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  • Author: Xiaoping Luo x
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Wenjun Long Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

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Tuo Zhou Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

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Xiuping Xuan Department of Endocrinology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China

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Qiuli Cao Department of Endocrinology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China

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Zuojie Luo Department of Endocrinology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China

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Yingfen Qin Department of Endocrinology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China

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Qin Ning Department of Infectious Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

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Xiaoping Luo Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China

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Xuemei Xie Department of Endocrinology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China

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Intrauterine growth restriction combined with postnatal accelerated growth (CG-IUGR) could lead to long-term detrimental metabolic outcomes characterized by insulin resistance. As an indispensable co-receptor of Wnt signaling, LRP6 plays a critical role in the susceptibility of metabolic disorders. However, whether LRP6 is involved in the metabolic programing is still unknown. We hypothesized that CG-IUGR programed impaired insulin sensitivity through the impaired LRP6-mediated Wnt signaling in skeletal muscle. A CG-IUGR rat model was employed. The transcriptional and translational alterations of the components of the Wnt and the insulin signaling in the skeletal muscle of the male CG-IUGR rats were determined. The role of LRP6 on the insulin signaling was evaluated by shRNA knockdown or Wnt3a stimulation of LRP6. Compared with controls, the male CG-IUGR rats showed an insulin-resistant phenotype, with impaired insulin signaling and decreased expression of LRP6/β-catenin in skeletal muscle. LRP6 knockdown led to reduced expression of the IR-β/IRS-1 in C2C12 cell line, while Wnt3a-mediated LRP6 expression increased the expression of IRS-1 and IGF-1R but not IR-β in the primary muscle cells of male CG-IUGR rats. The impaired LRP6/β-catenin/IGF-1R/IRS-1 signaling is probably one of the critical mechanisms underlying the programed impaired insulin sensitivity in male CG-IUGR.

Article Type:
Research Article
Collections:
Metabolic Syndrome and Diabetes
DOI:
https://doi.org/10.1530/EC-21-0203
Volume/Issue:
Volume 11: Issue 1
Open access