Endocrine Parameters and Phenotypes of the Growth Hormone Receptor Gene Disrupted (GHR−/−) Mouse

List, Edward O.; Sackmann-Sala, Lucila; Berryman, Darlene E.; Funk, Kevin; Kelder, Bruce; Gosney, Elahu S.; Okada, Shigeru; Ding, Juan; Cruz‐Topete, Diana; Kopchick, John J.

doi:10.1210/er.2010-0009

Cited by 162 publications

(179 citation statements)

References 211 publications

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“…In contrast, the Dlk1-TG mice displayed moderately improved insulin sensitivity rather than the insulin resistance predicted by multiple models of GH signaling ablation (45). In addition, linear growth was not affected in our model.…”

Section: Discussionmentioning

confidence: 51%

DLK1/PREF1 regulates nutrient metabolism and protects from steatosis

Charalambous

Rocha

Radford

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Significance Hepatosteatosis or nonalcoholic fatty liver disease (NAFLD) is an important health problem affecting approximately 20% of the population of the United States and is associated with cardiovascular risk factors such as insulin resistance and obesity. Using a Delta-like homologue (Dlk1) [also known as preadipocyte factor 1 (Pref1)] transgenic model, we identified a new player in the growth hormone (GH) signaling pathway that, when overexpressed, is protective against obesity and hepatosteatosis. Because the dosage of circulating DLK1 is naturally elevated in early life and during pregnancy, we believe that our transgenic model mimics endogenous mechanisms of DLK1-mediated GH signaling modulation that are used during periods of metabolic stress to protect from steatosis and alter fuel utilization in the whole organism.

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Section: Discussionmentioning

confidence: 51%

DLK1/PREF1 regulates nutrient metabolism and protects from steatosis

Charalambous

Rocha

Radford

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…Physiological changes between GHR-/-mice and wildtype littermates are indicative of GH's actions. The GHR-/-mice have been a productive tool to study GH action, resulting in more than 100 published studies (for a comprehensive review, see [2]). …”

Section: Ghr-/-micementioning

confidence: 99%

“…These mice have a number of striking features that have been recently reviewed [2]. First, they are extremely insulin sensitive [3][4][5][6][7][8][9][10][11][12].…”

Section: Ghr-/-micementioning

confidence: 99%

“…Thus, depending on the population and associated environmental factors, it appears that some humans with LS actually do have improved glucose metabolism similar to the GHR-/-mice. [2]. GH, growth hormone; GHA, GH receptor antagonist; GHR, growth hormone receptor; IGF, insulin-like growth factor; ND, not determined.…”

Section: Clinical: Ghr-/-versus Laron Syndrome (Ls)mentioning

confidence: 99%

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Growth Hormone and Translational Research: From the 'Bench' to the 'Bedside'

et al. 2011

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“…As glial cells express GHR (McLenachan et al 2009) and astrocytes in GHR-deficient mice are smaller and less abundant (List et al 2011), our aim was to analyse the effects of GH and GHRP-6 on astrocyte proliferation and differentiation. In addition, as rats treated with GH or GHRP-6 showed increased levels of phosphorylated Akt in the hypothalamus, hippocampus and cerebellum, but not of ERKs1/2 (Frago et al 2002), and Akt is a central regulator of survival, growth and proliferation (Pascual & Guerri 2007), we evaluated the possible involvement of Akt in these processes.…”

Section: Introductionmentioning

confidence: 99%

Differential effects of GH and GH-releasing peptide-6 on astrocytes

Baquedano¹,

Chowen²,

Argente³

et al. 2013

Journal of Endocrinology

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GH and GH secretagogues (GHSs) are involved in many cellular activities such as stimulation of mitosis, proliferation and differentiation. As astrocytes are involved in developmental and protective functions, our aim was to analyse the effects of GH and GH-releasing hexapeptide on astrocyte proliferation and differentiation in the hypothalamus and hippocampus. Treatment of adult male Wistar rats with GH (i.v., 100 mg/day) for 1 week increased the levels of glial fibrillary acidic protein (GFAP) and decreased the levels of vimentin in the hypothalamus and hippocampus. These changes were not accompanied by increased proliferation. By contrast, GH-releasing hexapeptide (i.v., 150 mg/day) did not affect GFAP levels but increased proliferation in the areas studied. To further study the intracellular mechanisms involved in these effects, we treated C6 astrocytoma cells with GH or GH-releasing hexapeptide and the phosphatidylinositol 3 0 -kinase (PI3K) inhibitor, LY294002, and observed that the presence of this inhibitor reverted the increase in GFAP levels induced by GH and the proliferation induced by GH-releasing hexapeptide. We conclude that although GH-releasing hexapeptide is a GHS, it may exert GH-independent effects centrally on astrocytes when administered i.v., although the effects of both substances appear to be mediated by the PI3K/Akt pathway.

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Endocrine Parameters and Phenotypes of the Growth Hormone Receptor Gene Disrupted (GHR−/−) Mouse

Cited by 162 publications

References 211 publications

DLK1/PREF1 regulates nutrient metabolism and protects from steatosis

DLK1/PREF1 regulates nutrient metabolism and protects from steatosis

Growth Hormone and Translational Research: From the 'Bench' to the 'Bedside'

Differential effects of GH and GH-releasing peptide-6 on astrocytes

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