Imperial College London
Alternate

ProfessorGuyRutter

Faculty of Medicine, Department of Medicine

Visiting Professor
 
 
 
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Contact

 

+44 (0)20 7594 3340g.rutter Website

 
 
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Location

 

ICTEM buildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Cruciani-Guglielmacci:2017:10.1016/j.molmet.2017.01.009,
author = {Cruciani-Guglielmacci, C and Bellini, L and Denom, J and Oshima, M and Fernandez, N and Normandie-Levi, P and Berney, XP and Kassis, N and Rouch, C and Dairou, J and Gorman, T and Smith, DM and Marley, A and Liechti, R and Kuznetsov, D and Wigger, L and Burdet, F and Lefèvre, AL and Wehrle, I and Uphues, I and Hildebrandt, T and Rust, W and Bernard, C and Ktorza, A and Rutter, GA and Scharfmann, R and Xenarios, I and Le, Stunff H and Thorens, B and Magnan, C and Ibberson, M},
doi = {10.1016/j.molmet.2017.01.009},
journal = {Molecular Metabolism},
pages = {340--351},
title = {Molecular phenotyping of multiple mouse strains under metabolic challenge uncovers a role for Elovl2 in glucose-induced insulin secretion},
url = {http://dx.doi.org/10.1016/j.molmet.2017.01.009},
volume = {6},
year = {2017}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Objective: In type 2 diabetes (T2D), pancreatic β cells become progressively dysfunctional, leading to a decline in insulin secretion over time. In this study, we aimed to identify key genes involved in pancreatic beta cell dysfunction by analyzing multiple mouse strains in parallel under metabolic stress. Methods: Male mice from six commonly used non-diabetic mouse strains were fed a high fat or regular chow diet for three months. Pancreatic islets were extracted and phenotypic measurements were recorded at 2 days, 10 days, 30 days, and 90 days to assess diabetes progression. RNA-Seq was performed on islet tissue at each time-point and integrated with the phenotypic data in a network-based analysis. Results: A module of co-expressed genes was selected for further investigation as it showed the strongest correlation to insulin secretion and oral glucose tolerance phenotypes. One of the predicted network hub genes was Elovl2, encoding Elongase of very long chain fatty acids 2. Elovl2 silencing decreased glucose-stimulated insulin secretion in mouse and human β cell lines. Conclusion: Our results suggest a role for Elovl2 in ensuring normal insulin secretory responses to glucose. Moreover, the large comprehensive dataset and integrative network-based approach provides a new resource to dissect the molecular etiology of β cell failure under metabolic stress.
AU  - Cruciani-Guglielmacci,C
AU  - Bellini,L
AU  - Denom,J
AU  - Oshima,M
AU  - Fernandez,N
AU  - Normandie-Levi,P
AU  - Berney,XP
AU  - Kassis,N
AU  - Rouch,C
AU  - Dairou,J
AU  - Gorman,T
AU  - Smith,DM
AU  - Marley,A
AU  - Liechti,R
AU  - Kuznetsov,D
AU  - Wigger,L
AU  - Burdet,F
AU  - Lefèvre,AL
AU  - Wehrle,I
AU  - Uphues,I
AU  - Hildebrandt,T
AU  - Rust,W
AU  - Bernard,C
AU  - Ktorza,A
AU  - Rutter,GA
AU  - Scharfmann,R
AU  - Xenarios,I
AU  - Le,Stunff H
AU  - Thorens,B
AU  - Magnan,C
AU  - Ibberson,M
DO  - 10.1016/j.molmet.2017.01.009
EP  - 351
PY  - 2017///
SN  - 2212-8778
SP  - 340
TI  - Molecular phenotyping of multiple mouse strains under metabolic challenge uncovers a role for Elovl2 in glucose-induced insulin secretion
T2  - Molecular Metabolism
UR  - http://dx.doi.org/10.1016/j.molmet.2017.01.009
UR  - http://hdl.handle.net/10044/1/44990
VL  - 6
ER  -
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