scholarly journals Severity of the Catabolic Condition Differentially Modulates Hypothalamic Expression of Growth Hormone-Releasing Hormone in the Fasted Mouse: Potential Role of Neuropeptide Y and Corticotropin-Releasing Hormone

Endocrinology ◽  
2007 ◽  
Vol 148 (1) ◽  
pp. 300-309 ◽  
Author(s):  
Raul M. Luque ◽  
Seungjoon Park ◽  
Rhonda D. Kineman
Keyword(s):  
Neuropeptide Y ◽  
Mrna Levels ◽  
Releasing Hormone ◽  
Ghrelin Receptor ◽  
Ghrh Receptor ◽  
Transient Rise ◽  
Biphasic Effect ◽  
Neuronal Systems ◽  
Induced Changes

To determine whether the severity of the catabolic condition differentially regulates the GH axis, male mice were either fed ad libitum or fasted for 12, 24, and 48 h. Hypothalami, pituitaries, and stomachs were collected for assessment of mRNA levels by quantitative real-time RT-PCR, and blood collected for measurement of plasma hormone and metabolite levels by commercial assay kits. Overnight (12 h) fasting resulted in a significant suppression of circulating glucose, insulin, IGF-I, and leptin levels and an increase in corticosterone, free fatty acids, and n-octanoyl ghrelin levels, and these directional changes were maintained at the 24- and 48-h time points. Fasting (24 h) also increased circulating GH levels, which was associated with an increase in pituitary mRNA levels for GHRH receptor and ghrelin receptor and a decrease in mRNA levels for somatostatin (SST) receptor (SSTR) subtypes, SSTR2, SSTR3, and SSTR5, where the changes in ghrelin receptor and SSTR expression persisted after 48 h fasting. Hypothalamic SST mRNA levels were not altered by fasting, whereas there was a transient rise in stomach SST mRNA levels 24 h after food withdrawal. In contrast, there was a biphasic effect of fasting on GHRH expression. GHRH mRNA levels were significantly elevated at 12 and 24 h but fell to ∼50% of fed controls 48 h after food withdrawal. A sequential rise in hypothalamic neuropeptide Y (NPY) and CRH mRNA levels preceded the fall in GHRH expression, where fasting-induced changes in CRH and GHRH mRNA levels were not observed in 48-h-fasted NPY knockout mice. These observations, in light of previous reports showing both NPY and CRH can inhibit GHRH expression and GH release, suggest that these neuronal systems may work in concert to control the ultimate impact of fasting on GH axis function.

In vivo action of a new octadecaneuropeptide antagonist on neuropeptide Y and corticotropin-releasing hormone mRNA levels in rat

2005 ◽  
Vol 141 (2) ◽  
pp. 156-160 ◽  
Author(s):  
V. Compère ◽  
S. Li ◽  
J. Leprince ◽  
M.C. Tonon ◽  
H. Vaudry ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Mrna Levels ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

Neutralization of TNF does not influence endotoxininduced changes in thyroid hormone metabolism in humans

1999 ◽  
Vol 276 (2) ◽  
pp. R357-R362 ◽  
Author(s):  
Tom van der Poll ◽  
Erik Endert ◽  
Susette M. Coyle ◽  
Jan M. Agosti ◽  
Stephen F. Lowry
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Stimulating Hormone ◽  
Hormone Metabolism ◽  
Thyroid Hormone Metabolism ◽  
Healthy Humans ◽  
Transient Rise ◽  
Induced Changes ◽  
Necrosis Factor ◽  
Control Study

To determine the role of tumor necrosis factor (TNF) in endotoxin-induced changes in plasma thyroid hormone and thyroid-stimulating hormone (TSH) concentrations, 24 healthy postabsorptive humans were studied on a control study day ( n= 6), after infusion of a recombinant TNF receptor IgG fusion protein (TNFR:Fc; 6 mg/m2; n = 6) after intravenous injection of endotoxin (2 ng/kg; n = 6), or after administration of endotoxin with TNFR:Fc ( n = 6). Administration of TNFR:Fc alone did not affect thyroid hormone or TSH levels when compared with the control day. Endotoxin induced a transient rise in plasma TNF activity (1.5 h: 219 ± 42 pg/ml), which was completely prevented by TNFR:Fc ( P < 0.05). After endotoxin administration, plasmal-thyroxine (T4), free T4, 3,5,3′-triiodothyronine (T3), and TSH were lower and 3,3′,5′-triiodothyronine was higher than on the control day (all P < 0.05). Coinfusion of TNFR:Fc with endotoxin did not influence these endotoxin-induced changes. Our results suggest that endogenous TNF does not play an important role in the alterations in plasma thyroid hormone and TSH concentrations induced by mild endotoxemia in healthy humans.

