| Exposure to a high-fat diet alters leptin sensitivity and elevates renal sympathetic nerve activity and arterial pressure in rabbits. | |
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MedLine Citation:
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PMID: 20194306 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The activation of the sympathetic nervous system through the central actions of the adipokine leptin has been suggested as a major mechanism by which obesity contributes to the development of hypertension. However, direct evidence for elevated sympathetic activity in obesity has been limited to muscle. The present study examined the renal sympathetic nerve activity and cardiovascular effects of a high-fat diet (HFD), as well as the changes in the sensitivity to intracerebroventricular leptin. New Zealand white rabbits fed a 13.5% HFD for 4 weeks showed modest weight gain but a 2- to 3-fold greater accumulation of visceral fat compared with control rabbits. Mean arterial pressure, heart rate, and plasma norepinephrine concentration increased by 8%, 26%, and 87%, respectively (P<0.05), after 3 weeks of HFD. Renal sympathetic nerve activity was 48% higher (P<0.05) in HFD compared with control diet rabbits and was correlated to plasma leptin (r=0.87; P<0.01). Intracerebroventricular leptin administration (5 to 100 microg) increased mean arterial pressure similarly in both groups, but renal sympathetic nerve activity increased more in HFD-fed rabbits. By contrast, intracerebroventricular leptin produced less neurons expressing c-Fos in HFD compared with control rabbits in regions important for appetite and sympathetic actions of leptin (arcuate: -54%, paraventricular: -69%, and dorsomedial hypothalamus: -65%). These results suggest that visceral fat accumulation through consumption of a HFD leads to marked sympathetic activation, which is related to increased responsiveness to central sympathoexcitatory effects of leptin. The paradoxical reduction in hypothalamic neuronal activation by leptin suggests a marked "selective leptin resistance" in these animals. |
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Authors:
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Larissa J Prior; Nina Eikelis; James A Armitage; Pamela J Davern; Sandra L Burke; Jean-Pierre Montani; Benjamin Barzel; Geoffrey A Head |
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Publication Detail:
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Type: Journal Article Date: 2010-03-01 |
Journal Detail:
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Title: Hypertension Volume: 55 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-03-18 Completed Date: 2010-04-09 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 862-8 Citation Subset: IM |
Affiliation:
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Baker IDI Heart and Diabetes Institute, PO Box 6492, St Kilda Rd Central, Melbourne, Victoria 8008, Australia. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Analysis of Variance Animals Blood Pressure / drug effects, physiology* Body Weight / physiology Catheters, Indwelling Dietary Fats / metabolism*, pharmacology Dose-Response Relationship, Drug Heart Rate / drug effects, physiology Hypothalamus / metabolism Injections, Intraventricular Intra-Abdominal Fat / metabolism Kidney / innervation* Leptin / administration & dosage, metabolism* Male Neurons / metabolism Proto-Oncogene Proteins c-fos / metabolism Rabbits Receptors, Leptin / metabolism* Sympathetic Nervous System / drug effects, metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Dietary Fats; 0/Leptin; 0/Proto-Oncogene Proteins c-fos; 0/Receptors, Leptin |
| Comments/Corrections | |
Comment In:
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Hypertension. 2010 Apr;55(4):844-5
[PMID:
20194295
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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