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

@article{Egecioglu2006GrowthHR,
  title={Growth hormone receptor deficiency results in blunted ghrelin feeding response, obesity, and hypolipidemia in mice.},
  author={Emil Egecioglu and Mikael Bjursell and Anna Ljungberg and Suzanne L. Dickson and John J. Kopchick and G{\"o}ran Bergstr{\"o}m and Lennart Svensson and Jan Oscarsson and Jan Törnell and M Bohlooly-y},
  journal={American journal of physiology. Endocrinology and metabolism},
  year={2006},
  volume={290 2},
  pages={
          E317-25
        }
}
We 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-/- and littermate control (+/+) mice to determine whether ghrelin's acute effects on appetite are dependent on GHR signaling. GHR-/- mice were also analyzed with respect to serum levels of lipoproteins… 

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Role of endogenous ghrelin in growth hormone secretion, appetite regulation and metabolism

Substantial data have implicated ghrelin as an important regulator of feeding behavior and energy equilibrium and this effect is mediated through hypothalamic neuropeptide Y (NPY) and Agouti-related peptide (AgRP).

Effect of Ghrelin on Glucose-Insulin Homeostasis: Therapeutic Implications

Mice with targeted deletion of either ghrelin or the GHSR exhibit an essentially normal metabolic phenotype when fed a regular chow diet, suggesting that gh Relin may have a redundant role in the regulation of food intake.

Central ghrelin regulates peripheral lipid metabolism in a growth hormone-independent fashion.

The existence of a new central nervous system-based neuroendocrine circuit, regulating metabolic homeostasis of adipose tissue, is suggested by the effect of central ghrelin administration on lipid metabolism in lipogenic tissues (liver and WAT) in the absence of GH.

The absence of GH signaling affects the susceptibility to high-fat diet-induced hypothalamic inflammation in male mice.

The GH/IGF-1 axis is important in determining not only adipose tissue accrual but also the inflammatory response to HFD, however, how hypothalamic inflammation/gliosis is defined will determine whether it can be considered a common feature of HFD-induced obesity.

Ghrelin-Induced Food Intake, But not GH Secretion, Requires the Expression of the GH Receptor in the Brain of Male Mice.

The findings indicate that GHR signaling in the brain is required for the orexigenic effect of ghrelin, independently of GH action on ARH AgRP/NPY neurons.

Effects of isolated GH deficiency on adipose tissue, feeding and adipokines in mice.

Effects of Growth Hormone Receptor Ablation in Corticotropin-Releasing Hormone Cells

GHR ablation, specifically in CRH-expressing neurons, does not lead to major alterations in metabolism, hypothalamic–pituitary–adrenal axis, acute stress response or anxiety in mice.

The Pentapeptide RM-131 Promotes Food Intake and Adiposity in Wildtype Mice but Not in Mice Lacking the Ghrelin Receptor

The data show that in wildtype mice RM-131 potently promotes weight gain and adiposity through stimulation of food intake, however, RM- 131 fails to affect food intake and body weight in mice lacking the GHR, underlining that the anabolic effects ofRM-131 are mediated via the ghrelin receptor in mice.
...

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