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Michael L. J. Ashford

Michael L. J. Ashford

D-Index & Metrics

Biology and Biochemistry

D-Index
62
Citations
18123
World Ranking
10607
National Ranking
809

Overview

Michael L. J. Ashford is affiliated with the University of Dundee in the United Kingdom. Their research predominantly spans the fields of Medicine and Biochemistry, Genetics and Molecular Biology, with substantial focus on subfields such as Physiology, Molecular Biology, Surgery, Neurology, and Endocrinology, Diabetes and Metabolism.

The main topics of their work include:

  • Adipose Tissue and Metabolism
  • Pancreatic function and diabetes
  • Alzheimer's disease research and treatments
  • Advanced Glycation End Products research
  • Genomics, phytochemicals, and oxidative stress
  • Adipokines, Inflammation, and Metabolic Diseases
  • Metabolism, Diabetes, and Cancer

Michael L. J. Ashford has published research in various venues, with the most frequent being:

  • Molecular Metabolism
  • Journal of Clinical Investigation
  • Diabetologia
  • Redox Biology
  • Cerebral Circulation - Cognition and Behavior

Recent papers authored or co-authored by Ashford include:

  • "Elevated circulating amyloid concentrations in obesity and diabetes promote vascular dysfunction," 2020, Journal of Clinical Investigation
  • "Non-canonical Keap1-independent activation of Nrf2 in astrocytes by mild oxidative stress," 2021, Redox Biology
  • "Adipocyte integrin-linked kinase plays a key role in the development of diet-induced adipose insulin resistance in male mice," 2021, Molecular Metabolism
  • "Metformin increases the uptake of glucose into the gut from the circulation in high-fat diet-fed male mice, which is enhanced by a reduction in whole-body Slc2a2 expression," 2023, Molecular Metabolism
  • "Chronic hyperglycaemia increases the vulnerability of the hippocampus to oxidative damage induced during post-hypoglycaemic hyperglycaemia in a mouse model of chemically induced type 1 diabetes," 2023, Diabetologia

Frequent co-authors in their research include Alison D. McNeilly, Rory J. McCrimmon, Jennifer Gallagher, Paul J. Meakin, and Zofia Tuharska. This network of collaborators suggests a sustained engagement with researchers focused on related metabolic and neurological studies.

Through their work, Ashford has contributed to a deeper understanding of metabolic dysfunctions linked to obesity, diabetes, and neurodegenerative conditions. Their interdisciplinary involvement spans experimental physiology, molecular biology, and clinical investigations related to metabolism and disease pathology.

Best Publications

  • Itaconate is an anti-inflammatory metabolite that activates Nrf2 via alkylation of KEAP1.

    Evanna L Mills;Dylan G Ryan;Hiran A Prag;Dina Dikovskaya

  • Insulin activates ATP-sensitive K+ channels in hypothalamic neurons of lean, but not obese rats.

    D. Spanswick;M. A. Smith;S. Mirshamsi;V. H. Routh;V. H. Routh

  • AMPK is essential for energy homeostasis regulation and glucose sensing by POMC and AgRP neurons

    Marc Claret;Mark A. Smith;Rachel L. Batterham;Colin Selman

  • Glucose-induced excitation of hypothalamic neurones is mediated by ATP-sensitive K+ channels.

    M. L. J. Ashford;P. R. Boden;J. M. Treherne

  • Adenosine-5′-triphosphate-sensitive ion channels in neonatal rat cultured central neurones

    M. L. J. Ashford;N. C. Sturgess;N. J. Trout;N. J. Gardner

  • AMPK: regulating energy balance at the cellular and whole body levels.

    D. Grahame Hardie;Michael L. J. Ashford

  • ATP-Sensitive K+ Channels in Pancreatic β-Cells: Spare-Channel Hypothesis

    D. L. Cook;L. S. Satin;M. L. J. Ashford;C. N. Hales

  • Loss of Nrf2 markedly exacerbates nonalcoholic steatohepatitis.

