Post-receptor crosstalk between growth hormone and insulin signal in rats born small for gestational age with catch-up growth.
OBJECTIVE: Insulin resistance has been observed in individuals born small for gestational age (SGA) with catch-up growth (CUG), yet the mechanisms involved remain unclear. This study examined the role of GH and insulin signaling crosstalk in insulin resistance of SGA rats with CUG. DESIGN AND METHOD...
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doaj-bf9345030ada463082046a26e1b17bd92020-11-24T21:43:49ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0196e10045910.1371/journal.pone.0100459Post-receptor crosstalk between growth hormone and insulin signal in rats born small for gestational age with catch-up growth.Hong-Zhu DengHong DengChao-Qun CenKai-Yun ChenMin-Lian DuOBJECTIVE: Insulin resistance has been observed in individuals born small for gestational age (SGA) with catch-up growth (CUG), yet the mechanisms involved remain unclear. This study examined the role of GH and insulin signaling crosstalk in insulin resistance of SGA rats with CUG. DESIGN AND METHODS: SGA rats were developed by dietary restriction in pregnant rats. GH receptor inhibition was performed on four-week old CUG-SGA and AGA rats. Phosphorylation of IRS-1, AKT, and ERK, and expression of SOCS3 in the skeletal muscle were determined via immunoblot analysis at baseline and after insulin stimulation in CUG-SGA, NCUG-SGA and AGA groups. RESULTS: Compared to AGA controls, phosphorylation of IRS-1 and AKT in response to insulin stimulation in CUG-SGA rats was significantly blunted (P<0.05), and phosphorylation of ERK at baseline was dramatically activated (P<0.05). SOCS3 expression was significantly increased in CUG-SGA compared to AGA (P = 0.001) and NCUG-SGA (P = 0.006) rats, and was significantly suppressed following GHR inhibition (P<0.05). Furthermore, phosphorylation of IRS-1 and AKT in response to insulin stimulation increased after GHR inhibition (P<0.05). CONCLUSIONS: Insulin resistance in CUG-SGA rats is associated with impairment of IRS-1-PI3K-AKT signaling, which may result from GH signaling-induced up-regulation of SOCS3.http://europepmc.org/articles/PMC4070916?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Hong-Zhu Deng Hong Deng Chao-Qun Cen Kai-Yun Chen Min-Lian Du |
spellingShingle |
Hong-Zhu Deng Hong Deng Chao-Qun Cen Kai-Yun Chen Min-Lian Du Post-receptor crosstalk between growth hormone and insulin signal in rats born small for gestational age with catch-up growth. PLoS ONE |
author_facet |
Hong-Zhu Deng Hong Deng Chao-Qun Cen Kai-Yun Chen Min-Lian Du |
author_sort |
Hong-Zhu Deng |
title |
Post-receptor crosstalk between growth hormone and insulin signal in rats born small for gestational age with catch-up growth. |
title_short |
Post-receptor crosstalk between growth hormone and insulin signal in rats born small for gestational age with catch-up growth. |
title_full |
Post-receptor crosstalk between growth hormone and insulin signal in rats born small for gestational age with catch-up growth. |
title_fullStr |
Post-receptor crosstalk between growth hormone and insulin signal in rats born small for gestational age with catch-up growth. |
title_full_unstemmed |
Post-receptor crosstalk between growth hormone and insulin signal in rats born small for gestational age with catch-up growth. |
title_sort |
post-receptor crosstalk between growth hormone and insulin signal in rats born small for gestational age with catch-up growth. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2014-01-01 |
description |
OBJECTIVE: Insulin resistance has been observed in individuals born small for gestational age (SGA) with catch-up growth (CUG), yet the mechanisms involved remain unclear. This study examined the role of GH and insulin signaling crosstalk in insulin resistance of SGA rats with CUG. DESIGN AND METHODS: SGA rats were developed by dietary restriction in pregnant rats. GH receptor inhibition was performed on four-week old CUG-SGA and AGA rats. Phosphorylation of IRS-1, AKT, and ERK, and expression of SOCS3 in the skeletal muscle were determined via immunoblot analysis at baseline and after insulin stimulation in CUG-SGA, NCUG-SGA and AGA groups. RESULTS: Compared to AGA controls, phosphorylation of IRS-1 and AKT in response to insulin stimulation in CUG-SGA rats was significantly blunted (P<0.05), and phosphorylation of ERK at baseline was dramatically activated (P<0.05). SOCS3 expression was significantly increased in CUG-SGA compared to AGA (P = 0.001) and NCUG-SGA (P = 0.006) rats, and was significantly suppressed following GHR inhibition (P<0.05). Furthermore, phosphorylation of IRS-1 and AKT in response to insulin stimulation increased after GHR inhibition (P<0.05). CONCLUSIONS: Insulin resistance in CUG-SGA rats is associated with impairment of IRS-1-PI3K-AKT signaling, which may result from GH signaling-induced up-regulation of SOCS3. |
url |
http://europepmc.org/articles/PMC4070916?pdf=render |
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