A liver-derived secretory protein, selenoprotein P, causes insulin resistance
Open accessAbstract
The liver may regulate glucose homeostasis by modulating the sensitivity/resistance of peripheral tissues to insulin, by way of the production of secretory proteins, termed hepatokines. Here, we demonstrate that selenoprotein P (SeP), a liver-derived secretory protein, causes insulin resistance. Using serial analysis of gene expression (SAGE) and DNA chip methods, we found that hepatic SeP mRNA levels correlated with insulin resistance in humans. Administration of purified SeP impaired insulin signaling and dysregulated glucose metabolism in both hepatocytes and myocytes. Conversely, both genetic deletion and RNA interference-mediated knockdown of SeP improved systemic insulin sensitivity and glucose tolerance in mice. The metabolic actions of SeP were mediated, at least partly, by inactivation of adenosine monophosphate-activated protein kinase (AMPK). In summary, these results demonstrate a role of SeP in the regulation of glucose metabolism and insulin sensitivity and suggest that SeP may be a therapeutic target for type 2 diabetes.
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Mice demonstrate increased hepatic expression of SeP in response to high-fat diet feeding, NAFLD, and type 2 diabetes.
“These findings coincide with studies in mice that demonstrate increased hepatic expression of SeP in response to high-fat diet feeding, NAFLD, and type 2 diabetes [29,260,265].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [260]
SeP is a glycoprotein secreted predominantly from the liver and is upregulated by selenium and glucose supplies but downregulated by insulin and adiponectin.
“Selenoprotein P (SeP) is a glycoprotein that is secreted predominantly from the liver and is upregulated by selenium and glucose supplies but downregulated by insulin and adiponectin [260,261].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [260]
Wild-type mice treated with SeP exhibit whole-body glucose intolerance and insulin resistance.
“Wild-type mice treated with SeP exhibited whole-body glucose intolerance and insulin resistance [260]”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [260]
SeP knockout mice show improved glucose tolerance and insulin resistance.
“whereas SeP knockout mice showed improved glucose tolerance and insulin resistance [260].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [260]
SeP is associated with insulin resistance and increased serum triglyceride, and patients with NAFLD, obesity, and type 2 diabetes have high circulating levels of SeP.
“SeP is associated with insulin resistance and increased serum triglyceride, and patients with NAFLD, obesity, and type 2 diabetes have high circulating levels of SeP [260,263,264] (Table 1).”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [260]
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- Authors
- Misu, H., Takamura, T., Takayama, H., Hayashi, H., Matsuzawa-Nagata, N., Kurita, S., Ishikura, K., Ando, H., Takeshita, Y., Ota, T., Sakurai, M., Yamashita, T., Mizukoshi, E., Yamashita, T., Honda, M., Miyamoto, K.-I., Kubota, T., Kubota, N., Kadowaki, T., Kim, H.-J., Lee, I.-K., Minokoshi, Y., Saito, Y., Takahashi, K., Yamada, Y., Takakura, N., & Kaneko, S.
- Affiliations
- Kanazawa University (JP)
- The University of Tokyo (JP)
- Kyungpook National University Hospital (KR)
- National Institute for Physiological Sciences (JP)
- Doshisha University (JP)
- Hokkaido Pharmaceutical University (JP)
- Research Institute for Microbial Diseases, The University of Osaka (JP)
- Corresponding author
- Takamura, Toshinari
- ORCID
- Misu, Hirofumi
- Takamura, Toshinari
- Takayama, Hiroaki
- Ando, Hitoshi
- Takeshita, Yumie
- Ota, Tsuguhito
- Sakurai, Masaru
- Yamashita, Tatsuya
- Mizukoshi, Eishiro
- Yamashita, Taro
- Honda, Masao
- Kubota, Tetsuya
- Kubota, Naoto
- Kadowaki, Takashi
- Lee, In-kyu
- Minokoshi, Yasuhiko
- Saito, Yoshiro
- Yamada, Yoshihiro
- Takakura, Nobuyuki
- Kaneko, Shuichi
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2010-11
- Volume
- 12
- Issue
- 5
- Pages
- 483-495
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2074936957
- Cited by
- 583
- References
- 43
- Citations by year
- 2026: 38 · 2025: 33 · 2024: 36 · 2023: 44 · 2022: 54 · 2021: 46 · 2020: 43 · 2019: 54 · 2018: 51 · 2017: 31 · 2016: 32 · 2015: 28 · 2014: 26 · 2013: 29 · 2012: 23
- FWCI
- 15.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1025 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Kanazawa University Repository for Academic Resources (DSpace) (Kanazawa University) (submittedVersion, cc-by-nc-nd)
- Funders
- Takeda Science Foundation
- Ministry of Education, Culture, Sports, Science and Technology
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Nursing › Nutrition and Dietetics › Selenium in Biological Systems
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- selenoprotein P, insulin resistance, hepatokines, glucose homeostasis, glucose tolerance, insulin signaling, muscle cells, hepatocytes, type 2 diabetes, hepatic gene expression
- MeSH terms
- Animals, Cell Line, Diabetes Mellitus, Type 2, Female, Gene Expression Regulation, Glucose, Humans, Insulin Resistance, Liver, Male, Mice, Inbred C57BL, Phosphorylation, RNA, Messenger, Gene Deletion, Palmitic Acid, Hepatocytes, RNA Interference, Selenoprotein P, Mice, Rats, AMP-Activated Protein Kinases
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