ArticleMolecular metabolism2015
Notch intracellular domain overexpression in adipocytes confers lipodystrophy in mice.
Article in Molecular metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Reprogramming in delipidated adipocytes: metabolism, regulation and progress.Cell death discovery · 2026Review
- Dedifferentiation of Mature Adipocytes and Their Future Potential for Regenerative Medicine Applications.Biomedicines · 2026Review
- Yeast hydrolysate and exercise ameliorate high-fat diet-induced obesity in C57BL/6 mice.BMC complementary medicine and therapies · 2025Article
- Gain of Function NOTCH3 Variants Cause Familial Partial Lipodystrophy Due to Activation of Senescence Pathways.Diabetes · 2025Article
- An organotypic atlas of human vascular cells.Nature medicine · 2024Article
- Review
- A Notch toward Progenitor D(G)FRentiation: Defining a NOTCH-PDGFR axis in brown adipogenesis.Developmental cell · 2024Article
- Article
- Forced Hepatic Expression of NRF2 or NQO1 Impedes Hepatocyte Lipid Accumulation in a Lipodystrophy Mouse Model.International journal of molecular sciences · 2023Article
- Primary diffuse large B-cell lymphoma of the breast: A retrospective study of outcomes and insulin resistance.Saudi medical journal · 2023Article
- Notch pathway inhibitor DAPT acceleratesOncology letters · 2021Article
- Cancer-Associated Adipocytes in Breast Cancer: Causes and Consequences.International journal of molecular sciences · 2021Review
- Hepatocyte high-mobility group box 1 protects against steatosis and cellular stress during high fat diet feeding.Molecular medicine (Cambridge, Mass.) · 2020Article
- Distinct roles for Notch1 and Notch3 in human adipose-derived stem/stromal cell adipogenesis.Molecular biology reports · 2020Article
- NOTCH Receptors and DLK Proteins Enhance Brown Adipogenesis in Mesenchymal C3H10T1/2 Cells.Cells · 2020Article
- Target genes associated with lipid and glucose metabolism in non-alcoholic fatty liver disease.Lipids in health and disease · 2019Article
- Adipocyte dedifferentiation in health and diseases.Clinical science (London, England : 1979) · 2019Review
- Comparison of cachectic and non-cachectic sarcoma patients reveals an important role of Notch signaling in metastasis and myogenesis.American journal of cancer research · 2019Article
- DLK proteins modulate NOTCH signaling to influence a brown or white 3T3-L1 adipocyte fate.Scientific reports · 2018Article
- Placode rotation in transitional lumbosacral lipomas: are there implications for origin and mechanism of deterioration?Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2018Article
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7 authors at 1 institution in 1 country.
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Abstract
objectiveThe Notch family of intermembrane receptors is highly conserved across species and is involved in cell fate and lineage control. Previous in vitro studies have shown that Notch may inhibit adipogenesis. Here we describe the role of Notch in adipose tissue by employing an in vivo murine model which overexpresses Notch in adipose tissue.
methodsAlbino C57BL/6J Rosa(NICD/NICD)::Adipoq-Cre (Ad-NICD) male mice were generated to overexpress the Notch intracellular domain (NICD) specifically in adipocytes. Male Rosa(NICD/NICD) mice were used as controls. Mice were evaluated metabolically at the ages of 1 and 3 months by assessing body weights, serum metabolites, body composition (EchoMRI), glucose tolerance and insulin tolerance. Histological sections of adipose tissue depots as well as of liver were examined. The mRNA expression profile of genes involved in adipogenesis was analyzed by quantitative real-time PCR.
resultsThe Ad-NICD mice were heavier with significantly lower body fat mass compared to the controls. Small amounts of white adipose tissue could be seen in the 1-month old Ad-NICD mice, but was almost absent in the 3-months old mice. The Ad-NICD mice also had higher serum levels of glucose, insulin, triglyceride and non-esterified fatty acids. These differences were more prominent in the older (3-months) than in the younger (1-month) mice. The Ad-NICD mice also showed severe insulin resistance along with a steatotic liver. Gene expression analysis in the adipose tissue depots showed a significant repression of lipogenic (Fasn, Acacb) and adipogenic pathways (C/ebpα, C/ebpβ, Pparγ2, Srebf1).
conclusionsIncreased Notch signaling in adipocytes in mice results in blocked expansion of white adipose tissue which leads to ectopic accumulation of lipids and insulin resistance, thus to a lipodystrophic phenotype. These results suggest that further investigation of the role of Notch signaling in adipocytes could lead to the manipulation of this pathway for therapeutic interventions in metabolic disease.
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