Continuous administration of growth hormone does not prevent the decrease of IGF-I gene expression in zinc-deprived rats despite normalization of liver GH binding

Ninh, Nguyen Xuan; Maiter, Dominique; Lause, Pascale; Chrzanowska, B; Underwood, Louis E.; Ketelslegers, Jean‐Marie; Thissen, Jean‐Paul

doi:10.1016/s1096-6374(98)80299-2

Cited by 18 publications

(20 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, in rats, as in humans, dietary zinc deprivation is associated with low serum IGF-I concentrations. Previous experiments of our group have shown that the decline in IGF-I caused by zinc deprivation results from a state of GH resistance (Ninh et al 1997).…”

Section: Introductionmentioning

confidence: 89%

“…Although the circulating levels of most major IGFBPs are decreased in response to zinc deprivation (Clegg et al 1995, Ninh et al 1997, it is possible that this decline in blood reflects an increase of IGFBPs (mainly IGFBP-3) at the cell surface where they could limit the access of IGF-I to the type 1 IGF receptor (Conover 1991). The marked decrease of serum IGFBP-3 levels in response to zinc deprivation together with the minimal changes in liver IGFBP-3 mRNA levels supports this possibility.…”

Section: Ctrlmentioning

confidence: 98%

See 1 more Smart Citation

Failure of exogenous IGF-I to restore normal growth in rats submitted to dietary zinc deprivation

Ninh

Maiter²,

Verniers³

et al. 1998

Journal of Endocrinology

View full text Add to dashboard Cite

Dietary zinc deficiency in rats causes growth retardation associated with decreased circulating IGF-I concentrations. To investigate the potential role of low IGF-I in this condition, we attempted to reverse the growth failure by administration of exogenous IGF-I. Rats were fed for 4 weeks a zinc-deficient diet (ZD, Zn 0 ppm) or were pair-fed a zinc-normal diet (PF, Zn 75 ppm). We compared the anabolic action of recombinant human (rh) IGF-I infused at the dose of 120 µg/day for the last experimental week in ZD, PF and freely fed control (CTRL) rats. Zinc deficiency caused growth stunting (weight gain 47% of PF; P<0·001), decreased circulating IGF-I (52% of PF; P<0·01) and liver IGF-I mRNA (67% of PF; P<0·01). Serum insulin-like growth factor-binding protein-3 (IGFBP-3) assessed by ligand blot was also reduced in ZD rats (65% of PF; P<0·01). While exogenous IGF-I increased body weight in CTRL (+12 g; P<0·01) and PF (+7 g; not significant) animals, growth was not stimulated in ZD rats ( 1·5 g) in comparison with the corresponding untreated groups. However, circulating IGF-I and IGFBP-3 levels were restored by IGF-I infusion to levels similar to those in untreated CTRL rats. In conclusion, restoration of normal circulating levels of IGF-I and IGFBP-3 by rhIGF-I infusion fails to reverse the growth retardation induced by zinc deficiency. These results suggest that growth retardation related to zinc deficiency is not only caused by low serum IGF-I concentrations, but also by inhibition of the anabolic actions of IGF-I.

show abstract

Section: Introductionmentioning

confidence: 89%

Section: Ctrlmentioning

confidence: 98%

Failure of exogenous IGF-I to restore normal growth in rats submitted to dietary zinc deprivation

Ninh

Maiter²,

Verniers³

et al. 1998

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…However, with regard to hormone-mediated alterations in cellular metabolism, changed patterns (concentrations) of individual nutrients/metabolites in a cell can in addition to the hormones affect gene expression by interaction with specific targets including nuclear receptors and response elements as depicted in Figure 1. The lack of an essential nutrient causing a sustained deficiency syndrome can also secondarily alter hormone secretion and action and thereby affect gene expression directly and indirectly in the most complex ways (Roth and Kirchgessner, 1994;Ninh et al, 1995Ninh et al, , 1998.…”

Section: How Do Nutrients Affect Gene Expression In General?mentioning

confidence: 99%

“…The zinc status in mammals is known to affect growth and this is mediated at least in part through the somatotropic axis with alterations in the level of circulating insulin-like growth factor I (IGF-I) (McNall et al, 1995;Ninh et al, 1995;Lefebvre et al, 1998Lefebvre et al, , 1999Ninh et al, 1998). Correspondingly, seven of the identified hepatic transcripts with reduced expression levels in zinc-deficient rats related to liver targets of growth regulation including the growth hormone receptor (GHR), the GHR binding protein (GHRBP), IGF-I, the IGF binding proteins IGFBP1 and IGFBP2 and a subunit of IGFPB (tom Dieck et al, 2003).…”

Section: From Growth Control To Metabolismmentioning

confidence: 99%

Nutrient-gene interactions: a single nutrient and hundreds of target genes

Daniel¹,

Dieck²

2004

Biological Chemistry

View full text Add to dashboard Cite

Based on the effects of a selective experimental zinc deficiency in a rodent model we explore the use of transcriptome profiling for assessing nutrient-gene interactions in the liver at the molecular and cellular levels. Zinc deficiency caused pleiotropic alterations in mRNA/protein levels of hundreds of genes. In the context of observed metabolic alterations in hepatic metabolism, possible mechanisms are discussed for how a low zinc status may be sensed and transmitted into changes in various metabolic pathways. However, it also becomes obvious that analysis of such complex nutrient-gene interactions beyond the descriptional level is a real challenge for systems biology.

show abstract

“…92 A controversy exists in the literature about whether the effect of zinc deficiency on IGF-1 hepatic expression is due to a dysregulation of the GH receptor pathway or to a direct action of zinc on IGF-1. 93 In other words, although GH biology certainly plays a role in the regulation of hepatic IGF-1 expression, nutritional zinc also contributes in a fashion independent of the GH pathway. The first study supplemented KunMing mice with zinc and found that while serum and hepatic IGF-1 mRNA levels increased in these animals, serum and hepatic GH receptor mRNA levels remained unchanged.…”

Section: Insulin-like Growth Factor-1mentioning

confidence: 99%