The forkhead transcription factor Foxo1 (Fkhr) confers insulin sensitivity onto glucose-6-phosphatase expression
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Type 2 diabetes is characterized by the inability of insulin to suppress glucose production in the liver and kidney.Insulin inhibits glucose production by indirect and direct mechanisms.The latter result in transcriptional suppression of key gluconeogenetic and glycogenolytic enzymes, phosphoenolpyruvate carboxykinase (Pepck) and glucose-6-phosphatase (G6p).The transcription factors required for this effect are incompletely characterized.We report that in glucogenetic kidney epithelial cells, Pepck and G6p expression are induced by dexamethasone (dex) and cAMP, but fail to be inhibited by insulin.The inability to respond to insulin is associated with reduced expression of the forkhead transcription factor Foxo1, a substrate of the Akt kinase that is inhibited by insulin through phosphorylation.Transduction of kidney cells with recombinant adenovirus encoding Foxo1 results in insulin inhibition of dex/cAMP-induced G6p expression.Moreover, expression of dominant negative Foxo1 mutant results in partial inhibition of dex/cAMP-induced G6p and Pepck expression in primary cultures of mouse hepatocyes and kidney LLC-PK1-FBPase + cells.These findings are consistent with the possibility that Foxo1 is involved in insulin regulation of glucose production by mediating the ability of insulin to decrease the glucocorticoid/cAMP response of G6p.
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Insulin represses expression of the phosphoenolpyruvate carboxykinase and G-6-Pase genes; PEPCK repression occurs by disrupting association of CREB and RNA polymerase II with the PEPCK gene promoter, whereas G-6-P suppression requires PKBα/Akt and FOXO1, whose expression is diminished by GSK-3 inhibition.
“The second liver-specific effect of insulin is to repress the expression of the phosphoenolpyruvate carboxykinase and G-6-Pase genes; the first by disrupting the association of cAMP response element-binding protein and RNA polymerase II with the phosphoenolpyruvate carboxykinase gene promoter,23 whereas G-6-P suppression requires PKBα/Akt and forkhead transcription factor (FOXO1),24, 25 whose”
From Pancreatic regulation of glucose homeostasis. (2016) · cites this paper as [24]
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Nuclear Receptors in Nonalcoholic Fatty Liver Disease
López-Velázquez, J. A., Carrillo-Córdova, L. D., Chávez-Tapia, N. C., Uribe, M., & Méndez-Sánchez, N. (2012) · Journal of Lipids · doi:10.1155/2012/139875 · Cited by 48 · see citing works
Goldsworthy, M., Bai, Y., Li, C.-M., Ge, H., Lamas, E., Hilton, H., Esapa, C. T., Baker, D., Baron, W., Juan, T., et al. (2016) · Diabetes · doi:10.2337/db15-1276 · Cited by 35 · see citing works
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- Authors
- Nakae, J., Kitamura, T., Silver, D. L., & Accili, D.
- Affiliations
- Columbia University (US)
- Corresponding author
- Accili, Domenico
- Venue
- Journal of Clinical Investigation
- Published
- 2001-11-01
- Volume
- 108
- Issue
- 9
- Pages
- 1359-1367
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC209440
- OpenAlex
- W2127337885
- Cited by
- 652
- References
- 71
- Citations by year
- 2026: 8 · 2025: 14 · 2024: 18 · 2023: 22 · 2022: 22 · 2021: 32 · 2020: 26 · 2019: 30 · 2018: 33 · 2017: 22 · 2016: 27 · 2015: 25 · 2014: 33 · 2013: 20 · 2012: 26
- FWCI
- 8.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK057539, DK 57539)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › FOXO transcription factor regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fibroblast Growth Factor Research
- Keywords
- FOXO1, forkhead transcription factor, insulin sensitivity, glucose-6-phosphatase, phosphoenolpyruvate carboxykinase, gluconeogenesis, type 2 diabetes, insulin signaling, Akt kinase, glucocorticoid response, cAMP signaling, renal epithelial cells, hepatocytes, insulin resistance
- MeSH terms
- Forkhead Box Protein O1, Cyclic AMP, Adenoviridae, Animals, Cells, Cultured, Dexamethasone, DNA-Binding Proteins, Dose-Response Relationship, Drug, Epithelial Cells, Gene Expression Regulation, Genes, Dominant, Glucocorticoids, Glucose, Glucose-6-Phosphatase, Humans, Insulin, Kidney, Nerve Tissue Proteins, Phosphorylation, Protein Binding, RNA, Messenger, Time Factors, Transcription Factors, Transcription, Genetic, Transduction, Genetic, Hepatocytes, Rats, Forkhead Transcription Factors
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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