    Sudhir Chowdhry;Maiiada H. Nazmy;Paul J. Meakin;Albena T. Dinkova-Kostova;Albena T. Dinkova-Kostova

  • The role of insulin receptor substrate 2 in hypothalamic and β cell function

    Agharul I. Choudhury;Helen Heffron;Mark A. Smith;Hind Al-Qassab

  • Susceptibility of Nrf2-Null Mice to Steatohepatitis and Cirrhosis upon Consumption of a High-Fat Diet Is Associated with Oxidative Stress, Perturbation of the Unfolded Protein Response, and Disturbance in the Expression of Metabolic Enzymes but Not with Insulin Resistance

    Paul J. Meakin;Sudhir Chowdhry;Ritu S. Sharma;Fiona B. Ashford

  • Cloning and functional expression of a rat heart KATP channel.

    M. L.J. Ashford;Chris Bond;T. A. Blair;J. P. Adelman

  • Dynamic imaging of free cytosolic ATP concentration during fuel sensing by rat hypothalamic neurones: evidence for ATP-independent control of ATP-sensitive K(+) channels.

    Edward K. Ainscow;Shirin Mirshamsi;Teresa Tang;Michael L. J. Ashford

  • Effects of sulphonylureas and diazoxide on insulin secretion and nucleotide-sensitive channels in an insulin-secreting cell line

    N.C. Sturgess;R.Z. Kozlowski;C.A. Carrington;C.N. Hales

  • Experimental Nonalcoholic Steatohepatitis and Liver Fibrosis Are Ameliorated by Pharmacologic Activation of Nrf2 (NF-E2 p45-Related Factor 2)

    Ritu S. Sharma;David J. Harrison;Dorothy Kisielewski;Diane M. Cassidy

  • Neuronal development is promoted by weakened intrinsic antioxidant defences due to epigenetic repression of Nrf2

    Karen F. S. Bell;Bashayer Al-Mubarak;Marc André Martel;Sean McKay

  • Leptin and insulin stimulation of signalling pathways in arcuate nucleus neurones: PI3K dependent actin reorganization and KATP channel activation.

    Shirin Mirshamsi;Hilary A Laidlaw;Ke Ning;Erin Anderson

  • Dominant Role of the p110β Isoform of PI3K over p110α in Energy Homeostasis Regulation by POMC and AgRP Neurons

    Hind Al-Qassab;Mark A. Smith;Mark A. Smith;Elaine E. Irvine;Julie Guillermet-Guibert

  • Essential Role of Phosphoinositide 3-Kinase in Leptin-inducedK ATP Channel Activation in the Rat CRI-G1 Insulinoma Cell Line

    Jennie Harvey;Neil G. McKay;Kay S. Walker;Jeroen Van der Kaay

  • Hydrogen peroxide induces intracellular calcium overload by activation of a non-selective cation channel in an insulin-secreting cell line.

    Paco S. Herson;Kevin Lee;Rob D. Pinnock;John Hughes

  • Reduction in BACE1 decreases body weight, protects against diet-induced obesity and enhances insulin sensitivity in mice.

    Paul J. Meakin;Alex J. Harper;D. Lee Hamilton;Jennifer Gallagher

Frequent Co-Authors

C. N. Hales
C. N. Hales University of Cambridge
John D. Hayes
John D. Hayes University of Dundee
Dominic J. Withers
Dominic J. Withers Imperial College London
Albena T. Dinkova-Kostova
Albena T. Dinkova-Kostova University of Dundee
Calum Sutherland
Calum Sutherland University of Dundee
Stephen K. Smith
Stephen K. Smith University of Cambridge
Paco S. Herson
Paco S. Herson University of Colorado Denver
Susan E. Ozanne
Susan E. Ozanne University of Cambridge
Gregory S. Barsh
Gregory S. Barsh Stanford University
David L. Hamilton
David L. Hamilton University of California, Santa Barbara

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