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Rashmi Prasad

Rashmi Prasad

Assistant researcher

Rashmi Prasad

Glucose-induced Changes in Gene Expression in Human Pancreatic Islets - Causes or Consequences of Chronic Hyperglycemia


  • Emilia Ottosson-Laakso
  • Ulrika Krus
  • Petter Storm
  • Rashmi B Prasad
  • Nikolay Oskolkov
  • Emma Ahlqvist
  • João Fadista
  • Ola Hansson
  • Leif Groop
  • Petter Vikman

Summary, in English

Dysregulation of gene expression in islets from type 2 diabetic patients might be causally involved in the development of hyperglycemia or it could develop as a consequence of hyperglycemia, i.e. glucotoxicity. To separate the genes potentially causally involved in pathogenesis from those likely to be secondary to the hyperglycemia we exposed islets from human donors to normal or high glucose concentrations for 24 hours and analyzed gene expression. We compared these findings with gene expression in islets from donors with normal glucose tolerance (NGT) and hyperglycemia (HG, including T2D). The genes whose expression changed in the same direction after short-term glucose exposure as in T2D were considered most likely to be a consequence of hyperglycemia. Genes whose expression changed in HG but not after short-term glucose exposure, in particular genes that also correlated with insulin secretion, were considered the strongest candidates for causal involvement in T2D. E.g. ERO1LB, DOCK10, IGSF11 and PRR14L were down-regulated in HG and correlated positively with insulin secretion suggesting a protective role while TMEM132C was up-regulated in HG and correlated negatively with insulin secretion suggesting a potential pathogenic role.This study provides a catalogue of gene expression changes in human pancreatic islets after exposure to glucose.


  • Genomics, Diabetes and Endocrinology
  • Diabetes - Islet Patophysiology
  • EXODIAB: Excellence in Diabetes Research in Sweden

Publishing year












Document type

Journal article


American Diabetes Association Inc.


  • Endocrinology and Diabetes



Research group

  • Genomics, Diabetes and Endocrinology
  • Diabetes - Islet Patophysiology


  • ISSN: 1939-327X