Central and Peripheral Regulation of Metabolism by Growth Hormone

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (31 October 2022) | Viewed by 3728

Special Issue Editor


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Guest Editor
Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo 05508-000, SP, Brazil
Interests: growth hormone; central nervous system; leptin; metabolism; hypothalamus

Special Issue Information

Dear Colleagues,

In several tissues, growth hormone (GH) action leads to protein synthesis, cell proliferation and tissue growth. Some of these effects are indirectly mediated by the insulin-like growth factor 1 (IGF-1). GH action also presents multiple metabolic effects, including the stimulation of lipolysis and insulin resistance. Furthermore, the brain is also involved in the metabolic effects of GH.

This Special Issue of Metabolites will be dedicated to publishing current advancements on the central and peripheral regulation of metabolism by GH. The topics that will be covered by this Special Issue include: the role of GH or IGF-1 in metabolically relevant tissues such as adipose tissue, skeletal muscle, pancreas and liver, the importance of the brain in mediating the metabolic effects of GH and IGF-1, the regulation of food intake by GH and/or IGF-1 and the association between metabolic diseases (e.g., diabetes, obesity, etc.) and dysfunctions in GH secretion. Manuscripts dealing with other challenging issues involving GH/IGF-1 and metabolism are also very welcome.

Dr. Jose Donato Jr.
Guest Editor

Manuscript Submission Information

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Keywords

  • IGF-1
  • GH
  • food intake
  • insulin resistance
  • diabetes
  • obesity
  • brain
  • liver
  • hypothalamus
  • adipose tissue

Published Papers (2 papers)

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Research

10 pages, 1416 KiB  
Article
Growth Hormone Alters Circulating Levels of Glycine and Hydroxyproline in Mice
by Jonathan A. Young, Silvana Duran-Ortiz, Stephen Bell, Kevin Funk, Yuan Tian, Qing Liu, Andrew D. Patterson, Edward O. List, Darlene E. Berryman and John J. Kopchick
Metabolites 2023, 13(2), 191; https://doi.org/10.3390/metabo13020191 - 28 Jan 2023
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Abstract
Growth hormone (GH) has established effects on protein metabolism, such as increasing protein synthesis and decreasing amino acid degradation, but its effects on circulating amino acid levels are less studied. To investigate this relationship, metabolomic analyses were used to measure amino acid concentrations [...] Read more.
Growth hormone (GH) has established effects on protein metabolism, such as increasing protein synthesis and decreasing amino acid degradation, but its effects on circulating amino acid levels are less studied. To investigate this relationship, metabolomic analyses were used to measure amino acid concentrations in plasma and feces of mice with alterations to the GH axis, namely bovine GH transgenic (bGH; increased GH action) and GH receptor knockout (GHRKO; GH resistant) mice. To determine the effects of acute GH treatment, GH-injected GH knockout (GHKO) mice were used to measure serum glycine. Furthermore, liver gene expression of glycine metabolism genes was assessed in bGH, GHRKO, and GH-injected GHKO mice. bGH mice had significantly decreased plasma glycine and increased hydroxyproline in both sexes, while GHRKO mice had increased plasma glycine in both sexes and decreased hydroxyproline in males. Glycine synthesis gene expression was decreased in bGH mice (Shmt1 in females and Shmt2 in males) and increased in GHRKO mice (Shmt2 in males). Acute GH treatment of GHKO mice caused decreased liver Shmt1 and Shmt2 expression and decreased serum glycine. In conclusion, GH alters circulating glycine and hydroxyproline levels in opposing directions, with the glycine changes at least partially driven by decreased glycine synthesis. Full article
(This article belongs to the Special Issue Central and Peripheral Regulation of Metabolism by Growth Hormone)
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11 pages, 1567 KiB  
Article
Childhood-Onset GH Deficiency versus Adult-Onset GH Deficiency: Relevant Differences Regarding Insulin Sensitivity
by Heraldo Mendes Garmes, Alejandro Rosell Castillo, Sarah Monte Alegre, Aglecio Luiz de Souza, Yeelen Ballesteros Atala and Denise Engelbrecht Zantut-Wittmann
Metabolites 2022, 12(12), 1251; https://doi.org/10.3390/metabo12121251 - 11 Dec 2022
Cited by 2 | Viewed by 1090
Abstract
The results of the studies on the pattern of insulin sensitivity (IS) are contradictory in patients with GH deficiency (GHD); however, the interference of the GHD onset stage, childhood or adulthood in the IS has not been assessed by euglycemic hyperinsulinemic clamp (EHC), [...] Read more.
The results of the studies on the pattern of insulin sensitivity (IS) are contradictory in patients with GH deficiency (GHD); however, the interference of the GHD onset stage, childhood or adulthood in the IS has not been assessed by euglycemic hyperinsulinemic clamp (EHC), a gold-standard method for the assessment of insulin sensitivity. In a prospective cross-sectional study, we assessed IS and body composition in 17 adults with hypopituitarism without GH replacement, ten with childhood-onset (COGHD) and seven with adulthood-onset (AOGHD) and compared them to paired control groups. COGHD presented higher IS (p = 0.0395) and a similar percentage of fat mass (PFM) to AOGHD. COGHD showed higher IS than the control group (0.0235), despite a higher PFM (0.0022). No differences were found between AODGH and the control group. In AOGHD and the control group, IS was negatively correlated with PFM (rs: −0.8214, p = 0.0234 and rs: −0.3639, p < 0.0344), while this correlation was not observed with COGHD (rs: −0.1152, p = 0.7514). Despite the higher PFM, patients with COGHD were more sensitive to insulin than paired healthy individuals, while patients with AOGHD showed similar IS compared to controls. The lack of GH early in life could modify the metabolic characteristics of tissues related to the glucose metabolism, inducing beneficial effects on IS that persist into adulthood. Thus, the glycometabolic findings in patients with COGHD seems to be not applicable to AOGHD. Full article
(This article belongs to the Special Issue Central and Peripheral Regulation of Metabolism by Growth Hormone)
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