Advanced search

Filter By:

Journal Check one or more journals to show results from those journals only.

Choose more journals

Article type Check one or more article types to show results from those article types only.
Subject Check one or more subjects to show results from those subjects only.
Date Choose a date option to show results from those dates only.

Custom date range

Clear all filters
Sort by:
Showing 1–8 of 8 results
Advanced filters: Author: Jesper Gromada Clear advanced filters

  • Genetic variation in ANGPTL4 is associated with lipid traits. Here, the authors find that predicted loss-of-function variants in ANGPTL4 are associated with glucose homeostasis and reduced risk of type 2 diabetes and that Angptl4−/− mice on a high-fat diet show improved insulin sensitivity.

    • Viktoria Gusarova
    • Colm O’Dushlaine
    • Jesper Gromada
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-11

  • Inhibition of GDF8 increases muscle mass in mice, but is less effective in monkeys and humans. Here the authors show that activin A also inhibits muscle hypertrophy and that concomitant inhibition of activin A and GDF8 synergistically increases muscle mass in mice and non-human primates.

    • Esther Latres
    • Jason Mastaitis
    • Jesper Gromada
    ResearchOpen Access
    Nature Communications
    Volume: 8, P: 1-13

  • The rare loss-of-function allele p.Arg138* in SLC30A8 (encoding ZnT8) mediates protection against type 2 diabetes (T2D) through promoting better insulin secretion and enhanced glucose responsiveness, suggesting ZnT8 as a target for T2D treatment.

    • Om Prakash Dwivedi
    • Mikko Lehtovirta
    • Leif Groop
    Research
    Nature Genetics
    Volume: 51, P: 1596-1606

  • Helga Ellingsgaard et al. show that secretion of interleukin-6 by muscle in response to exercise, or injection of recombinant protein, increases the expression of the incretin GLP-1 by both intestinal cells and by pancreatic alpha cells, thus potentiating insulin release and improving glycemic control. These results identify a new endocrine loop linking energy demands to homeostatic control while also suggesting further targets for type 2 diabetes therapy.

    • Helga Ellingsgaard
    • Irina Hauselmann
    • Marc Y Donath
    Research
    Nature Medicine
    Volume: 17, P: 1481-1489

  • Over the past 10 years, evidence has accumulated to suggest that α-cells are involved in the development of diabetes mellitus. This Review outlines our current understanding of α-cells and discusses how they could be targeted in the treatment of diabetes mellitus.

    • Jesper Gromada
    • Pauline Chabosseau
    • Guy A. Rutter
    Reviews
    Nature Reviews Endocrinology
    Volume: 14, P: 694-704

  • Persistent ER stress in pancreatic β-cells contributes to the pathogenesis of type 2 diabetes. Fonseca and colleagues show that the ER membrane glycoprotein WFS1, which is mutated in people with Wolfram syndrome, has a known role in the ER stress response. It regulates insulin production and secretion in β-cells by associating with adenylyl cyclase 8 at the plasma membrane and generating cAMP. ER stress prevents WFS1 plasma membrane localization, attenuating cAMP production and insulin secretion.

    • Sonya G. Fonseca
    • Fumihiko Urano
    • Mark Burcin
    Research
    Nature Cell Biology
    Volume: 14, P: 1105-1112

  • hPSCs model of Maturity Onset Diabetes of the Young caused by mutations in the transcription factor HNF1A (HNF1A-MODY), regulates the expression of genes required for the formation of dense-core insulin granules and calcium-dependent insulin secretion, demonstrating a basis to treat HNF1A-MODY patients with sulfonylureas.

    • Bryan J. González
    • Haoquan Zhao
    • Dieter Egli
    ResearchOpen Access
    Communications Biology
    Volume: 5, P: 1-17