STAFF

Dr. Iván Quesada Moll

Professor, Universidad Miguel Hernandez

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Unit
Molecular Diagnosis, Prognosis and Therapy

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Subunit
Diabetes and Metabolic Disorders

Group
Diabetes Research Unit

ivanq@umh.es

+34 965 222 003

RESEARCH FIELDS 

  • Mechanisms that regulate the function of pancreatic alpha and beta-cells.
  • Alterations, adaptations and/or failure of beta cells in pathologic conditions such as diabetes and obesity.

PROFESSIONAL BACKGROUND

  • Previous positions:
    1. Visiting Assistant Professor. Department of Bioengineering, University of Washington, Seattle, USA, 2004.
    2. Research Faculty (Ramón y Cajal Program), 2004-2008.
    3. Associate Professor in Nutrition. Miguel Hernandez University, Elche, Spain, 2009-2018.
  • Postdoctoral positions:
    1. Postdoctoral Fellow. Department of Bioengineering, University of Washington, Seattle, USA.
  • PhD in Biology (2000), Miguel Hernández University, Elche, Spain.
  • Degree in Biology (1996), University of Alicante, Alicante, Spain.

REPRESENTATIVE PUBLICATIONS

Merino B., et al. (2015)

Scientific Reports, DOI: 10.1038/srep11622

Pancreatic alpha-cells from female mice undergo morphofunctional changes during compensatory adaptations of the endocrine pancreas to diet-induced obesity.

Vieira E., Burris T.P. and Quesada I. (2014)

Trends in Molecular Medicine, DOI: 10.1016/j.molmed.2014.10.007

Clock genes, pancreatic function and diabetes.

Rafacho A., et al. (2014)

PLoS One, DOI: 10.1371/journal.pone.0093531

Pancreatic alpha-cell dysfunction contributes to the disruption of glucose homeostasis and compensatory insulin hypersecretion in glucocorticoid-treated rats.

Gonzalez A., et al. (2013)

Endocrinology, DOI: 10.1210/en.2013-1424

Insulin hypersecretion in islets from diet-induced hyperinsulinemic female obese mice is associated to several functional adaptations in individual beta-cells.

Marroquí L., et al. (2012)

Endocrinology, DOI: 10.1210/en.2011-1623

The eFunctional and structural adaptations in the pancreatic alpha-cell and changes in glucagon signaling during protein malnutrition.