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Specific subpopulations of hypothalamic leptin receptor-expressing neurons mediate the effects of early developmental leptin receptor deletion on energy balance.

Alan C Rupp | Margaret B Allison | Justin C Jones | Christa M Patterson | Chelsea L Faber | Nadejda Bozadjieva | Lora K Heisler | Randy J Seeley | David P Olson | Martin G Myers
Molecular metabolism | 2018

To date, early developmental ablation of leptin receptor (LepRb) expression from circumscribed populations of hypothalamic neurons (e.g., arcuate nucleus (ARC) Pomc- or Agrp-expressing cells) has only minimally affected energy balance. In contrast, removal of LepRb from at least two large populations (expressing vGat or Nos1) spanning multiple hypothalamic regions produced profound obesity and metabolic dysfunction. Thus, we tested the notion that the total number of leptin-responsive hypothalamic neurons (rather than specific subsets of cells with a particular molecular or anatomical signature) subjected to early LepRb deletion might determine energy balance.

Pubmed ID: 29914853

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Associated grants

  • Agency: NIDDK NIH HHS, United States
    Id: T32 DK071212
  • Agency: Biotechnology and Biological Sciences Research Council, United Kingdom
    Id: BB/NO17838/1
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK056731
  • Agency: Wellcome Trust, United Kingdom
    Id: 098012
  • Agency: NIDDK NIH HHS, United States
    Id: F30 DK097861
  • Agency: NIDDK NIH HHS, United States
    Id: R37 DK056731
  • Agency: NIDDK NIH HHS, United States
    Id: P30 DK034933
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK104999
  • Agency: NIDDK NIH HHS, United States
    Id: U2C DK110768
  • Agency: NIDDK NIH HHS, United States
    Id: P30 DK020572
  • Agency: Wellcome Trust, United Kingdom

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Phoenix Pharmaceuticals (tool)

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Fiji (tool)

RRID:SCR_002285

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