Modulation of Growth Hormone-Releasing Factor Stimulated Growth Hormone Secretion by Plasma Glucose and Free Fatty Acid Concentrations in Sheep

Title
Modulation of Growth Hormone-Releasing Factor Stimulated Growth Hormone Secretion by Plasma Glucose and Free Fatty Acid Concentrations in Sheep
Publication Date
1988
Author(s)
Sartin, JL
Bartol, FF
Kemppainen, RJ
Dieberg, Gudrun
( author )
OrcID: https://orcid.org/0000-0001-7191-182X
Email: gdieberg@une.edu.au
UNE Id une-id:gdieberg
Buxton, D
Soyoola, E
Type of document
Journal Article
Language
en
Entity Type
Publication
Publisher
S Karger AG
Place of publication
Switzerland
DOI
10.1159/000125073
UNE publication id
une:10975
Abstract
Effects of plasma glucose and free fatty acid (FFA) concentrations on bovine growth hormone-releasing factor (bGRF)-induced release of growth hormone (GH) were examined in ovariohysterectomized sheep. In experiment 1, the effects of an infusion of insulin (0.025 U/kg BW·h⁻¹), glucose (40 mg/kg BW·h⁻¹), insulin plus glucose or saline on the subsequent effects of bGRF on plasma GH concentrations were determined. Insulin-induced hypoglycemia inhibited GRF effects on plasma GH concentrations while glucose infusion enhanced bGRF actions. Infusing a higher glucose dose (120 mg/kg BW·h⁻¹) had no effect on GRF actions. Subsequently, infusion of FFA (0.25 g/kg/·h⁻¹), nicotinic acid (50 mg/kg BW) or saline for 1 h prior to bGRF injection demonstrated that FFA inhibited GRF actions but FFA depletion by nicotinic acid infusion had no effect on GRF actions. Nicotinic acid (40 mg/kg BW·h⁻¹) infused for 2 h prior to bGRF injection significantly enhanced bGRF-stimulated GH secretion. Finally, to determine whether central nervous system glucopenia produced similar effects to insulin-induced hypoglycemia, 2-deoxyglucose (500 mg) was injected into the lateral ventricle followed in 1 h by the i.v. injection of bGRF. The central glucopenia produced by 2-DG inhibited GRF-stimulated GH release. These data demonstrate that decreased peripheral or central nervous system glucose availability and exogenous administration of FFA antagonized GRF-induced release of GH. And, pharmacologic depletion of circulating FFA for at least 2 h facilitated GRF-induced release of GH.
Link
Citation
Neuroendocrinology, 48(6), p. 627-633
ISSN
1423-0194
0028-3835
Start page
627
End page
633

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