Changes in Serum Growth Hormone Levels from Fetal to Adult Age in the Rat

Blázquez, Enrique; Simon, Frederic A.; Blázquez, Mercedes; Foà, Piero P.

doi:10.3181/00379727-147-38437

Cited by 54 publications

(26 citation statements)

References 9 publications

(9 reference statements)

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“…These patterns observed here are similar to those observed in previous reports [39,40]. Although fetal pituitary rGH is detected by RIA [39] and rGH mRNA-positive cells appear in the fetal pituitary [41] during the last three days of pregnancy, the source of fetal serum rGH is not clear. Furthermore, no information is available about the physiological role of rGH in the fetal circulation.…”

Section: Discussionsupporting

confidence: 88%

Gestational Profiles of Rat Placental Lactogen-II(rPL-ll) and Growth Hormone(GH) im Maternal and Fetal Serum, Amniotic Fluid, and Placental Tissue.

1991

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Section: Discussionsupporting

confidence: 88%

Gestational Profiles of Rat Placental Lactogen-II(rPL-ll) and Growth Hormone(GH) im Maternal and Fetal Serum, Amniotic Fluid, and Placental Tissue.

1991

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“…Plasma insulin decreases and glucagon increases in the immediate postnatal period in most species including humans, rats, rabbits, sheep, and pigs (10,11). Perinatal decreases in insulin and increases in glucagon have been suggested to be the result of the stress of birth and through the activation of the sympathetic nervous system (12,13).…”

Section: From the Cardiovascular Research Group University Of Albertmentioning

confidence: 99%

gAd-globular Head Domain of Adiponectin Increases Fatty Acid Oxidation in Newborn Rabbit Hearts

Onay-Beşi̇kçi̇¹,

Altarejos

Lopaschuk

2004

Journal of Biological Chemistry

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Adiponectin is an adipocyte-derived hormone that has a number of metabolic effects in the body, including the control of both glucose and fatty acid metabolism. The globular head domain of adiponectin, gAd, has also been shown to increase fatty acid oxidation in skeletal muscle. Within days after birth, a rapid increase in fatty acid oxidation occurs in the heart. We examined whether adiponectin or gAd plays a role in this maturation of cardiac fatty acid oxidation. Plasma adiponectin increased in newborn rabbits following birth: 1.2 ؎ 0.3 g/ml in 1-day-old, 6.8 ؎ 1.8 g/ml in 7-day-old, and 45 ؎ 5 g/ml in 6-week-old rabbits. Because plasma insulin levels decrease and remain low throughout the suckling period, and because this decrease may contribute to the maturation of fatty acid oxidation, we examined the effects of adiponectin and gAd on fatty acid oxidation in isolated perfused 1-day-old rabbit hearts in the presence or absence of 100 microunits/ml insulin. Adiponectin (10 g/ml) did not alter fatty acid oxidation in the presence of insulin. In the absence of insulin, the addition of recombinant gAd (1.5 g/ml) increased fatty acid oxidation compared with control (129 ؎ 18 versus 66 ؎ 11 nmol⅐g dry weight ؊1 ⅐min ؊1 , respectively (p < 0.05). In 7-day-old hearts, where fatty acid oxidation rates were 5-fold higher than 1-day-old hearts, gAd did not alter fatty acid oxidation rates. The increase in fatty acid oxidation in 1-day-old hearts occurred independently of changes in 5-AMP-activated protein kinase, acetyl-CoA carboxylase, or malonyl-CoA. The effect of gAd on fatty acid oxidation was reversed in the presence of 100 microunits/ml insulin. These results suggest that a decrease in plasma insulin and increase in gAd are involved in the increase of cardiac fatty acid oxidation in the immediate newborn period.Adiponectin is an adipocyte-derived polypeptide hormone of ϳ30-kDa (1). It has a signal sequence at the N terminus, a small nonhelical region, a stretch of repeated collagens, and a C-terminal globular head domain (gAd) that makes up for the majority of the protein (2). Recently, gAd has been shown to increase fatty acid oxidation in muscle and cause weight loss in mice (3). Yamauchi et al. (4) demonstrated that gAd and fulllength adiponectin stimulate 5Ј-AMP-activated protein kinase (AMPK) 1 in skeletal muscle. Activation of AMPK increases the phosphorylation of acetyl-CoA carboxylase (ACC), fatty acid oxidation, glucose uptake, and lactate production in C2C12 myocytes. When administered in vivo, both full-length adiponectin and gAd stimulated AMPK and increased the phosphorylation of ACC in the mouse soleus muscle (4). Moreover, stimulation of AMPK with full-length adiponectin also reduces gluconeogenesis in the liver and plasma glucose (4). In agreement with these findings, Tomas et al. (5) reported that gAd stimulates fatty acid oxidation in skeletal muscle by activating AMPK and inactivating ACC. Recently, Yamauchi et al. (6) cloned complementary DNAs encoding two adiponectin receptors, AdipoR1 an...

