Decreased fasting blood glucose is associated with impaired hepatic glucose production in thyroid-stimulating hormone receptor knockout mice
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- Wang Tingting
- Department of Endocrinology, Provincial Hospital Affiliated to Shandong University, Jinan, China Institute of Endocrinology, Shandong Academy of Clinical Medicine, Jinan, China
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- Xu Jin
- Department of Endocrinology, Provincial Hospital Affiliated to Shandong University, Jinan, China
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- Bo Tao
- Central Laboratory, Provincial Hospital Affiliated to Shandong University, Jinan, China
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- Zhou Xiaoming
- Central Laboratory, Provincial Hospital Affiliated to Shandong University, Jinan, China
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- Jiang Xiuyun
- Department of Endocrinology, Provincial Hospital Affiliated to Shandong University, Jinan, China Institute of Endocrinology, Shandong Academy of Clinical Medicine, Jinan, China
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- Gao Ling
- Central Laboratory, Provincial Hospital Affiliated to Shandong University, Jinan, China Institute of Endocrinology, Shandong Academy of Clinical Medicine, Jinan, China
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- Zhao Jiajun
- Department of Endocrinology, Provincial Hospital Affiliated to Shandong University, Jinan, China Institute of Endocrinology, Shandong Academy of Clinical Medicine, Jinan, China
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Our previous study reported that thyroid-stimulating hormone (TSH) promotes cholesterol synthesis via the cyclic adenosine monophosphate/protein kinase A/cAMP regulatory element-binding protein (cAMP/PKA/CREB) pathway after binding to TSH receptors (TSHR) in the liver. The hepatic cAMP/PKA/CREB pathway also plays an important role in maintaining fasting glucose homeostasis. These findings implied a possible role for TSH in hepatic glucose metabolism. In this study, we used TSH receptor knockout mice (Tshr-ko mice) to clarify the effect of Tshr deletion on hepatic glucose metabolism, and investigated whether the effects of TSH directly regulate hepatic gluconeogenesis in HepG2 cells. Tshr-ko mice exhibited decreased fasting blood glucose levels, increased insulin sensitivity but normal level of fasting plasma insulin. Tshr deletion impaired hepatic glucose production by down-regulating the expression of glucose-6-phosphatase (G6P) and phosphoenolpyruvate pyruvate carboxylase (PEPCK) mRNA, two rate-limiting enzymes in hepatic gluconeogenesis, and enhancing the abundance of hepatic glucokinase (GK), the first enzyme regulating glycogen synthesis. Moreover, Tshr deletion inhibited the protein expression of hepatic phospho-CREB and increased the protein expression of hepatic phospho-AMP-activated protein kinase (p-AMPK), two up-stream regulators of PEPCK and G6P mRNA. In HepG2 cells, TSH increased the expression of G6P and PEPCK at mRNA level. These results indicated the simulative effects of TSH on hepatic glucose production in vivo and in vitro, suggesting a novel role for TSH in hepatic glucose metabolism.
収録刊行物
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- Endocrine Journal
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Endocrine Journal 60 (8), 941-950, 2013
一般社団法人 日本内分泌学会
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詳細情報 詳細情報について
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- CRID
- 1390001206299617152
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- NII論文ID
- 10031195763
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- NII書誌ID
- AA10901436
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- COI
- 1:STN:280:DC%2BC3snjtVOntg%3D%3D
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- ISSN
- 13484540
- 09188959
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- PubMed
- 23665701
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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- 使用不可