛酮可以防止不应性的逆转,这表明β-内啡肽或相关肽可能发挥作用。进行这些实验是为了确定这些肽的来源,这些肽同样可能在应激反应中从垂体、肾上腺髓质或神经末梢释放。由于肾上腺切除术与应激一样,也会导致促肾上腺皮质激素 (ACTH) 和相关肽的分泌增加,因此我们研究了 GH 对取自肾上腺切除术大鼠的脂肪组织中葡萄糖氧化的影响,并发现在肾上腺切除术 4 天后研究的组织中对 GH 出现了显着的胰岛素样反应。这种效应并非由于 GH 缺乏所致,因为肾上腺切除术仅略微降低了血浆浓度。在处死前 30 或 60 分钟给予纳洛酮(250 µg/大鼠),或在处死前 60 和 120 分钟给予地塞米松(100 µg/注射),可防止对 GH 的反应,而不影响 GH 的循环水平。肾上腺切除术的效果不能通过将来自正常无应激大鼠的脂肪组织与ACTH和β-内啡肽预孵育来重现,但通过将脂肪组织在垂体预先在促肾上腺皮质激素释放激素(0.1 µM)和精氨酸加压素(0.2 µM)存在下孵育的培养基中预孵育15分钟来重复。添加纳洛酮 (250 µg/ml) 可阻断这种作用。无论是在没有下丘脑肽的情况下培养垂体的培养基,还是单独的下丘脑肽,都不能有效诱导正常大鼠脂肪组织中对 GH 的胰岛素样反应。用于这些研究的垂体是从 3-5 周前进行甲状腺切除的大鼠身上获得的,因此几乎不含 GH。数据表明,在肾上腺切除或应激的大鼠中,与 ACTH 一起释放的物质可以急剧逆转正常脂肪组织对 GH 的胰岛素样作用的抵抗力。
In its initial encounter with growth hormone (GH) in vitro, epididymal fat excised from GH-deficient rats responds with an insulin-like increase in glucose metabolism. Tissues freshly excised from normal rats are refractory to the insulin-like effects of GH, but become sensitive immediately after surgical stress. Reversal of refractoriness is prevented by administration of the opioid antagonist, naloxone, just prior to stress, suggesting a possible role of β-endorphin or related peptides. These experiments were undertaken to determine the source of these peptides which might equally well be released from the pituitary, adrenal medullae, or nerve endings in response to stress. Since adrenalectomy, like stress, also results in increased secretion of adrenocorticotropic hormone (ACTH) and related peptides, we studied the effects of GH on glucose oxidation in adipose tissue obtained from adrenalectomized rats and found a significant insulin-like response to GH in tissues studied 4 days after adrenalectomy. This effect was not due to GH deficiency, since plasma concentrations were only slightly reduced by adrenalectomy. Administration of naloxone (250 µg/rat), 30 or 60 min before sacrifice, or dexamethasone (100 µg/injection), 60 and 120 min before sacrifice, prevented a response to GH without affecting circulating levels of GH. The effects of adrenalectomy could not be reproduced by preincubation of adipose tissue from normal nonstressed rats with ACTH and β-endorphin, but were duplicated by preincubation of adipose tissue for 15 min in medium in which pituitary glands had previously incubated in the presence of corticotropin-releasing hormone (0.1 µM) and arginine vasopressin (0.2 µM). Addition of naloxone (250 µg/ml) blocked this effect. Neither medium, in which pituitary glands had been incubated in the absence of hypothalamic peptides, nor the hypothalamic peptides alone were effective in inducing an insulin-like response to GH in adipose tissue of normal rats. The pituitary glands used for these studies were obtained from rats that had been thyroidectomized 3–5 weeks earlier and hence were virtually devoid of GH. The data suggest that substances released along with ACTH in the adrenalectomized or stressed rat can acutely reverse the refractoriness of normal adipose tissue to the insulin-like effects of GH.