ArticleMolecular metabolism2019
A spontaneous leptin receptor point mutation causes obesity and differentially affects leptin signaling in hypothalamic nuclei resulting in metabolic dysfunctions distinct from db/db mice.
Article in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Leptin Receptor b (LEPRb) Mutations Disrupt Hypothalamic Control of the Reproductive Axis.International journal of molecular sciences · 2026Review
- Gender-Associated Differences in the Regulation of Potassium Channels in Astrocytes of Type 2 Diabetic Mice.Cells · 2026Article
- Comparison of the characteristics of non-alcoholic fatty liver disease in C57BL/6J-LeprExperimental animals · 2025Article
- Daraesoon (shoot of hardy kiwi) mitigates hyperglycemia in db/db mice by alleviating insulin resistance and inflammation.Nutrition research and practice · 2024Article
- Association of the Human Leptin Receptor Gene (rs1137101; Gln223Arg) Polymorphism and Circulating Leptin in Patients with Metabolic Syndrome in the Indian Population.Indian journal of clinical biochemistry : IJCB · 2023Article
- A Novel Mouse Model of Intrahepatic Cholangiocarcinoma Induced by Azoxymethane.International journal of molecular sciences · 2023Article
- Comprehensive mutations analyses ofFrontiers in nutrition · 2022Article
- Metabolic Syndrome: Lessons from Rodent andBioMed research international · 2022Review
- Blackcurrant Improves Diabetic Cardiovascular Dysfunction by Reducing Inflammatory Cytokines in Type 2 Diabetes Mellitus Mice.Nutrients · 2021Article
- Association between Single Nucleotide Polymorphism rs9891119 of STAT3 Gene and the Genetic Susceptibility to Type 2 Diabetes in Chinese Han Population from Guangdong.Journal of healthcare engineering · 2021Article
- A big-data approach to understanding metabolic rate and response to obesity in laboratory mice.eLife · 2020Article
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Authors and funding
8 authors at 3 institutions in 1 country.
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Abstract
objectiveLeptin (Lep) plays a crucial role in controlling food intake and energy expenditure. Defective Lep/LepRb-signaling leads to fat accumulation, massive obesity, and the development of diabetes. We serendipitously noticed spontaneous development of obesity similar to LepR-deficient (db/db) mice in offspring from a C57BL/6J breeding and transmittance of the phenotype in a Mendelian manner. Candidate gene sequencing revealed a spontaneous point mutation in the LepRb gene. We investigated leptin responsiveness, leptin receptor signaling and metabolic phenotype of this novel LepRb mutant mouse variant.
methodsOverexpression and functional tests of the mutant LepRb in 3T3 cells. Measurement of leptin responsiveness in hypothalamic nuclei, glucose tolerance, food uptake and energy expenditure in the mutant mice.
resultsThe mutation results in the exchange of a glycine for serine (G506S) and introduces an alternative splice acceptor which, when used, encodes for a protein with a 40aa deletion that is retained in the cytoplasm. LepRb signaling was abrogated in the hypothalamic ventromedial nucleus (VMN) and dorsomedial nucleus (DMN), but only partially reduced in the hypothalamic arcuate nucleus (ARC) of LepRb
conclusionsThis study provides further insight into differences of the leptin responsiveness in VMN, DMN, and ARC and its metabolic consequences.
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