ArticleDiabetes2013
Identification of a loss-of-function mutation in Ube2l6 associated with obesity resistance.
Article in Diabetes, 2013. 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, 20 citations in OpenAlex.
- Combined pharmacological targeting of CD9Cell reports. Medicine · 2025Article
- Differential effects of industrial and ruminant trans fatty acids on appetitive memory.Metabolic brain disease · 2025Article
- FGFR1 Signaling Facilitates Obesity-Driven Pulmonary Outgrowth in Metastatic Breast Cancer.Molecular cancer research : MCR · 2024Article
- Integration of multi-omics approaches for functional characterization of muscle related selective sweep genes in Nanchukmacdon.Scientific reports · 2021Article
- Integrated analysis of mRNA and miRNA expression profiles in livers of Yimeng black pigs with extreme phenotypes for backfat thickness.Oncotarget · 2017Article
- Obesity alters immune and metabolic profiles: New insight from obese-resistant mice on high-fat diet.Obesity (Silver Spring, Md.) · 2016Article
- Epigenetic downregulation of the ISG15-conjugating enzyme UbcH8 impairs lipolysis and correlates with poor prognosis in nasopharyngeal carcinoma.Oncotarget · 2015Article
- The genetic basis of obesity-associated type 2 diabetes (diabesity) in polygenic mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2014Review
- Central action of FGF19 reduces hypothalamic AGRP/NPY neuron activity and improves glucose metabolism.Molecular metabolism · 2014Article
- Genetic and epigenetic control of metabolic health.Molecular metabolism · 2013Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We previously mapped a locus on BALB/c chromosome 2 associated with protection from leptin-deficiency-induced obesity. Here, we generated the corresponding congenic mouse strain by introgression of a segment of C57BL/6J chromosome 2 to the BALB/c background to confirm the genotype-phenotype associations. We found that the BALB/c alleles decreased fat mass expansion by limiting adipocyte hyperplasia and adipocyte hypertrophy. This was concomitant to an increase in adipocyte triglyceride lipase (ATGL)-mediated triglyceride breakdown and prolongation of ATGL half-life in adipose tissue. In addition, BALB/c alleles on chromosome 2 exerted a cell-autonomous role in restraining the adipogenic potential of preadipocytes. Within a 9.8-Mb critical interval, we identified a nonsynonymous coding single nucleotide polymorphism in the gene coding for the ubiquitin-conjugating enzyme E2L6 (Ube2l6, also known as Ubch8) and showed that the BALB/c allele of Ube2l6 is a hypomorph leading to the lack of UBE2L6 protein expression. Ube2l6 knockdown in 3T3-L1 adipocytes repressed adipogenesis. Thus, altered adipogenic potential caused by Ube2l6 knockdown is likely critically involved in BALB/c obesity resistance by inhibiting adipogenesis and reducing adipocyte numbers. Overall, we have identified a loss-of-function mutation in Ube2l6 that contributes to the chromosome 2 obesity quantitative trait locus.
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