Author

D. B. Savage

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cell Biology· 3 Physiology· 2

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 4 Organism:mouse· 4 Research Focus:host-pathogen & immune response· 3 Research Focus:cell type annotation· 2 Research Focus:metabolism & bioenergetics· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:differential expression· 1

Frequent Co-Authors

S. Patel· 4 shared A. Alvarez-Guaita· 3 shared A. Haider· 3 shared S. O'Rahilly· 3 shared S. Virtue· 3 shared F. Scurria· 2 shared J. P. Mann· 2 shared J. Prudent· 2 shared

Activity by Year

2019-2022 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 43 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

4 shared papersCell Biology

S. Patel

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

Loss of Mfn1 but not Mfn2 enhances adipogenesis

J. P. Mann, L. Tabara, A. Alvarez-Guaita, L. Dong, A. Haider, K. Lim, P. Tandon, J. E. Minchin, S. O'Rahilly, S. Patel, D. J. Fazakerley, J. Prudent, R. K. Semple, D. B. Savage

The paper shows that loss of Mfn1 promotes adipogenesis in cultured cells, while loss of Mfn2 does not, indicating distinct roles for Mfn1 and Mfn2 in adipocyte differentiation.

bioRxiv · Nov 4, 2022 · PreprintCell Biology

A mouse model of human mitofusin 2-related lipodystrophy exhibits adipose-specific mitochondrial stress and reduced leptin secretion

J. P. Mann, X. Duan, A. Alvarez-Guaita, A. Haider, I. Luijten, M. Page, S. Patel, F. Scurria, M. Protasoni, L. C. Tabara, S. Virtue, S. I. O'Rahilly, M. Armstrong, J. Prudent, R. K. Semple, D. B. Savage

This study uses a mouse model to show that a MFN2 mutation causes adipose-specific mitochondrial stress and reduced leptin secretion, linking mitochondrial dysfunction to metabolic disease.

bioRxiv · Sep 20, 2022Cell Biology

Endogenous GDF15 and FGF21 additively alleviate hepatic steatosis and insulin resistance in obese mice.

S. Patel, A. Haider, A. Alvarez-Guaita, G. Bidault, J. S. El-Sayed Moustafa, E. Guiu-Jurado, J. A. Tadross, J. Warner, J. Harrison, S. Virtue, F. Scurria, I. Zvetkova, M. Blüher, K. S. Small, S. O'Rahilly, D. B. Savage

This study shows that GDF15 and FGF21, secreted by the liver in obese mice, reduce hepatic steatosis and insulin resistance when both are active.

bioRxiv · Jun 8, 2022 · PreprintPhysiology

The architecture of Cidec-mediated interfaces between lipid droplets

I. Ganeva, K. Lim, J. Boulanger, P. C. Hoffmann, D. B. Savage, W. Kukulski

The paper visualizes lipid droplet interfaces using cryo-ET and shows lipid transfer occurs through closely apposed monolayers with exponential kinetics, suggesting a pressure-driven mechanism.

bioRxiv · Mar 23, 2021Cell Biology

GDF15 and the beneficial actions of metformin in pre-diabetes

A. P. Coll, M. Chen, P. Taskar, D. Rimmington, S. Patel, J. Tadross, I. Cimino, M. Yang, P. Welsh, S. Virtue, D. A. Goldspink, E. Miedzybrodzka, Y. C. L. Tung, S. Rodriguez-Cuenca, R. A. Tomaz, , S. O'Rahilly

This study shows metformin increases GDF15 levels, which is necessary for its weight loss and insulin-sensitizing effects in both humans and mice.

bioRxiv · Jun 21, 2019Physiology