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The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

Inhibition of Notch signaling ameliorates insulin resistance in a FoxO1-dependent manner

Pajvani, Utpal B, Shawber, Carrie J, Samuel, Varman T, Birkenfeld, Andreas L, Shulman, Gerald I, Kitajewski, Jan, Accili, Domenico·2011·Nature Medicine
DOI 10.1038/nm.2378PMC PMC3387563
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  • GSI treatment of diet-induced or genetic mouse models of obesity improved hepatic insulin sensitivity, likely through inhibition of Notch co-activation of FoxO1-mediated hepatic glucose production.

    “For instance, we found that GSI treatment of diet-induced or genetic mouse models of obesity improved hepatic insulin sensitivity, likely through inhibition of Notch co-activation of FoxO1-mediated hepatic glucose production (Pajvani et al., 2011).”

    From γ-secretase inhibition lowers plasma triglyceride-rich lipoproteins by stabilizing the LDL receptor (2018) · cites this paper as Pajvani et al., 2011

    The Results section on γ-secretase inhibitors reports improved glucose levels and tolerance in diet-induced obese and genetically obese ob/ob mice, with findings suggestive of increased hepatic insulin sensitivity. The Discussion describes Notch–FoxO1 cooperation in regulating hepatic glucose production, but the Results and Discussion also state that GSI reduced glucose production in FoxO1-deficient hepatocytes. Thus, the proposed FoxO1-mediated mechanism is not established as the explanation for the GSI effect. (LLM, conf=0.88)

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Research works printed but not linked: 39

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  3. Haeusler, R.A., Kaestner, K.H. & Accili, D. FoxOs function synergistically to promote hepatic glucose production. J. Biol. Chem. 285, 35245–35248 (2010). · DOI
  4. Nakae, J. et al. Regulation of insulin action and pancreatic beta-cell function by mutated alleles of the gene encoding forkhead transcription factor Foxo1. Nat. Genet. 32, 245–253 (2002). · DOI
  5. Nakae, J., Park, B.C. & Accili, D. Insulin stimulates phosphorylation of the forkhead transcription factor FKHR on serine 253 through a Wortmannin-sensitive pathway. J. Biol. Chem. 274, 15982–15985 (1999). · DOI
  6. Altomonte, J. et al. Inhibition of Foxo1 function is associated with improved fasting glycemia in diabetic mice. Am. J. Physiol. Endocrinol. Metab. 285, E718–E728 (2003). · DOI
  7. Matsumoto, M., Pocai, A., Rossetti, L., Depinho, R.A. & Accili, D. Impaired regulation of hepatic glucose production in mice lacking the forkhead transcription factor Foxo1 in liver. Cell Metab. 6, 208–216 (2007). · DOI
  8. Fortini, M.E. Notch signaling: the core pathway and its posttranslational regulation. Dev. Cell 16, 633–647 (2009). · DOI
  9. Dufraine, J., Funahashi, Y. & Kitajewski, J. Notch signaling regulates tumor angiogenesis by diverse mechanisms. Oncogene 27, 5132–5137 (2008). · DOI
  10. Weinmaster, G. & Kopan, R. A garden of Notch-ly delights. Development 133, 3277–3282 (2006). · DOI
  11. Zong, Y. et al. Notch signaling controls liver development by regulating biliary differentiation. Development 136, 1727–1739 (2009). · DOI
  12. Loomes, K.M. et al. Bile duct proliferation in liver-specific Jag1 conditional knockout mice: effects of gene dosage. Hepatology 45, 323–330 (2007). · DOI
  13. Xue, Y. et al. Embryonic lethality and vascular defects in mice lacking the Notch ligand Jagged1. Hum. Mol. Genet. 8, 723–730 (1999). · DOI
  14. Oka, C. et al. Disruption of the mouse RBP-J kappa gene results in early embryonic death. Development 121, 3291–3301 (1995). · DOI
  15. Postic, C. & Magnuson, M.A. DNA excision in liver by an albumin-Cre transgene occurs progressively with age. Genesis 26, 149–150 (2000). · DOI
  16. Das, I. et al. Notch oncoproteins depend on γ-secretase/presenilin activity for processing and function. J. Biol. Chem. 279, 30771–30780 (2004). · DOI
  17. Wang, J. et al. Effects of adenovirus-mediated liver-selective overexpression of protein tyrosine phosphatase-1b on insulin sensitivity in vivo. Diabetes Obes. Metab. 3, 367–380 (2001). · DOI
  18. Rand, M.D. et al. Calcium depletion dissociates and activates heterodimeric notch receptors. Mol. Cell. Biol. 20, 1825–1835 (2000). · DOI
  19. Wolfe, M.S. γ-Secretase in biology and medicine. Semin. Cell Dev. Biol. 20, 219–224 (2009). · DOI
  20. van Es, J.H. et al. Notch/γ-secretase inhibition turns proliferative cells in intestinal crypts and adenomas into goblet cells. Nature 435, 959–963 (2005). · DOI
  21. Milano, J. et al. Modulation of notch processing by γ-secretase inhibitors causes intestinal goblet cell metaplasia and induction of genes known to specify gut secretory lineage differentiation. Toxicol. Sci. 82, 341–358 (2004). · DOI
  22. Samuel, V.T. et al. Targeting foxo1 in mice using antisense oligonucleotide improves hepatic and peripheral insulin action. Diabetes 55, 2042–2050 (2006). · DOI
  23. Accili, D. & Arden, K.C. FoxOs at the crossroads of cellular metabolism, differentiation, and transformation. Cell 117, 421–426 (2004). · DOI
  24. Huang, A. et al. Functional silencing of hepatic microsomal glucose-6-phosphatase gene expression in vivo by adenovirus-mediated delivery of short hairpin RNA. FEBS Lett. 558, 69–73 (2004). · DOI
  25. Chopra, A.R. et al. Absence of the SRC-2 coactivator results in a glycogenopathy resembling Von Gierke's disease. Science 322, 1395–1399 (2008). · DOI
  26. Kim, J.J. et al. FoxO1 haploinsufficiency protects against high-fat diet-induced insulin resistance with enhanced peroxisome proliferator-activated receptor gamma activation in adipose tissue. Diabetes 58, 1275–1282 (2009). · DOI
  27. Nakae, J. et al. Forkhead transcription factor FoxO1 in adipose tissue regulates energy storage and expenditure. Diabetes 57, 563–576 (2008). · DOI
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  35. Krebs, L.T. et al. Notch signaling is essential for vascular morphogenesis in mice. Genes Dev. 14, 1343–1352 (2000). · DOI
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  37. Lin, H.V. et al. Divergent regulation of energy expenditure and hepatic glucose production by insulin receptor in agouti-related protein and POMC neurons. Diabetes 59, 337–346 (2010). · DOI
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Metadata

Authors
Pajvani, U. B., Shawber, C. J., Samuel, V. T., Birkenfeld, A. L., Shulman, G. I., Kitajewski, J., & Accili, D.
Venue
Nature Medicine
Publisher
Springer Science and Business Media LLC
Published
2011-07-31
Volume
17
Issue
8
Pages
961-967
ISSN
  • 1078-8956
  • 1546-170X
DOI
10.1038/nm.2378
PMC
PMC3387563
Cited by
193
References
7
Language
en
Update notices
correction (2023-12-01)
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