scholarly journals Intracerebroventricular Administration of Growth Hormone Releasing Peptide-6 (GHRP-6) Inhibits Food Intake, but not Food Retention of Crop and Stomach in Neonatal Chicks

2006 ◽  
Vol 43 (1) ◽  
pp. 35-40 ◽  
Author(s):  
Md. Sakirul Islam Khan ◽  
Koh-Ichi Dodo ◽  
Kazuki Yahata ◽  
Sayuri Nishimoto ◽  
Hiroshi Ueda ◽  
...  
2002 ◽  
Vol 453 (1) ◽  
pp. 75-79 ◽  
Author(s):  
Ei-suke Saito ◽  
Hiroyuki Kaiya ◽  
Tomo Takagi ◽  
Izumi Yamasaki ◽  
D.Michael Denbow ◽  
...  

2001 ◽  
Vol 301 (2) ◽  
pp. 123-126 ◽  
Author(s):  
Mitsuhiro Furuse ◽  
Tetsuya Tachibana ◽  
Atsushi Ohgushi ◽  
Ryuichi Ando ◽  
Takao Yoshimatsu ◽  
...  

Endocrinology ◽  
1996 ◽  
Vol 137 (11) ◽  
pp. 5155-5158 ◽  
Author(s):  
K Okada ◽  
S Ishii ◽  
S Minami ◽  
H Sugihara ◽  
T Shibasaki ◽  
...  

1979 ◽  
Vol 26 (1) ◽  
pp. 133-136 ◽  
Author(s):  
YOSHIAKI OKADA ◽  
KAZUO WATANABE ◽  
TORU TAKEUCHI ◽  
TOSHIO ONISHI ◽  
KIYOJI TANAKA ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Xiyao Zhang ◽  
Wensong Li ◽  
Ping Li ◽  
Manli Chang ◽  
Xu Huang ◽  
...  

As a regulator of food intake and energy metabolism, the role of ghrelin in glucose metabolism is still not fully understood. In this study, we determined the in vivo effect of ghrelin on incretin effect. We demonstrated that ghrelin inhibited the glucose-stimulated release of glucagon-like peptide-1 (GLP-1) when infused into the portal vein of Wistar rat. Hepatic vagotomy diminished the inhibitory effect of ghrelin on glucose-stimulated GLP-1 secretion. In addition, phentolamine, a nonselective α receptor antagonist, could recover the decrease of GLP-1 release induced by ghrelin infusion. Pralmorelin (an artificial growth hormone release peptide) infusion into the portal vein could also inhibit the glucose-stimulated release of GLP-1. And growth hormone secretagogue receptor antagonist, [D-lys3]-GHRP-6, infusion showed comparable increases of glucose stimulated GLP-1 release compared to ghrelin infusion into the portal vein. The data showed that intraportal infusion of ghrelin exerted an inhibitory effect on GLP-1 secretion through growth hormone secretagogue receptor 1α (GHS1α receptor), which indicated that the downregulation of ghrelin secretion after food intake was necessary for incretin effect. Furthermore, our results suggested that the enteric neural net involved hepatic vagal nerve and sympathetic nerve mediated inhibition effect of ghrelin on incretin effect.


2009 ◽  
Vol 297 (2) ◽  
pp. R352-R361 ◽  
Author(s):  
Munetaka Shimizu ◽  
Kathleen A. Cooper ◽  
Walton W. Dickhoff ◽  
Brian R. Beckman

We examined postprandial changes in circulating growth hormone (GH), insulin, insulin-like growth factor (IGF)-I, and IGF-binding proteins (IGFBPs) in yearling coho salmon under different feeding regimes. Fish were initially fasted for 1 day, 1 wk, or 3 wk. Fasted fish were then fed, and blood was collected at 4-h intervals over 26 h. After the various periods of fasting, basal levels of insulin were relatively constant, whereas those of IGF-I, IGFBPs and GH changed in proportion to the duration of the fast. A single meal caused a rapid, large increase in the circulating insulin levels, but the degree of the increase was influenced by the fasting period. IGF-I showed a moderate increase 2 h after the meal but only in the regularly fed fish. Plasma levels of 41-kDa IGFBP were increased in all groups within 6 h after the single meal. The fasting period did not influence the response of 41-kDa IGFBP to the meal. IGFBP-1 and GH decreased after the meal to the same extent among groups regardless of the fasting period. The present study shows that insulin and IGF-I respond differently to long (weeks)- and short (hours)-term nutritional changes in salmon; insulin maintains its basal level but changes acutely in response to food intake, whereas IGF-I adjusts its basal levels to the long-term nutritional status and is less responsive to acute nutritional input. IGFBPs maintain their sensitivity to food intake, even after prolonged fasting, suggesting their critical role in the nutritional regulation of salmon growth.


2009 ◽  
Vol 123 (5) ◽  
pp. 1058-1065 ◽  
Author(s):  
Alexander W. Johnson ◽  
Rebecca Canter ◽  
Michela Gallagher ◽  
Peter C. Holland

1987 ◽  
Vol 253 (3) ◽  
pp. R516-R522 ◽  
Author(s):  
J. E. Morley ◽  
E. N. Hernandez ◽  
J. F. Flood

Neuropeptide Y (NPY) stimulates eating in a number of species. In the studies reported here, intracerebroventricular administration of porcine NPY increased eating in mice. In the presence of food, NPY caused enhancement of water intake, whereas in the absence of food, NPY suppressed water intake. Behavioral analysis showed that NPY decreased the latency to eat, increased the time spent eating, and decreased grooming. Human NPY also increased food intake, whereas the free acid of NPY was inactive. Although some minor discrepancies in response were noted overall, NPY was as effective at stimulating food intake in genetically obese (ob/ob) mice compared with their lean littermates (ob/-), in genetically diabetic mice (db/db) and their nondiabetic heterozygote control (db/m), in streptozocin-induced diabetic mice and their controls, and in adult (8 mo old) compared with old (25 mo old) mice.


2011 ◽  
Vol 197 (12) ◽  
pp. 1143-1147 ◽  
Author(s):  
L. Emadi ◽  
H. Jonaidi ◽  
E. Hosseini Amir Abad

1998 ◽  
Vol 275 (1) ◽  
pp. R120-R128
Author(s):  
Karina Jandziszak ◽  
Carlos Suarez ◽  
Ethan Wasserman ◽  
Ross Clark ◽  
Bonnie Baker ◽  
...  

Severe chronic metabolic acidosis (CMA) in rats is associated with poor food intake and downregulation of growth hormone (GH), insulin-like growth factors (IGFs), and liver receptors; the administration of recombinant GH (rGH) fails to improve the growth failure. In mice with carbonic anhydrase II deficiency (CAD), a model of moderate CMA with food intake close to normal, we studied serum levels of GH, IGFs, and IGF-binding proteins, and the growth response to rGH. CAD was associated with low serum levels of GH in males. Randomized administration of rGH from ∼5 to ∼12 wk to CAD mice improved food efficiency and increased serum IGF-I levels, final length, and weight compared with placebo without affecting blood pH. Although administration of rGH also increased linear growth in healthy animals, the effect was less than that in CAD mice and was only observed when started before 6 wk of life. Thus growth failure in CAD mice is associated with a decrease in GH secretion in males but not in females. Long-term administration of rGH increases linear growth in CAD mice despite persistent CMA.


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