ArticleNutrition & diabetes2016
Transgenic mice overexpressing nesfatin/nucleobindin-2 are susceptible to high-fat diet-induced obesity.
Article in Nutrition & diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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9 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Systematic review: pain, cognition, and cardioprotection-unpacking oxytocin's contributions in a sport context.Frontiers in physiology · 2024Pooled it
- Nesfatin-1 as a Cardiovascular-Metabolic-Immune Integrator: Insights from Cellular Cross-talk to Precision Medicine.Journal of cardiovascular translational research · 2026Review
- 17Beta-Estradiol Regulates NUCB2/ Nesfatin-1 Expression in Mouse Oviduct.Development & reproduction · 2020Article
- Nesfatin-1 suppresses peripheral arterial remodeling without elevating blood pressure in mice.Endocrine connections · 2019Article
- Tissue-Specific Localization NUCB2/nesfatin-1 in the Liver and Heart of Mouse Fetus.Development & reproduction · 2018Article
- Nesfatin-1/Nucleobindin-2 Is a Potent Prognostic Marker and Enhances Cell Proliferation, Migration, and Invasion in Bladder Cancer.Disease markers · 2018Article
- Increased blood pressure in nesfatin/nuclebindin-2-transgenic mice.Hypertension research : official journal of the Japanese Society of Hypertension · 2017Article
- Testosterone Regulates NUCB2 mRNA Expression in Male Mouse Hypothalamus and Pituitary Gland.Development & reproduction · 2017Article
- SERUM NESFATIN-1 LEVEL IN HEALTHY SUBJECTS WITH WEIGHT-RELATED ABNORMALITIES AND NEWLY DIAGNOSED PATIENTS WITH TYPE 2 DIABETES MELLITUS; A CASE-CONTROL STUDY.Acta endocrinologica (Bucharest, Romania : 2005)Article
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3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNesfatin/Nucleobindin-2 (Nesf/NUCB2), a precursor of nesfatin-1, an anorexigenic protein, is ubiquitously expressed in peripheral tissues in addition to the hypothalamus. However, the role of intracellular Nesf/NUCB2 has not been established in the periphery.
methodsNesf/NUCB2-transgenic (Tg) mice were generated, and chronological changes of body weight and daily food intake were measured in Nesf/NUCB2-Tg mice fed normal laboratory chow or 45% high-fat diet (HFD). In addition, changes of metabolic markers were evaluated in those mice.
resultsNo differences were observed in daily food intake and body weight between Nesf/NUCB2-Tg mice (n=11) and their non-Tg littermates (n=11) fed normal chow. Nesf/NUCB2-Tg mice showed increased mRNA expression of oxytocin and corticotropin-releasing hormone and decreased mRNA expression of cocaine- and amphetamine-related transcript in the hypothalamus. Nesf/NUCB2-Tg mice fed 45% HFD (n=6) showed significantly higher increase in body weight than their non-Tg littermates fed the same diet (n=8); however, no difference was observed in daily food intake between these two groups. Further, Nesf/NUCB2-Tg mice fed 45% HFD showed a significant increase in the weight of the liver, subcutaneous fat, and brown adipose tissue and decrease in the expression of uncoupling protein-1 in the subcutaneous fat. Blood glucose levels of Nesf/NUCB2-Tg mice fed 45% HFD were not different from those of their non-Tg littermates fed the same diet. Insulin levels of these Tg mice were significantly higher than those of their non-Tg littermates. Histological analysis showed marked fat deposition in the hepatocytes surrounding the hepatic central veins in Nesf/NUCB2-Tg mice fed 45% HFD.
conclusionsOverexpression of Nesf/NUCB2 did not change food intake, but increased body weight only in Nesf/NUCB2-Tg mice fed HFD. The results of this study indicate that Nesf/NUCB2 was involved in the development of insulin resistance and fat deposition in the liver, independent of the modulation of energy intake.
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