ArticleMolecular metabolism2020
Identification of the leptin receptor sequences crucial for the STAT3-Independent control of metabolism.
Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Molecular mechanisms and neural mediators of leptin action.Genes & development · 2025Review
- Role of circadian clock in female embryo implantation.Frontiers in cell and developmental biology · 2025Review
- Fetal growth restriction and placental defects in obese mice are associated with impaired decidualisation: the role of increased leptin signalling modulators SOCS3 and PTPN2.Cellular and molecular life sciences : CMLS · 2024Article
- Evidence That Peripheral Leptin Resistance in Omental Adipose Tissue and Liver Correlates with MASLD in Humans.International journal of molecular sciences · 2024Article
- AgRP neuron cis-regulatory analysis across hunger states reveals that IRF3 mediates leptin's acute effects.Nature communications · 2024Article
- Regulatory Basis of Adipokines Leptin and Adiponectin in Epilepsy: from Signaling Pathways to Glucose Metabolism.Neurochemical research · 2023Review
- Exercise training modulates adipokine dysregulations in metabolic syndrome.Sports medicine and health science · 2022Review
- Is LRP2 Involved in Leptin Transport over the Blood-Brain Barrier and Development of Obesity?International journal of molecular sciences · 2021Article
- Tissue-Specific Effects of Leptin on Glucose and Lipid Metabolism.Endocrine reviews · 2021Review
- Roles of Gangliosides in Hypothalamic Control of Energy Balance: New Insights.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
backgroundLeptin acts via its receptor, LepRb, on specialized neurons in the brain to modulate energy balance and glucose homeostasis. LepRb→STAT3 signaling plays a crucial role in leptin action, but LepRb also mediates an additional as-yet-unidentified signal (Signal 2) that is important for leptin action. Signal 2 requires LepRb regions in addition to those required for JAK2 activation but operates independently of STAT3 and LepRb phosphorylation sites.
methodsTo identify LepRb sequences that mediate Signal 2, we used CRISPR/Cas9 to generate five novel mouse lines containing COOH-terminal truncation mutants of LepRb. We analyzed the metabolic phenotype and measures of hypothalamic function for these mouse lines.
resultsWe found that deletion of LepRb sequences between residues 921 and 960 dramatically worsens metabolic control and alters hypothalamic function relative to smaller truncations. We also found that deletion of the regions including residues 1013-1053 and 960-1013 each decreased obesity compared to deletions that included additional COOH-terminal residues.
conclusionsLepRb sequences between residues 921 and 960 mediate the STAT3 and LepRb phosphorylation-independent second signal that contributes to the control of energy balance and metabolism by leptin/LepRb. In addition to confirming the inhibitory role of the region (residues 961-1013) containing Tyr
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