Further Evidence That Thyrotropin-Releasing Hormone Participates in the Regulation of Growth Hormone Secretion in the Rat

Bluet‐Pajot, Marie‐Thérèse; Durand, Dominique; Drouva, Sophia V.; Mounier, Françoise; Pressac, M; Kordon, C.

doi:10.1159/000124624

Cited by 29 publications

(21 citation statements)

References 22 publications

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“…Two days before data collection, an indwelling cannula was inserted into the right atrium under ether anesthesia, as previously described [25]. On the day of the experiments, 2 h before the sampling period, the distal extremity of the cannula was connected to a polyethylene catheter filled with 25 IU/ml of heparinized saline.…”

Section: Methodsmentioning

confidence: 99%

Delayed Age-Associated Decrease in Growth Hormone Pulsatile Secretion and Increased Orexigenic Peptide Expression in the Lou C/Jall Rat

et al. 2004

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Since modifications in the growth hormone/insulin-like growth factor 1 (GH/IGF-1) axis and/or caloric restriction are involved in the ageing process, GH secretory profiles, total IGF-1, ghrelin, and leptin plasma levels and expression of genes implicated in somatotrope axis and food intake regulation in hypothalamus and pituitary were compared in 3-, 12-, and 24-month-old male Lou C/Jall rats and their parent strain, the Wistar rats. The Lou C/Jall strain may appear as a healthy ageing model, since it does not become obese with age and maintains its caloric intake at 2 years of age. The GH pulsatile secretion decreased from 3 months in Wistar, but only after 12 months in Lou C/Jall rats. The IGF-1 levels were lower in Lou C/Jall rats and decreased more steeply with ageing as compared with Wistar rats. The total ghrelin levels were higher in young Lou C/Jall rats than in Wistar rats, but increased similarly with age in both strains. The leptin concentrations increased with ageing only in Wistar rats. By semiquantitative reverse-transcription polymerase chain reaction, pituitary GH secretagogue receptors and GH mRNA levels were more abundant in Lou C/Jall rats, and the latter decreased with ageing in Wistar rats only. Hypothalamic growth-hormone-releasing hormone and GH secretagogue receptor mRNA levels were similar in both strains and transiently increased only in middle-aged Wistar rats. Agouti-related peptide, neuropeptide Y, and orexin mRNA levels were more abundant in the Lou C/Jall rat hypothalamus, and the two former tended to further increase with age only in this strain. Conversely, the hypothalamic pro-opiomelanocortin mRNA levels were higher in old Wistar rats. In conclusion, ageing in Lou C/Jall rats is associated with a delayed decrease in pulsatile GH secretion in the presence of a lower IGF-1 tone and an increase in the expression of orexigenic neuropeptides in the hypothalamus.

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Section: Methodsmentioning

confidence: 99%

Delayed Age-Associated Decrease in Growth Hormone Pulsatile Secretion and Increased Orexigenic Peptide Expression in the Lou C/Jall Rat

et al. 2004

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“…Experiments were performed on freely moving rats implanted with an indwelling cannula inserted into the right atrium 2 days earlier under ether anesthesia, as previously described [7]. The distal extremity of the cannula was connected to a polyethylene catheter filled with 25 IU/ml heparinized saline 2 h before the beginning of sampling.…”

Section: Methodsmentioning

confidence: 99%

In vivo and in vitro Effects of Ghrelin/Motilin-Related Peptide on Growth Hormone Secretion in the Rat

et al. 2001

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Ghrelin (Ghr), a 28 amino acid gastric peptide with an n-octanoylation on Ser 3, has recently been identified as an endogenous ligand of the growth hormone secretagogue (GHS) receptor. A cDNA was also isolated from a mouse stomach library encoding a protein named prepromotilin-related peptide (ppMTLRP) which shares sequence similarities with prepromotilin. Mouse and rat ppMTLRP sequences (rGhr) are identical and show 89% identity with human ghrelin (hGhr). By analogy with promotilin, cleavage of proMTLRP into an 18 amino acid endogenous processed peptide can be assumed on the basis of a conserved dibasic motif in position 9–10 of its sequence. In the present work, we compared the GH-releasing activity of rGhr28/MTLRP and of hGhr28/MTRLP with that of a shorter form of the peptide, hGhr18. A short peptide devoid of Ser-3 n-octanoylation hGhr18[–] was also tested. Addition of rGhr28, hGhr28 and hGhr18 stimulated GH release to the same extent from superfused pituitaries. The effect was dose dependent in a 10^–8 to 10^–6M concentration range. In contrast, hGhr 18[–] was inactive. In freely moving animals, both rGhr28 and hGhr28 (10 µg, i.v.) stimulated GH release, whereas the same dose of hGhr18 or of hGhr18[–] was ineffective. After rGhr28, GH plasma levels increased as early as 5 min after injection and returned to basal values within 40–60 min. Expressed as percent stimulation, administration of rGhr28 was equally effective when injected during troughs or peaks of GH. Plasma concentrations of prolactin, adrenocorticotropin and leptin were not modified. Spontaneous GH secretory episodes were no longer observed within 3 h of rGhr28 treatment, but repeated administration of the secretagogue at 3- to 4-hour intervals resulted in a similar GH response. Activation of somatostatin (SRIH) release by ether stress did not blunt the GH response to rGhr28. This suggests that the secretagogue acts in part by inhibiting endogenous SRIH, as further substantiated by the ability of rGhr28 (10^–6M), to decrease the amplitude of 25 mM K⁺-induced SRIH release from perifused hypothalami. In conclusion, (1) n-octanoylation of Ghrs and the shorter form hGhr18 is essential for the direct pituitary GH-releasing effect of this new family of endogenous GHSs; (2) only the longer forms are active in vivo and (3) inhibition of SRIH release appears involved in the mechanism of Ghr action.

