Activity of human growth hormone and related polypeptides on the adipose conversion of 3T3 cells.

Morikawa, Minoru; Green, H; Lewis, U J

doi:10.1128/mcb.4.2.228

Cited by 60 publications

(34 citation statements)

References 23 publications

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“…Consistent with the clinical features of GHD patients, several reports have suggested a stimulatory effect of GH on adipogenesis (Morikawa et al 1984, Nixon & Green 1984. While GHD patients show a decreased number of adipocytes, they can form adipose tissue (Bonnet et al 1974, Salomon et al 1989, Bengtsson et al 1993.…”

Section: Discussionmentioning

confidence: 58%

“…As GH replacement increases the number of adipocytes in GHD patients, this indicates a stimulatory effect of GH on adipogenesis. To date, adipogenic activity of GH has been reported in studies in vitro (Morikawa et al 1984, Nixon & Green 1984. GH is strictly required in the conversion of preadipocytes to adipocytes and is thought to play a role in priming the cells to become responsive to insulin and insulin-like growth factor-I (IGF-I) in 3T3-F442A cells (Guller et al 1989, Corin et al 1990, Wabitsch et al 1995.…”

Section: Introductionmentioning

confidence: 99%

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Growth hormone stimulates adipogenesis of 3T3-L1 cells through activation of the Stat5A/5B-PPARγ pathway

Kawai¹,

Namba²,

Mushiake³

et al. 2007

Journal of Molecular Endocrinology

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Growth hormone-deficient (GHD) patients show a decreased number of adipocytes, which is normalized by GH replacement, indicating an adipogenic effect of GH. However, the precise mechanisms underlying this effect remain to be clarified. In this study, we investigated the adipogenic effect of GH. GH stimulated MDI (3-isobutyl-1-methylxanthine, dexamethasone, and insulin)-induced adipogenesis of 3T3-L1 cells with early induction of peroxisome proliferator-activated receptors (PPAR)g2 expression. This adipogenic effect of GH was suppressed by overexpression of Stat5A mutant (Stat5A-Y694F), a transcriptional suppressor for the GH-Stat5A/5B signaling pathway, with the reduction of PPARg2 expression. Next, we investigated the relationship between Stat5A/5B and CCAAT/enhancer binding protein (C/EBP)b/d or PPARg in 3T3-L1 cells. Stat5A/5B stimulated C/EBPb-and C/EBPd-induced adipogenesis with enhancement of PPARg2 expression. In addition, Stat5A/5B enhanced the transcriptional activity of C/EBPb/d in the PPARg gene promoter. Furthermore, Stat5A/5B stimulated PPARg-induced adipogenesis and enhanced the transcriptional activity of PPARg. These results suggest that the GH-Stat5A/5B signaling pathway stimulates adipogenesis in cooperation with C/EBPb/d and PPARg. To completely understand the effect of GH, cDNA microarray analysis was performed to screen genes affected by GH during MDI-induced adipogenesis. Among 4277 genes, 18 and 19 genes were up-and down-regulated respectively. cDNA microarray analysis also indicated the up-regulation of PPARg and the modulation of expression of genes coding for growth factors or growth factor receptors, suggesting that GH stimulates adipogenesis in association with the modulation of cell growth. Thus, the GHStat5A/B signaling pathway stimulates adipogenesis through two distinct steps. In addition, cDNA microarray data provide us the further insights underlying the adipogenic effect of GH.

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Section: Discussionmentioning

confidence: 58%

Section: Introductionmentioning

confidence: 99%

Growth hormone stimulates adipogenesis of 3T3-L1 cells through activation of the Stat5A/5B-PPARγ pathway

Kawai¹,

Namba²,

Mushiake³

et al. 2007

Journal of Molecular Endocrinology

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“…6) This fact indicates the possibility that 3T3 preadipocytes can be used as standard cells for assaying the activity of GHs from species other than mammals and various variants of hGH derived by means of mutagenesis.7)…”

Section: Several Laboratoriesmentioning

confidence: 99%

Adipogenic Activity of Fish Growth Hormones on Mouse Preadipose 3T3 Cells

Morikawa

Sugimoto

Yokoo

et al. 1992

NSUGAF

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“…Also, as referred to in the literature, biological tests of adipogenic activity in culture cells use cat serum (which contains FCGH) instead of bovine serum, because FCGH lacks adipogenicity (17).…”

Section: Feline Growth Hormone (Fcgh)mentioning

confidence: 99%

“…These are in turn used by the fetus for his/her development. It also generates free fatty acids (by lipolytic effect), which are used as an energy source by the fetus (17,18). Little is known about the HCS physiological role, and still is not known its action mechanism.…”

Section: Human Chorionic Somatomammotropin (Hcs)mentioning

confidence: 99%