دورية أكاديمية
Metabolism and Energy Expenditure, But Not Feeding or Glucose Tolerance, Are Impaired in Young Kiss1r KO Female Mice.
العنوان: | Metabolism and Energy Expenditure, But Not Feeding or Glucose Tolerance, Are Impaired in Young Kiss1r KO Female Mice. |
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المؤلفون: | Tolson KP; Department of Reproductive Medicine, University of California, San Diego, La Jolla, California 92093., Garcia C; Department of Reproductive Medicine, University of California, San Diego, La Jolla, California 92093., Delgado I; Department of Reproductive Medicine, University of California, San Diego, La Jolla, California 92093., Marooki N; Department of Reproductive Medicine, University of California, San Diego, La Jolla, California 92093., Kauffman AS; Department of Reproductive Medicine, University of California, San Diego, La Jolla, California 92093. |
المصدر: | Endocrinology [Endocrinology] 2016 Nov; Vol. 157 (11), pp. 4192-4199. Date of Electronic Publication: 2016 Sep 20. |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: Oxford University Press Country of Publication: United States NLM ID: 0375040 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1945-7170 (Electronic) Linking ISSN: 00137227 NLM ISO Abbreviation: Endocrinology Subsets: MEDLINE |
أسماء مطبوعة: | Publication: 2017- : New York : Oxford University Press Original Publication: Los Angeles, Calif. : Association for the Study of Internal Secretions, |
مواضيع طبية MeSH: | Energy Metabolism/*physiology , Leptin/*blood , Receptors, G-Protein-Coupled/*metabolism, Adiposity/physiology ; Animals ; Body Composition/genetics ; Body Composition/physiology ; Body Weight/physiology ; Eating/physiology ; Energy Metabolism/genetics ; Female ; Glucose Intolerance/genetics ; Glucose Intolerance/physiopathology ; Glucose Tolerance Test ; Male ; Mice ; Mice, Knockout ; Receptors, G-Protein-Coupled/genetics ; Receptors, Kisspeptin-1 ; Signal Transduction |
مستخلص: | Kisspeptin regulates reproduction via signaling through the receptor, Kiss1r, in GnRH neurons. However, both kisspeptin and Kiss1r are produced in several peripheral tissues, and recent studies have highlighted a role for kisspeptin signaling in metabolism and glucose homeostasis. We recently reported that Kiss1r knockout (KO) mice display a sexually dimorphic metabolic phenotype, with KO females displaying obesity, impaired metabolism, and glucose intolerance at 4-5 months of age. However, it remains unclear when this metabolic phenotype first emerges in development, or which aspects of the pleiotropic phenotype underlie the metabolic defects and which are secondary to the obesity. Here, we studied Kiss1r KO females at different ages, including several weeks before the emergence of body weight (BW) differences and later when obesity is present. We determined that at young adult ages (6 wk old), KO females already exhibit altered adiposity, leptin levels, metabolism, and energy expenditure, despite having normal BWs at this time. In contrast, food intake, water intake, and glucose tolerance are normal at young ages and only show impairments at older adult ages, suggesting that these impairments may be secondary to earlier alterations in metabolism and adiposity. We also demonstrate that, in addition to BW, all other facets of the adult metabolic phenotype persist even when gonadal sex steroids are similar between genotypes. Collectively, these data highlight the developmental emergence of a metabolic phenotype induced by disrupted kisspeptin signaling and reveal that multiple, but not all, aspects of this phenotype are already disrupted before detectable changes in BW. |
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معلومات مُعتمدة: | R01 HD082567 United States HD NICHD NIH HHS; T32 HD007203 United States HD NICHD NIH HHS; F32 HD076606 United States HD NICHD NIH HHS; P30 DK063491 United States DK NIDDK NIH HHS; P50 HD012303 United States HD NICHD NIH HHS; U54 HD012303 United States HD NICHD NIH HHS |
المشرفين على المادة: | 0 (Kiss1r protein, mouse) 0 (Leptin) 0 (Receptors, G-Protein-Coupled) 0 (Receptors, Kisspeptin-1) |
تواريخ الأحداث: | Date Created: 20160921 Date Completed: 20170519 Latest Revision: 20181113 |
رمز التحديث: | 20221213 |
مُعرف محوري في PubMed: | PMC5086529 |
DOI: | 10.1210/en.2016-1501 |
PMID: | 27649089 |
قاعدة البيانات: | MEDLINE |
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