Role of neuropeptide Y in the regulation of gonadotropin-releasing hormone gene expression in the rat preoptic area

1994 ◽  
Vol 26 (1-2) ◽  
pp. 69-73 ◽  
Author(s):  
Songyun Li ◽  
Min Hong ◽  
Alain Fournier ◽  
Serge St-Pierre ◽  
Georges Pelletier
Keyword(s):  
Gene Expression ◽  
Neuropeptide Y ◽  
Preoptic Area ◽  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone

The role of neuropeptides in the regulation of adrenal zona glomerulosa function: effects of substance P, neuropeptide Y, neurotensin, Met-enkephalin, Leu-enkephalin and corticotrophin-releasing hormone on aldosterone secretion in the intact perfused rat adrenal

1994 ◽  
Vol 140 (1) ◽  
pp. 91-96 ◽  
Author(s):  
J P Hinson ◽  
L A Cameron ◽  
A Purbrick ◽  
S Kapas
Keyword(s):  
Substance P ◽  
Neuropeptide Y ◽  
Mammalian Species ◽  
Dose Range ◽  
Zona Glomerulosa ◽  
Aldosterone Secretion ◽  
Cortical Cells ◽  
Releasing Hormone ◽  
Adrenal Cortical Cells

Abstract A range of neuropeptides has been identified in the adrenal glands of many mammalian species. In many cases these peptides have been located in nerves supplying the adrenal cortical cells, or within clusters of chromaffin cells within the zona glomerulosa. The function of these neuropeptides has yet to be determined, but from their location within the gland it is clearly possible that they may have a role in the regulation of aldosterone secretion. The effects of Met-enkephalin, Leu-enkephalin, neuropeptide Y, substance P, corticotrophin-releasing hormone (CRH) and neurotensin on aldosterone secretion were investigated using the intact perfused rat adrenal gland in situ. All the peptides tested, except CRH, caused a significant increase in aldosterone secretion over the dose range of 1 pmol to lOnmol, with a maximum response of about a twofold increase in secretion. Met-enkephalin, however, at a dose of 10 nmol caused a 350% increase in aldosterone secretion, a response comparable with that seen in response to angiotensin II in this preparation. These results suggest that, while substance P, neuropeptide Y, neurotensin and Leu-enkephalin all have the capacity to cause modest increases in the rate of steroid secretion by the zona glomerulosa, these neuropeptides probably do not have a major role in the acute regulation of aldosterone secretion, at least under basal conditions. Met-enkephalin, on the other hand, was a more potent stimulus to aldosterone secretion, and thus may have a role in the control of aldosterone secretion. Journal of Endocrinology (1994) 140, 91–96

Corticotropin-releasing hormone mimics stress-induced colonic epithelial pathophysiology in the rat

1999 ◽  
Vol 277 (2) ◽  
pp. G391-G399 ◽  
Author(s):  
Javier Santos ◽  
Paul R. Saunders ◽  
Nico P. M. Hanssen ◽  
Ping-Chang Yang ◽  
Derrick Yates ◽  
...  
Keyword(s):  
Mast Cells ◽  
Stress Responses ◽  
Restraint Stress ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Ussing Chambers ◽  
Ion Secretion ◽  
Epithelial Physiology ◽  
Induced Changes

We examined the effect of stress on colonic epithelial physiology, the role of corticotropin-releasing hormone (CRH), and the pathways involved. Rats were restrained or injected intraperitoneally with CRH or saline. Colonic segments were mounted in Ussing chambers, in which ion secretion and permeability (conductance and probe fluxes) were measured. To test the pathways involved in CRH-induced changes, rats were pretreated with hexamethonium, atropine, bretylium, doxantrazole, α-helical CRH-(9—41) (all intraperitoneally), or aminoglutethimide (subcutaneously). Restraint stress increased colonic ion secretion and permeability to ions, the bacterial peptide FMLP, and horseradish peroxidase (HRP). These changes were prevented by α-helical CRH-(9—41) and mimicked by CRH (50 μg/kg). CRH-induced changes in ion secretion were abolished by α-helical CRH-(9—41), hexamethonium, atropine, or doxantrazole. CRH-stimulated conductance was significantly inhibited by α-helical CRH-(9—41), hexamethonium, bretylium, or doxantrazole. CRH-induced enhancement of HRP flux was significantly reduced by all drugs but aminoglutethimide. Peripheral CRH reproduced stress-induced colonic epithelial pathophysiology via cholinergic and adrenergic nerves and mast cells. Modulation of stress responses may be relevant to the management of colonic disorders.

Sign in / Sign up

Export Citation Format

Share Document