Author

D. Nasteska

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

Physiology· 4 Cell Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 5 Research Focus:cell type annotation· 4 Organism:mouse· 4 Organism:human· 3 Research Focus:metabolism & bioenergetics· 3 Assay:metabolomics· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1

Frequent Co-Authors

D. J. Hodson· 4 shared I. Akerman· 3 shared D. A. Tennant· 2 shared F. B. Ashford· 2 shared F. Cuozzo· 2 shared G. G. Lavery· 2 shared K. Viloria· 2 shared N. H. F. Fine· 2 shared

Activity by Year

2019-2022 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 31 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 papersPhysiology

D. J. Hodson

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

High-resolution glucose tracing and in situ imaging reveals regulated lactate production in human pancreatic β cells

F. Cuozzo, K. Viloria, A. H. Shilleh, D. Nasteska, C. Frazer-Morris, Z. Jiao, A. Boufersaoui, B. Marzullo, H. R. Smith, C. Bonner, J. Kerr-Conte, F. Pattou, R. Nano, L. Piemonti, P. R. Johnson, , D. J. Hodson

The paper uses metabolic tracing and imaging to show that human pancreatic β cells produce lactate, regulated by LDHB expression, which affects Ca2+ spiking without altering ATP/ADP levels.

bioRxiv · Dec 21, 2022 · PreprintPhysiology

The prolyl hydroxylase PHD3 maintains β-cell glucose metabolism during fatty acid excess

D. Nasteska, F. Cuozzo, A. Thakker, R. Bany Bakar, R. Westbrook, I. Akerman, J. Cantley, D. A. Tennant, D. J. Hodson

This paper shows that PHD3 deletion in beta-cells impairs glucose homeostasis under high fat diet by altering fuel utilization and metabolic pathways.

bioRxiv · Apr 30, 2020 · PreprintPhysiology

Vitamin D-binding protein is required for the maintenance of α-cell function and glucagon secretion

K. Viloria, D. Nasteska, L. J. B. Briant, S. Helsing, D. Larner, N. H. F. Fine, F. B. Ashford, G. da Silva Xavier, M. Jimenez Ramos, J. E. Manning Fox, P. E. MacDonald, I. Akerman, G. G. Lavery, C. Flaxman, N. G. Morgan, , D. J. Hodson

This study shows that vitamin D-binding protein (DBP) is essential for maintaining β-cell function and glucagon secretion, with reduced DBP expression observed in late-onset type 1 diabetes.

bioRxiv · Dec 19, 2019 · PreprintPhysiology

Maternal hypothyroidism in mice influences glucose metabolism in adult offspring

Y. Kemkem, D. Nasteska, D. Hodson, A. Guillou, P. Mollard, P. Bargi-Souza, R. A. Peliciari-Garcia, A. De Bray, M. Schaeffer

This study shows that maternal hypothyroidism in mice leads to altered glucose metabolism in adult offspring, with persistent effects across generations.

bioRxiv · Sep 28, 2019Physiology

LUXendins reveal endogenous glucagon-like peptide-1 receptor distribution and dynamics

J. Ast, A. Arvaniti, N. H. F. Fine, D. Nasteska, F. B. Ashford, Z. Stamataki, Z. Koszegi, A. Bacon, S. Trapp, B. J. Jones, B. Hastoy, A. Tomas, C. Reissaus, A. K. Linnemann, E. D'Este, , D. J. Hodson

The paper introduces LUXendin peptides that label and visualize endogenous GLP1R with high specificity, revealing receptor organization and dynamics.

bioRxiv · May 8, 2019Cell Biology