دورية أكاديمية
Effects of chronic high fat diet on mediobasal hypothalamic satiety neuron function in POMC-Cre mice.
| العنوان: | Effects of chronic high fat diet on mediobasal hypothalamic satiety neuron function in POMC-Cre mice. |
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| المؤلفون: | Başer Ö; Yeditepe University, Faculty of Medicine, Department of Physiology, Istanbul, Türkiye., Yavuz Y; Yeditepe University, Faculty of Medicine, Department of Physiology, Istanbul, Türkiye., Özen DÖ; Yeditepe University, Faculty of Medicine, Department of Physiology, Istanbul, Türkiye., Özgün HB; Yeditepe University, Faculty of Medicine, Department of Physiology, Istanbul, Türkiye., Ağuş S; Yeditepe University, Faculty of Medicine, Department of Physiology, Istanbul, Türkiye., Civaş CC; Yeditepe University, Faculty of Medicine, Department of Physiology, Istanbul, Türkiye., Atasoy D; University of Iowa, Carver College of Medicine, Department of Neuroscience and Pharmacology, Iowa City, USA., Yılmaz B; Yeditepe University, Faculty of Medicine, Department of Physiology, Istanbul, Türkiye; Izmir Biomedicine and Genome Center, Izmir, Türkiye. Electronic address: byilmaz@yeditepe.edu.tr. |
| المصدر: | Molecular metabolism [Mol Metab] 2024 Apr; Vol. 82, pp. 101904. Date of Electronic Publication: 2024 Feb 21. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier GmbH Country of Publication: Germany NLM ID: 101605730 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2212-8778 (Electronic) Linking ISSN: 22128778 NLM ISO Abbreviation: Mol Metab Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: [München] : Elsevier GmbH, 2012- |
| مواضيع طبية MeSH: | Diet, High-Fat*/adverse effects , Leptin*/metabolism, Mice ; Animals ; Pro-Opiomelanocortin/metabolism ; Hypothalamus/metabolism ; Obesity ; Neurons/metabolism ; Mice, Transgenic |
| مستخلص: | Objective: The prevalence of obesity has increased over the past three decades. Proopiomelanocortin (POMC) neurons in the hypothalamic arcuate nucleus (ARC) play a vital role in induction of satiety. Chronic consumption of high-fat diet is known to reduce hypothalamic neuronal sensitivity to hormones like leptin, thus contributing to the development and persistence of obesity. The functional and morphological effects of a high-calorie diet on POMC neurons and how these effects contribute to the development and maintenance of the obese phenotype are not fully understood. For this purpose, POMC-Cre transgenic mice model was exposed to high-fat diet (HFD) and at the end of a 3- and 6-month period, electrophysiological and morphological changes, and the role of POMC neurons in homeostatic nutrition and their response to leptin were thoroughly investigated. Methods: Effects of HFD on POMC-satiety neurons in transgenic mice models exposed to chronic high-fat diet were investigated using electrophysiological (patch-clamp), chemogenetic and Cre recombinase advanced technological methods. Leptin, glucose and lipid profiles were determined and analyzed. Results: In mice exposed to a high-fat diet for 6 months, no significant changes in POMC dendritic spine number or projection density from POMC neurons to the paraventricular hypothalamus (PVN), lateral hypothalamus (LH), and bed nucleus stria terminalis (BNST) were observed. It was revealed that leptin hormone did not change the electrophysiological activities of POMC neurons in mice fed with HFD for 6 months. In addition, chemogenetic stimulation of POMC neurons increased HFD consumption. In the 3-month HFD-fed group, POMC activation induced an orexigenic response in mice, whereas switching to a standard diet was found to abolish orexigenic behavior in POMC mice. Conclusions: Chronic high fat consumption disrupts the regulation of POMC neuron activation by leptin. Altered POMC neuron activation abolished the neuron's characteristic behavioral anorexigenic response. Change in nutritional content contributes to the reorganization of developing maladaptations. Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (Copyright © 2024 The Authors. Published by Elsevier GmbH.. All rights reserved.) |
| معلومات مُعتمدة: | R01 DK126740 United States DK NIDDK NIH HHS |
| فهرسة مساهمة: | Keywords: Behavioral; Chemogenetic; Electrophysiology; High fat diet; Obesity; POMC neurons |
| المشرفين على المادة: | 0 (Leptin) 66796-54-1 (Pro-Opiomelanocortin) |
| تواريخ الأحداث: | Date Created: 20240223 Date Completed: 20240402 Latest Revision: 20240416 |
| رمز التحديث: | 20240416 |
| مُعرف محوري في PubMed: | PMC10910127 |
| DOI: | 10.1016/j.molmet.2024.101904 |
| PMID: | 38395148 |
| قاعدة البيانات: | MEDLINE |
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Full Text Finder | تدمد: | 2212-8778 |
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| DOI: | 10.1016/j.molmet.2024.101904 |