Growth hormone (GH) immunoreactivity in the rodent and primate CNS: Distribution, characterization and presence posthypophysectomy

Hojvat, Sally; Baker, George P.; Kirsteins, L.; Lawrence, A. M.

doi:10.1016/0006-8993(82)90529-7

Cited by 85 publications

(52 citation statements)

References 18 publications

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“…GH and GH receptor (GHR) are present in regions known to participate in the regulation of feeding behavior, energy balance and motivation (Gossard et al, 1987;Hojvat et al, 1982;Lobie et al, 1993). Besides, GH positively regulates AgRP and NPY (Bohlooly et al, 2005;Chan et al, 1996) which are appetite-stimulating neuropeptides.…”

Section: Introductionmentioning

confidence: 99%

Increased food intake in growth hormone-transgenic common carp (Cyprinus carpio L.) may be mediated by upregulating Agouti-related protein (AgRP)

Zhong

Song

Wang

et al. 2013

General and Comparative Endocrinology

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Section: Introductionmentioning

confidence: 99%

Increased food intake in growth hormone-transgenic common carp (Cyprinus carpio L.) may be mediated by upregulating Agouti-related protein (AgRP)

Zhong

Song

Wang

et al. 2013

General and Comparative Endocrinology

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“…In rodents, GH increases food intake (3, 10) and alters the pattern of feeding (46). In both human and rat brain, GH and the GH receptor (GHR) are present in regions known to participate in the regulation of feeding behavior, energy balance, and motivation, including the hypothalamus, hippocampus, and amygdala (19,23,28,29,35,36), raising the possibility that GH may exert its effects on feeding in these central nervous system (CNS) areas.It is possible that the GH effects in CNS on feeding will include an interaction with the hypothalamic circuits regulating appetite and energy balance including also those involved in the action of ghrelin, an endogenous ligand for the GH secretagogue receptor (GHSR) (27). In addition to stimulating GH secretion, ghrelin and ghrelin mimetics (the GH secretagogues) increase food intake and body weight gain (via increasing fat accumulation) upon intracerebroventricular (ICV) injection and peripheral administration (30, 49), suggesting that it has a role in the regulation of feeding behavior and energy balance.…”

mentioning

confidence: 99%

Growth hormone receptor deficiency results in blunted ghrelin feeding response, obesity, and hypolipidemia in mice

Egecioglu

Bjursell²,

Ljungberg³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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Growth hormone receptor deficiency results in blunted ghrelin feeding response, obesity, and hypolipidemia in mice. Am J Physiol Endocrinol Metab 290: E317-E325, 2006. First published September 20, 2005 doi:10.1152/ajpendo.00181.2005We have previously shown that growth hormone (GH) overexpression in the brain increased food intake, accompanied with increased hypothalamic agouti-related protein (AgRP) expression. Ghrelin, which stimulates both appetite and GH secretion, was injected intracerebroventricularly to GHR Ϫ/Ϫ and littermate control (ϩ/ϩ) mice to determine whether ghrelin's acute effects on appetite are dependent on GHR signaling. GHR Ϫ/Ϫ mice were also analyzed with respect to serum levels of lipoproteins, apolipoprotein (apo)B, leptin, glucose, and insulin as well as body composition. Central injection of ghrelin into the third dorsal ventricle increased food consumption in ϩ/ϩ mice, whereas no change was observed in GHR Ϫ/Ϫ mice. After ghrelin injection, AgRP mRNA expression in the hypothalamus was higher in ϩ/ϩ littermates than in GHR Ϫ/Ϫ mice, indicating a possible importance of AgRP in the GHR-mediated effect of ghrelin. Compared with controls, GHR Ϫ/Ϫ mice had increased food intake, leptin levels, and total and intraabdominal fat mass per body weight and deceased lean mass. Moreover, serum levels of triglycerides, LDL and HDL cholesterol, and apoB, as well as glucose and insulin levels were lower in the GHR Ϫ/Ϫ mice. In summary, ghrelin's acute central action to increase food intake requires functionally intact GHR signaling. Long-term GHR deficiency in mice is associated with high plasma leptin levels, obesity, and increased food intake but a marked decrease in all lipoprotein fractions. agouti-related protein; appetite regulation; intracerebroventriclar injection GROWTH HORMONE (GH) IS ACTIVE in the central nervous system, influencing feeding behavior and the sense of well-being in humans (9, 48). In rodents, GH increases food intake (3, 10) and alters the pattern of feeding (46). In both human and rat brain, GH and the GH receptor (GHR) are present in regions known to participate in the regulation of feeding behavior, energy balance, and motivation, including the hypothalamus, hippocampus, and amygdala (19,23,28,29,35,36), raising the possibility that GH may exert its effects on feeding in these central nervous system (CNS) areas.It is possible that the GH effects in CNS on feeding will include an interaction with the hypothalamic circuits regulating appetite and energy balance including also those involved in the action of ghrelin, an endogenous ligand for the GH secretagogue receptor (GHSR) (27). In addition to stimulating GH secretion, ghrelin and ghrelin mimetics (the GH secretagogues) increase food intake and body weight gain (via increasing fat accumulation) upon intracerebroventricular (ICV) injection and peripheral administration (30, 49), suggesting that it has a role in the regulation of feeding behavior and energy balance.Expression of bovine (b)GH under transcriptional control of t...

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“…Both GH production and GH receptors are found in the brain. mRNA for GH can be found in different parts of the brain (17), and the most abundant GH immunoreactivity is found in the amygdala, hippocampus, and hypothalamus (18). GH receptors are also present in multiple locations in the rodent (19,20) and human brain (21,22).…”

mentioning

confidence: 99%

Growth Hormone Overexpression in the Central Nervous System Results in Hyperphagia-Induced Obesity Associated With Insulin Resistance and Dyslipidemia

et al. 2005

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It is well known that peripherally administered growth hormone (GH) results in decreased body fat mass. However, GH-deficient patients increase their food intake when substituted with GH, suggesting that GH also has an appetite stimulating effect. Transgenic mice with an overexpression of bovine GH in the central nervous system (CNS) were created to investigate the role of GH in CNS. This study shows that overexpression of GH in the CNS differentiates the effect of GH on body fat mass from that on appetite. The transgenic mice were not GH-deficient but were obese and showed increased food intake as well as increased hypothalamic expression of agouti-related protein and neuropeptide Y. GH also had an acute effect on food intake following intracerebroventricular injection of C57BL/6 mice. The transgenic mice were severely hyperinsulinemic and showed a marked hyperplasia of the islets of Langerhans. In addition, the transgenic mice displayed alterations in serum lipid and lipoprotein levels and hepatic gene expression. In conclusion, GH overexpression in the CNS results in hyperphagia-induced obesity indicating a dual effect of GH with a central stimulation of appetite and a peripheral lipolytic effect. Diabetes 54:51-62, 2005

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Growth hormone (GH) immunoreactivity in the rodent and primate CNS: Distribution, characterization and presence posthypophysectomy

Cited by 85 publications

References 18 publications

Increased food intake in growth hormone-transgenic common carp (Cyprinus carpio L.) may be mediated by upregulating Agouti-related protein (AgRP)

Increased food intake in growth hormone-transgenic common carp (Cyprinus carpio L.) may be mediated by upregulating Agouti-related protein (AgRP)

Growth hormone receptor deficiency results in blunted ghrelin feeding response, obesity, and hypolipidemia in mice

Growth Hormone Overexpression in the Central Nervous System Results in Hyperphagia-Induced Obesity Associated With Insulin Resistance and Dyslipidemia

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