ArticleCell reports2018
Loss of Nucleobindin-2 Causes Insulin Resistance in Obesity without Impacting Satiety or Adiposity.
Article in Cell reports, 2018. 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, 27 citations in OpenAlex.
- Research progress on the relationship between Nesfatin-1 and glucose metabolism.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Proteins: Neglected active ingredients in edible bird's nest.Chinese herbal medicines · 2023Review
- Zinc Supplementation Improved Neuropeptide Y, Nesfatin-1, Leptin, C-reactive protein, and HOMA-IR of Diet-Induced Obese Rats.Biological trace element research · 2022Article
- NUCB2/Nesfatin-1 Reduces Obesogenic Diet Induced Inflammation in Mice Subcutaneous White Adipose Tissue.Nutrients · 2022Article
- The molecular signaling of exercise and obesity in the microbiota-gut-brain axis.Frontiers in endocrinology · 2022Review
- Metabolic differences and differentially expressed genes between C57BL/6J and C57BL/6N mice substrains.PloS one · 2022Article
- Characterization and Extraction Influence Protein Profiling of Edible Bird's Nest.Foods (Basel, Switzerland) · 2021Article
- Article
- Altered adipose tissue and adipocyte function in the pathogenesis of metabolic syndrome.The Journal of clinical investigation · 2019Review
- Nesfatin-1 suppresses peripheral arterial remodeling without elevating blood pressure in mice.Endocrine connections · 2019Article
- Current Understanding of the Role of Nesfatin-1.Journal of the Endocrine Society · 2018Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Inducers of satiety are drug targets for weight loss to mitigate obesity-associated diseases. Nucleobindin-2 (Nucb2) is thought to be post-translationally processed into bioactive nesfatin-1 peptide, which reportedly induces satiety, causes weight loss, and thus improves insulin sensitivity. Here, we show that deletion of Nucb2 did not affect food intake or adiposity and, instead, caused insulin resistance in mice fed a high-fat diet. In addition, ablation of Nucb2 in orexigenic hypothalamic Agrp neurons did not affect food intake, and nesfatin-1 was detectable in serum, despite global deletion of Nucb2 protein. Upon high-fat diet feeding, the loss of Nucb2 exacerbated metabolic inflammation in adipose tissue macrophages in an NFκB-dependent manner without inducing classical M1 or alternative M2-like macrophage polarization. Furthermore, the loss of Nucb2 in myeloid cells but not in adipocytes mediated the insulin resistance in response to a high-fat diet. Our study reveals that Nucb2 links metabolic inflammation to insulin resistance without affecting weight gain and food intake.
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