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11. |
Pituitary Secretions Related to Adrenocorticotropic Hormone Induce Sensitivity of Adipose Tissue to the Insulin-Like Actions of Growth Hormone |
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Neuroendocrinology,
Volume 45,
Issue 2,
1987,
Page 165-171
Vittorio Coiro,
H. Maurice Goodman,
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摘要:
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 effec
ISSN:0028-3835
DOI:10.1159/000124719
出版商:S. Karger AG
年代:1987
数据来源: Karger
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12. |
Immunocytochemical Localization of the Gonadotropin-Releasing Hormone-Associated Peptide of the LHRH Precursor |
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Neuroendocrinology,
Volume 45,
Issue 2,
1987,
Page 172-175
Madhabananda Sar,
Michael D. Culler,
William C. McGimsey,
Andres Negro-Vilar,
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摘要:
Using specific rabbit anti-GAP (gonadotropin-releasing hormone-associated peptide) serum, we have immunocytochemically localized GAP in the rat brain. Immunostaining of neuronal perikarya, fibers and terminals was demonstrated with GAP antiserum under conditions of tissue preparation which make immunostaining with LHRH anti-sera difficult or undectectable. GAP-immunoreactive perikarya were observed in sections of perfused or nonperfused brains without colchicine pretreatment. Using a double immunoperoxidase staining method, both GAP and LHRH immunoreactivities were shown to coexist in the same neurons. The common distributionof LHRH and GAP immunoreactivity in the rat brain is strongly supportive of GAP representing the non-LHRH portion of the LHRH precursor. The use of GAP antisera that can distinguish between LHRH and the remaining portion of its prohormone represents a valuable tool for studies of LHRH-prohormone processing and distribution.
ISSN:0028-3835
DOI:10.1159/000124720
出版商:S. Karger AG
年代:1987
数据来源: Karger
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13. |
International Society of Endocriology |
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Neuroendocrinology,
Volume 45,
Issue 2,
1987,
Page 176-176
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PDF (151KB)
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ISSN:0028-3835
DOI:10.1159/000124721
出版商:S. Karger AG
年代:1987
数据来源: Karger
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