Loss of mPer2 increases plasma insulin levels by enhanced glucose‐stimulated insulin secretion and impaired insulin clearance in mice
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The existence of peripheral oscillators has been shown, and they are critically important for organizing the metabolism of the whole body. Here we show that mice deficient in mPer2 markedly increase circulatory levels of insulin compared with wild type mice. Insulin secretion was more effectively stimulated by glucose, and alloxan, a glucose analogue, induced more severe hyperglycemia in mPer2-deficient mice. Hepatic insulin degrading enzyme (Ide) displayed an obvious day and night rhythm, which was impaired in mPer2-deficient mice, leading to a decrease in insulin clearance. Deficiency in mPer2 caused increased Clock expression and decreased expression of Mkp1 and Ide1, possibly underlying the observed phenotypes and suggesting that mPer2 plays a role in regulation of circulating insulin levels.
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Per2 mutant mice show reduced fasting glycemia, loss of rhythmic glycogen accumulation in the liver, elevated plasma insulin levels and impaired gluconeogenesis.
“Per2 mutant mice show reduced fasting glycemia, a loss of rhythmic glycogen accumulation in the liver, elevated plasma insulin levels and impaired gluconeogenesis [20–22]”
From Circadian control of glucose metabolism (2014) · cites this paper as [22]
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- Authors
- Zhao, Y., Zhang, Y., Zhou, M., Wang, S., Hua, Z., & Zhang, J.
- Affiliations
- Nanjing University of Science and Technology (CN)
- State Key Laboratory of Pharmaceutical Biotechnology (CN)
- Corresponding author
- Zhang, Jianfa
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2012-04-05
- Volume
- 586
- Issue
- 9
- Pages
- 1306-1311
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W2015784158
- Cited by
- 57
- References
- 37
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 5 · 2023: 3 · 2022: 3 · 2021: 1 · 2020: 7 · 2019: 5 · 2018: 1 · 2017: 6 · 2016: 7 · 2015: 4 · 2014: 4 · 2013: 5
- FWCI
- 1.84
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- FEBS Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (973 Program, 31071130)
- National Key Research and Development Program of China (2012CB517505)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- mPer2, circadian clock, peripheral oscillators, plasma insulin, glucose-stimulated insulin secretion, insulin clearance, insulin-degrading enzyme, clocks, MKP-1, alloxan-induced hyperglycemia, insulin resistance
- MeSH terms
- Insulin Secretion, Animals, Female, Gluconeogenesis, Glucose, Glycogen, Insulin, Insulysin, Liver, Male, Mice, Inbred C57BL, Gene Expression Regulation, Enzymologic, Glucose Transporter Type 2, Mice, Period Circadian Proteins
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