Growth Hormone
Prolactin and Growth Hormone

Author: Gianpiero Pescarmona
Date: 23/01/2008

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Growth Hormone

Age dependence of serum GH

Pulsatile GH release

Growth and GH

LH pulsatile secretion

Sexually Dimorphic Regulation of Hepatic Isoforms of Human Cytochrome P450 by Growth Hormone 2005

Role of exercise on GH pulsatile release 1997

Metabolic relationships

A functional common polymorphism in the Vitamin D-Responsive Element of the GH1 promoter contributes to Isolated Growth Hormone Deficiency. 2007

Our results, both from the association analysis and from functional experiments, point to a
primary involvement of the -57T sequence in the VDRE for the low GH production of the IGHD patients.
Actually, the substitution by site specific mutagenesis of the T with a G at position -57
on the hp#1 context completely abolished the vitamin D induced inhibitory response of this
haplotype (Fig. 2). The functional relevance of the –57 sequence was also indicated by
EMSA (Fig. 3) showing that the T and the G alleles had a different protein binding affinity.
Since the associated allele has a high binding affinity for the vitamin D receptor and VDR is expressed in GH producing pituitary cells [35], the gene encoding the VDR is an obvious further candidate.


Seoane S, Alonso M, Segura C, Perez-Fernandez R 2002 Localization of a negative
vitamin D response sequence in the human growth hormone gene. Biochem Biophys Res
Commun 292: 250-255.

The synergistic regulation of the rat GH gene
involves protein-DNA interactions, as well as physical
association between nuclear receptors (RAR, RXR, and
TR) and GHF-1/Pit-1. Thus, it has been shown that
vitamin D interferes with growth hormone gene expression
induced by T3 and retinoic acid in the rat
GH4C1 pituitary cell line, probably through interference
by VDR with the binding of the thyroid receptor or
RA receptor to a common hormone response element
(13). This repressive role of VDR is also observed in the
retinoic acid-dependent activation of the retinoic acid
receptor-2 promoter (30). In our case, the VDRE located
on the hGH promoter is only 3-bp downstream of
the Pit-1 proximal site. For this reason, it is tempting
to speculate that VDR binding to the hGH gene may
also interfere with the binding of Pit-1 to its GH response
element. This hypothesis is supported by the
fact that MCF-7 cells express the Pit-1 transcription
factor, as has recently been demonstrated by our group
In conclusion, our results indicate that vitamin D
inhibits human GH gene transcription in the MCF-7
strain of human breast adenocarcinoma cells. The
1,25(OH)2 D3 responsive region in the hGH gene is
located between 62 and 29 bp upstream of the transcription
start site. This region overlaps with the
TATA box and is situated near the Pit-1 proximal
response element site. Although our data do not demonstrate
that the vitamin D receptor interferes with
transcriptional factors to inhibit induction of transcription
induction, this hypothesis should not be excluded.

Colnot S, Lambert M, Blin C, Thomasset M and Perret C 1995 Identification of DNA
sequences that bind retinoid X receptor-1,25 (OH)2D3-receptor heterodimers with high
affinity. Mol Cell Endocrinol 113: 85-98.

Shaffer PL, Gewirth DT 2002 Structural basis of VDR-DNA interactions on direct repeat
response elements. EMBO J 21: 2242-2252

Perez-Fernandez R, Alonso M, Segura C, Munoz I, Garcia-Caballero T, Diguez C 1997
Vitamin D receptor gene expression in human pituitary gland. Life Sci.60: 35-42.

Vitamin D interferes with transactivation of the growth hormone gene by thyroid hormone and retinoic acid. 1996

Genes under VDRE control

Large-scale in silico and microarray-based identification of direct 1,25-dihydroxyvitamin D3 target genes. 2005

growth hormone releasing hormone preproprotein
vascular endothelial growth factor B
placental growth factor, vascular endothelial growth factor-related protein
growth hormone inducible transmembrane protein
growth hormone releasing hormone receptor
growth hormone receptor
growth hormone 1 isoform 1-6

Linear growth in relation to the circulating concentrations of insulin-like growth factor I, parathyroid hormone, and 25-hydroxy vitamin D in children with nutritional rickets before and after treatment: endocrine adaptation to vitamin D deficiency. 2008

h3.GH. IGF-I and Vitamin D

The lower plasma 24,25(OH)(2)D(3) concentrations could be explained by the higher plasma GH and IGF-I concentrations in the large- vs. small-breed dogs, and these hormones are known to suppress 24-hydroxylation.(from Vitamin D3 metabolism in dogs 2002)

Assessment of endocrine and nutritional status in age-related catabolic states of muscle and bone. 2007

Inverse correlation between serum free IGF-I and IGFBP-3 levels and blood pressure in patients affected with type 1 diabetes. 2006

Decreased fractional urinary calcium excretion and serum 1,25-dihydroxyvitamin D and IGF-I levels in preeclampsia. 2007

GH loss with urine

Studies on the renal kinetics of growth hormone (GH) and on the GH receptor and related effects in animals. 1997

Urinary growth hormone measurements in children with renal insufficiency. 1995

GH effect on tubular functions

On the mechanism of growth hormone-induced stimulation of renal acidification in humans: effect of dietary NaCl. 2000

Metabolic bone disease associated with systemic disorders. 1991

Control of cell growth and differentiation

Papers corticosteroid therapy acromegaly

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