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Norway

PMID:21266325  

Deletion of Lkb1 in pro-opiomelanocortin neurons impairs peripheral glucose homeostasis in mice.

Marc Claret | Mark A Smith | Claude Knauf | Hind Al-Qassab | Angela Woods | Amanda Heslegrave | Kaisa Piipari | Julian J Emmanuel | André Colom | Philippe Valet | Patrice D Cani | Ghazala Begum | Anne White | Phillip Mucket | Marco Peters | Keiko Mizuno | Rachel L Batterham | K Peter Giese | Alan Ashworth | Remy Burcelin | Michael L Ashford | David Carling | Dominic J Withers
Diabetes | 2011

AMP-activated protein kinase (AMPK) signaling acts as a sensor of nutrients and hormones in the hypothalamus, thereby regulating whole-body energy homeostasis. Deletion of Ampkα2 in pro-opiomelanocortin (POMC) neurons causes obesity and defective neuronal glucose sensing. LKB1, the Peutz-Jeghers syndrome gene product, and Ca(2+)-calmodulin-dependent protein kinase kinase β (CaMKKβ) are key upstream activators of AMPK. This study aimed to determine their role in POMC neurons upon energy and glucose homeostasis regulation.

Pubmed ID: 21266325

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Associated grants

  • Agency: Wellcome Trust, United Kingdom
  • Agency: Medical Research Council, United Kingdom
    Id: MC_U120027537
  • Agency: Breast Cancer Now, United Kingdom
    Id: BREAST CANCER NOW RESEARCH CENTRE
  • Agency: Medical Research Council, United Kingdom
    Id: G0601342
  • Agency: Medical Research Council, United Kingdom
    Id: MC_U120097114
  • Agency: Medical Research Council, United Kingdom
    Id: G0600866
  • Agency: Biotechnology and Biological Sciences Research Council, United Kingdom

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Phoenix Pharmaceuticals (tool)

RRID:SCR_001141

Commercial antibody supplier that specializes in peptide-related products for research in obesity, cardiovascular disease, and diabetes.

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