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“…After 18 days, a Silastic cannula was inserted, under isoflurane anesthesia (1.8%, air flow: 500 ml/min), through the right external jugular vein to approach or enter the right atrium and was exteriorized to the back of the neck, as previously described (6). After surgery, the rats were returned to their individual home cages for recovery of 1 day during which they received no further treatment.…”

Section: Experiments 3: Effect Of Meal Feeding Patterns On Circulatingmentioning

confidence: 99%

Scheduled feeding results in adipogenesis and increased acylated ghrelin

Verbaeys

Tolle

Swennen

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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Verbaeys I, Tolle V, Swennen Q, Zizzari P, Buyse J, Epelbaum J, Cokelaere M. Scheduled feeding results in adipogenesis and increased acylated ghrelin. Am J Physiol Endocrinol Metab 300: E1103-E1111, 2011. First published March 22, 2011; doi:10.1152/ajpendo.00551.2010.-Ghrelin, known to stimulate adipogenesis, displays an endogenous secretory rhythmicity closely related to meal patterns. Therefore, a chronic imposed feeding schedule might induce modified ghrelin levels and consequently adiposity. Growing Wistar rats were schedule-fed by imposing a particular fixed feeding schedule of 3 meals/day without caloric restriction compared with total daily control intake. After 14 days, their body composition was measured by DEXA and compared with ad libitum-fed controls and to rats daily intraperitoneal injection with ghrelin. Feeding patterns, circadian activity, and pulsatile acylated ghrelin variations were monitored. After 14 days, rats on the imposed feeding schedule displayed, despite an equal daily calorie intake, a slower growth rate compared with ad libitum-fed controls. Moreover, schedule-fed rats exhibiting a feeding pattern with intermittent fasting periods had a higher fat/lean ratio compared with ad libitum-fed controls. Interestingly, ghrelin-treated rats also showed an increase in fat mass, but the fat/lean ratio was not significantly increased compared with controls. In the schedule-fed rats, spontaneous activity and acylated ghrelin levels were increased and associated with the scheduled meals, indicating anticipatory effects. Our results suggest that scheduled feeding, associated with intermittent fasting periods, even without nutrient/ calorie restriction on a daily basis, results in adipogenesis. This repartitioning effect is associated with increased endogenous acylated ghrelin levels. This schedule-fed model points out the delicate role of meal frequency in adipogenesis and provides an investigative tool to clarify any effects of endogenous ghrelin without the need for ghrelin administration. metabolism; obesity; feeding patterns; meal frequency; dual-energy X-ray absorptiometry IN HUMANS, THE CORRELATION between meal patterns and obesity was pointed out in 1964, when Fábry et al. (19) reported that individuals consuming three meals or less per day were more overweight and more prone to hyperinsulinemia and glucose intolerance than those consuming five or more meals a day. Later on, an inverse relationship was shown between meal frequency and BMI in some (39) but not all populations studied (5, 18). Limited scientific literature on scheduled feeding, some going back more than 50 years, showed that force-fed rats also display a completely different metabolism with a concomitant change in body composition compared with freely fed rats despite similar caloric intake (2, 4, 10, 11).Previous research investigating the characteristics of a newly synthesized anorectic peptide, polyethylene glycol-cholecystokinin 9 (PEG-CCK 9 ) (28, 48 -50), revealed that rats fed a scheduled feeding to mimic the 3-to 6...

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Further Evidence That Thyrotropin-Releasing Hormone Participates in the Regulation of Growth Hormone Secretion in the Rat

Cited by 29 publications

References 22 publications

Delayed Age-Associated Decrease in Growth Hormone Pulsatile Secretion and Increased Orexigenic Peptide Expression in the Lou C/Jall Rat

Delayed Age-Associated Decrease in Growth Hormone Pulsatile Secretion and Increased Orexigenic Peptide Expression in the Lou C/Jall Rat

In vivo and in vitro Effects of Ghrelin/Motilin-Related Peptide on Growth Hormone Secretion in the Rat

Scheduled feeding results in adipogenesis and increased acylated ghrelin

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