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“…In neonatal rats, serum growth hormone (GH) concentrations are high after birth, and then there is a decline by 15±20 days of age (1,2). In the first days of life, GH secretion is stimulated by g-amino butyric acid (GABA) (3), thyroliberin (TRH) (4,5), growth hormone-releasing hormone (GHRH) (6) and excitatory amino acids (EAAs) (7).…”

Section: Introductionmentioning

confidence: 99%

5-HT1 and 5-HT2 receptor agonists blunt +/- -alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-stimulated GH secretion in prepubertal male rats

Pinilla

González²,

Tena‐Sempere³

et al. 2001

European Journal of Endocrinology

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Objective: Excitatory amino acids, g-amino butyric acid (GABA), serotonin and catecholamines are involved in the control of GH secretion. The actions of these neurotransmitters are interconnected, and recently we showed that the stimulatory effect of GABA was blocked by MK-801, an antagonist of N-methyl-D-aspartate receptors. The present experiments were carried out to analyze the interrelationships between (^)-a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors and serotoninergic and catecholaminergic pathways in the control of GH secretion in prepubertal (16±23-day-old) male rats. Design and Methods: The GH response to AMPA was analyzed in animals pretreated with 5-hydroxytryptophan methyl ester (5-HTP) plus fluoxetine (a precursor of 5-hydroxytryptamine (5-HT) synthesis and a blocker of 5-HT re-uptake), R (+)-8-hydroxydipropylaminotetralin hydrobromide (8-OH-DPAT, an agonist of the 5-HT 1 receptors), (^)-2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) and a-methyl-5-hydroxytryptamine (agonists of 5-HT 2 receptors), I-phenylbiguanide (an agonist of 5-HT 3 receptors), or a-methyl-p-tyrosine (a-MPT) and diethyldithiocarbamate (DDC) (blockers of catecholamine synthesis). Results: Basal GH secretion remained unchanged in prepubertal rats after activation of the serotoninergic system or blockade of catecholamine synthesis. The stimulatory effect of AMPA on GH secretion was blocked after activation of the serotoninergic system, through specific 5-HT 1 and 5-HT 2 receptor agonists. In contrast, activation of 5-HT 3 receptors potentiated AMPA-stimulated GH secretion. Conclusions: Serotoninergic receptors modulate the stimulatory effect of AMPA on GH secretion in prepubertal male rats.

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Changes in Serum Growth Hormone Levels from Fetal to Adult Age in the Rat

Cited by 54 publications

References 9 publications

Gestational Profiles of Rat Placental Lactogen-II(rPL-ll) and Growth Hormone(GH) im Maternal and Fetal Serum, Amniotic Fluid, and Placental Tissue.

Gestational Profiles of Rat Placental Lactogen-II(rPL-ll) and Growth Hormone(GH) im Maternal and Fetal Serum, Amniotic Fluid, and Placental Tissue.

gAd-globular Head Domain of Adiponectin Increases Fatty Acid Oxidation in Newborn Rabbit Hearts

5-HT1 and 5-HT2 receptor agonists blunt +/- -alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-stimulated GH secretion in prepubertal male rats

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