Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/12597
Title: Implications of diet modification on sympathoinhibitory mechanisms and hypertension in obesity.
Authors: Sfrantzis, K D;How, J M Y;Sartor, Daniela M
Affiliation: Department of Medicine, Austin Health, University of Melbourne, Heidelberg, 3084 Victoria, Australia.
Department of Medicine, Austin Health, University of Melbourne, Heidelberg, 3084 Victoria, Australia. Electronic address: dsartor@unimelb.edu.au.
Issue Date: 10-Jan-2015
Citation: Autonomic Neuroscience : Basic & Clinical 2015; 189(): 25-30
Abstract: We 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.
Internal ID Number: 25623383
URI: http://ahro.austin.org.au/austinjspui/handle/1/12597
DOI: 10.1016/j.autneu.2015.01.001
URL: http://www.ncbi.nlm.nih.gov/pubmed/25623383
Type: Journal Article
Subjects: cholecystokinin
hypertension
leptin
obesity
sympathetic nerve
Appears in Collections:Journal articles

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