The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here:

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Nils Wierup

Nils Wierup

Research team manager

Nils Wierup

A Central Role for GRB10 in Regulation of Islet Function in Man.


  • Inga Prokopenko
  • Wenny Poon
  • Reedik Mägi
  • Rashmi Prasad
  • S Albert Salehi
  • Peter Almgren
  • Peter Osmark
  • Nabila Bouatia-Naji
  • Nils Wierup
  • Tove Fall
  • Alena Stančáková
  • Adam Barker
  • Vasiliki Lagou
  • Clive Osmond
  • Weijia Xie
  • Jari Lahti
  • Anne U Jackson
  • Yu-Ching Cheng
  • Jie Liu
  • Jeffrey R O'Connell
  • Paul A Blomstedt
  • Joao Fadista
  • Sami Alkayyali
  • Tasnim Dayeh
  • Emma Ahlqvist
  • Jalal Taneera
  • Cecile Lecoeur
  • Ashish Kumar
  • Ola Hansson
  • Karin B Hansson
  • Benjamin F Voight
  • Hyun Min Kang
  • Claire Levy-Marchal
  • Vincent Vatin
  • Aarno Palotie
  • Ann-Christine Syvänen
  • Andrea Mari
  • Michael N Weedon
  • Ruth J F Loos
  • Ken K Ong
  • Peter Nilsson
  • Bo Isomaa
  • Tiinamaija Tuomi
  • Nicholas J Wareham
  • Michael Stumvoll
  • Elisabeth Widen
  • Timo A Lakka
  • Claudia Langenberg
  • Anke Tönjes
  • Rainer Rauramaa
  • Johanna Kuusisto
  • Timothy M Frayling
  • Philippe Froguel
  • Mark Walker
  • Johan G Eriksson
  • Charlotte Ling
  • Peter Kovacs
  • Erik Ingelsson
  • Mark I McCarthy
  • Alan R Shuldiner
  • Kristi D Silver
  • Markku Laakso
  • Leif Groop
  • Valeriya Lyssenko

Summary, in English

Variants in the growth factor receptor-bound protein 10 (GRB10) gene were in a GWAS meta-analysis associated with reduced glucose-stimulated insulin secretion and increased risk of type 2 diabetes (T2D) if inherited from the father, but inexplicably reduced fasting glucose when inherited from the mother. GRB10 is a negative regulator of insulin signaling and imprinted in a parent-of-origin fashion in different tissues. GRB10 knock-down in human pancreatic islets showed reduced insulin and glucagon secretion, which together with changes in insulin sensitivity may explain the paradoxical reduction of glucose despite a decrease in insulin secretion. Together, these findings suggest that tissue-specific methylation and possibly imprinting of GRB10 can influence glucose metabolism and contribute to T2D pathogenesis. The data also emphasize the need in genetic studies to consider whether risk alleles are inherited from the mother or the father.


  • Genomics, Diabetes and Endocrinology
  • Islet cell physiology
  • Neuroendocrine Cell Biology
  • Diabetes - Epigenetics
  • Division of Molecular Medicine and Gene Therapy
  • Internal Medicine - Epidemiology
  • EXODIAB: Excellence of Diabetes Research in Sweden
  • EpiHealth: Epidemiology for Health

Publishing year





PLoS Genetics





Document type

Journal article


Public Library of Science (PLoS)


  • Endocrinology and Diabetes



Research group

  • Genomics, Diabetes and Endocrinology
  • Islet cell physiology
  • Neuroendocrine Cell Biology
  • Diabetes - Epigenetics
  • Internal Medicine - Epidemiology


  • ISSN: 1553-7404