Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12597
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dc.contributor.authorSfrantzis, K Den
dc.contributor.authorHow, J M Yen
dc.contributor.authorSartor, Daniela Men
dc.date.accessioned2015-05-16T02:18:49Z-
dc.date.available2015-05-16T02:18:49Z-
dc.date.issued2015-01-10en
dc.identifier.citationAutonomic Neuroscience : Basic & Clinical 2015; 189: 25-30en
dc.identifier.govdoc25623383en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/12597en
dc.description.abstractWe have previously demonstrated that a number of rats fed a moderately high-fat diet (MHFD) become obese and hypertensive and had compromised sympathoinhibitory and vasodilator responses to the gut hormones cholecystokinin (CCK) and gastric leptin. This has implications for increased resistance in vascular beds that attract a large proportion of cardiac output after a meal and may be an important mechanism underlying the development of hypertension in obesity in which food consumption is greatly increased. The aim of this study was to determine whether swapping a MHFD for a low-fat diet (LFD) would induce weight loss in obese animals, reverse the signs of hypertension and restore sympathoinhibitory reflexes. Male Sprague-Dawley rats were placed on a LFD (controls; n=8) or a MHFD (n=24) for 11weeks after which the latter displayed either an obesity-prone (OP) or obesity-resistant (OR) phenotype. All animals were fed a LFD for a further 6weeks after which they were anaesthetised with isoflurane and artificially ventilated for evaluation of resting arterial pressure (AP) and renal sympathetic nerve responses to CCK (0.1-4μg/kg) and leptin (15μg/kg). Weight gain in OP animals remained higher than OR or controls following diet switch (P<0.05 for both). Resting AP was not significantly different between OP (103±4mmHg), OR (102±3mmHg) or control (104±3mmHg) animals and sympathoinhibitory responses to CCK or leptin were not different between the groups (P>0.05). These results demonstrate that diet modification can have beneficial effects on sympathetic function and restore normotension without the need for weight reduction.en
dc.language.isoenen
dc.subject.othercholecystokininen
dc.subject.otherhypertensionen
dc.subject.otherleptinen
dc.subject.otherobesityen
dc.subject.othersympathetic nerveen
dc.titleImplications of diet modification on sympathoinhibitory mechanisms and hypertension in obesity.en
dc.typeJournal Articleen
dc.identifier.journaltitleAutonomic neuroscience : basic & clinicalen
dc.identifier.affiliationDepartment of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1016/j.autneu.2015.01.001en
dc.description.pages25-30en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/25623383en
dc.type.austinJournal Articleen
item.grantfulltextnone-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
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