Abstract
The regulation of growth hormone (GH) release during prenatal development and during early postnatal life is not entirely clarified. In this study plasma GH concentrations in pigs with inherited pseudo vitamin D deficiency type I (PDDR-I), which regularly show growth retardation, were compared during ontogeny with unaffected pigs of the same breed (German Landrace, DL) as control. Plasma GH concentrations were measured in plasma of chronically catheterized fetuses (beginning on day 101 after mating or after artificial insemination) and in piglets (day 37 postpartum (p.p.)—day 42 p.p.) of both lines. A growth curve beginning at day 7 p.p. was recorded for both lines. The relative amount of GH receptor (GHR) mRNA in liver was quantified by competitive reverse transcription polymerase chain reaction in piglets at day 42 p.p. A trend for higher GH concentrations was observed in PDDR-I fetuses (p < 0.1). In PDDR-I piglets compared to DL piglets higher plasma GH values (p < 0.01), were observed despite lower body weight. The relative quantity of GHR mRNA in liver was not significantly different between the two lines. Piglets with an inherited defect of vitamin D synthesis showed higher GH concentrations. A hormonal imprinting by low 1,25(OH)2D3 could be one reason for our observations and should be analysed in detail in future.
Highlights
Inadequate vitamin D sustenance is currently a global problem in humans [1]
It was suggested that vitamin D treatment may improve the management of growth hormone (GH) deficiency in humans because it increases the secretion of circulating insulin-like growth factor-I (IGF-I) [6]
Experiments were conducted in fetuses and piglets with a defect in 25-hydroxyvitamin D3 1α hydroxylation (PDDR-I) in comparison to unaffected pigs of the same breed (DL)
Summary
Inadequate vitamin D sustenance is currently a global problem in humans [1]. Deficits depend for example on the exposition to sunlight, affecting diseases beyond calcium metabolism, as discussed by Sowah et al [2]. Lower birth weight and disturbed neonatal growth in humans are associated with maternal vitamin D deficiency [3,4,5]. It was suggested that vitamin D treatment may improve the management of GH deficiency in humans because it increases the secretion of circulating insulin-like growth factor-I (IGF-I) [6]. Nutrients 2018, 10, 617 stages of development and that GH-deficient newborns have abnormal growth pattern [7]. In late gestation growth is mostly related to hormones influencing maternal nutrient partition via placental blood flow to the fetus [8]. The GH receptor (GHR) mRNA abundance is linked with the nutritional status of the piglet. Fasting for 20–24 h reduces the amount of GHR mRNA in the liver of 7 weeks old piglets [11]. The IGF-I response to recombinant porcine GH challenge is only moderate up to day 37 postpartum (p.p.) but increases progressively afterwards [12]
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