دورية أكاديمية
أعرض في EDS

Unaltered Hypothalamic Metabolic Gene Expression in Kiss1r Knockout Mice Despite Obesity and Reduced Energy Expenditure.

التفاصيل البيبلوغرافية
العنوان: Unaltered Hypothalamic Metabolic Gene Expression in Kiss1r Knockout Mice Despite Obesity and Reduced Energy Expenditure.
المؤلفون: De Bond JP; School of Anatomy, Physiology and Human Biology, University of Western Australia, Perth, Australia., Tolson KP; Department of Reproductive Medicine, University of California San Diego, La Jolla, CA, USA., Nasamran C; Department of Reproductive Medicine, University of California San Diego, La Jolla, CA, USA., Kauffman AS; Department of Reproductive Medicine, University of California San Diego, La Jolla, CA, USA., Smith JT; School of Anatomy, Physiology and Human Biology, University of Western Australia, Perth, Australia. jeremy.smith@uwa.edu.au.
المصدر: Journal of neuroendocrinology [J Neuroendocrinol] 2016 Oct; Vol. 28 (10).
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Wiley & Sons Country of Publication: United States NLM ID: 8913461 Publication Model: Print Cited Medium: Internet ISSN: 1365-2826 (Electronic) Linking ISSN: 09538194 NLM ISO Abbreviation: J Neuroendocrinol Subsets: MEDLINE
أسماء مطبوعة: Publication: <2010->: Malden, MA : Wiley & Sons
Original Publication: Eynsham, Oxon, UK : Oxford University Press, c1989-
مواضيع طبية MeSH: Energy Metabolism* , Gene Expression*, Hypothalamus/*metabolism , Obesity/*metabolism , Receptors, Kisspeptin-1/*metabolism, Animals ; Appetite ; Body Weight ; Female ; Gonads/metabolism ; Leptin/blood ; Male ; Mice ; Mice, Knockout ; Neuropeptide Y/genetics ; Neuropeptide Y/metabolism ; Obesity/genetics ; Pro-Opiomelanocortin/genetics ; Pro-Opiomelanocortin/metabolism ; Receptor, Melanocortin, Type 3/genetics ; Receptor, Melanocortin, Type 3/metabolism ; Receptor, Melanocortin, Type 4/genetics ; Receptor, Melanocortin, Type 4/metabolism ; Receptors, Ghrelin/genetics ; Receptors, Ghrelin/metabolism ; Receptors, Kisspeptin-1/genetics
مستخلص: Kisspeptin controls reproduction by stimulating gonadotrophin-releasing hormone neurones via its receptor Kiss1r. Kiss1r is also expressed other brain areas and in peripheral tissues, suggesting additional nonreproductive roles. We recently determined that Kiss1r knockout (KO) mice develop an obese and diabetic phenotype. In the present study, we investigated whether Kiss1r KOs develop this metabolic phenotype as a result of alterations in the expression of metabolic genes involved in the appetite regulating system of the hypothalamus, including neuropeptide Y (Npy) and pro-opiomelanocortin (Pomc), as well as leptin receptor (Lepr), ghrelin receptor (Ghsr), and melanocortin receptors 3 and 4 (Mc3r, Mc4r). Body weights, leptin levels and hypothalamic gene expression were measured in both gonad-intact and gonadectomised (GNX) mice at 8 and 20 weeks of age that had received either normal chow or a high-fat diet. We detected significant increases in Pomc expression in gonad-intact Kiss1r KO mice at 8 and 20 weeks, although there were no alterations in the other metabolic-related genes. However, the Pomc increases appeared to reflect genotype differences in circulating sex steroids, because GNX wild-type and Kiss1r KO mice exhibited similar Pomc levels, along with similar Npy levels. The altered Pomc gene expression in gonad-intact Kiss1r KO mice is consistent with previous reports of reduced food intake in these mice and may serve to increase the anorexigenic drive, perhaps compensating for the obese state. However, the surprising overall lack of changes in any of the hypothalamic metabolic genes in GNX KO mice suggests that the aetiology of obesity in the absence of kisspeptin signalling may reflect peripheral rather than central metabolic impairments.
(© 2016 British Society for Neuroendocrinology.)
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معلومات مُعتمدة: F32 HD076606 United States HD NICHD NIH HHS; P30 DK063491 United States DK NIDDK NIH HHS; P50 HD012303 United States HD NICHD NIH HHS; T32 HD007203 United States HD NICHD NIH HHS
فهرسة مساهمة: Keywords: Kiss1; GPR54; kisspeptin; leptin; metabolism
المشرفين على المادة: 0 (Kiss1r protein, mouse)
0 (Leptin)
0 (MC4R protein, mouse)
0 (Mc3r protein, mouse)
0 (Neuropeptide Y)
0 (Receptor, Melanocortin, Type 3)
0 (Receptor, Melanocortin, Type 4)
0 (Receptors, Ghrelin)
0 (Receptors, Kisspeptin-1)
66796-54-1 (Pro-Opiomelanocortin)
تواريخ الأحداث: Date Created: 20160908 Date Completed: 20180108 Latest Revision: 20181113
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC5083214
DOI: 10.1111/jne.12430
PMID: 27601011
قاعدة البيانات: MEDLINE
الوصف
تدمد:1365-2826
DOI:10.1111/jne.12430