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Publication
Growth Hormone Deficiency and Excess Alter the Gut Microbiome in Adult Male
Mice.
Authors Jensen EA, Young JA, Jackson Z, Busken J, List EO, Carroll RK, Kopchick JJ,
Murphy ER, Berryman DE
Submitted By Submitted Externally on 9/28/2020
Status Published
Journal Endocrinology
Year 2020
Date Published 4/1/2020
Volume : Pages 161 : Not Specified
PubMed Reference 32100023
Abstract The gut microbiome has been implicated in host metabolism, endocrinology, and
pathophysiology. Furthermore, several studies have shown that gut bacteria
impact host growth, partially mediated through the growth hormone
(GH)/insulin-like growth factor 1 (IGF-1) axis. Yet, no study to date has
examined the specific role of GH on the gut microbiome. Our study thus
characterized the adult gut microbial profile and intestinal phenotype in GH
gene-disrupted (GH-/-) mice (a model of GH deficiency) and bovine GH transgenic
(bGH) mice (a model of chronic, excess GH action) at 6 months of age. Both the
GH-/- and bGH mice had altered microbial signatures, in opposing directions at
the phylum and genus levels. For example, GH-/- mice had significantly reduced
abundance in the Proteobacteria, Campylobacterota, and Actinobacteria phyla,
whereas bGH mice exhibited a trending increase in those phyla compared with
respective controls. Analysis of maturity of the microbial community
demonstrated that lack of GH results in a significantly more immature microbiome
while excess GH increases microbial maturity. Several common bacterial genera
were shared, although in opposing directions, between the 2 mouse lines (e.g.,
decreased in GH-/- mice and increased in bGH mice), suggesting an association
with GH. Similarly, metabolic pathways like acetate, butyrate, heme B, and
folate biosynthesis were predicted to be impacted by GH. This study is the first
to characterize the gut microbiome in mouse lines with altered GH action and
indicates that GH may play a role in the growth of certain microbiota thus
impacting microbial maturation and metabolic function.




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