title: Implications of diet modification on sympathoinhibitory mechanisms and hypertension in obesity.
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 11 weeks after which the latter displayed either an obesity-prone (OP) or obesity-resistant (OR) phenotype. All animals were fed a LFD for a further 6 weeks after which they were anaesthetised with isoflurane and artificially ventilated for evaluation of resting arterial pressure (AP) and renal sympathetic nerve responses to CCK (0.1-4 μg/kg) and leptin (15 μg/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 ± 4 mmHg), OR (102 ± 3 mmHg) or control (104 ± 3 mmHg) 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.
authors.affiliation: Department of Medicine, Austin Health, University of Melbourne, Heidelberg, 3084 Victoria, Australia.
authors.forename: K D
authors.initials: KD
authors.lastname: Sfrantzis
authors.affiliation: Department of Medicine, Austin Health, University of Melbourne, Heidelberg, 3084 Victoria, Australia.
authors.forename: J M Y
authors.initials: JM
authors.lastname: How
authors.affiliation: Department of Medicine, Austin Health, University of Melbourne, Heidelberg, 3084 Victoria, Australia. Electronic address: dsartor@unimelb.edu.au.
authors.forename: D M
authors.initials: DM
authors.lastname: Sartor
mesh_terms: D000818:Animals; D062186:Arterial Pressure / Q000502:physiology; D001337:Autonomic Agents / Q000494:pharmacology; D001835:Body Weight; D002766:Cholecystokinin / Q000494:pharmacology; D018752:Diet, Fat-Restricted; D059305:Diet, High-Fat / Q000009:adverse effects; D004195:Disease Models, Animal; D005765:Gastrointestinal Agents / Q000494:pharmacology; D020022:Genetic Predisposition to Disease; D006973:Hypertension / Q000178:diet therapy* / Q000503:physiopathology*; D020738:Leptin / Q000494:pharmacology; D008297:Male; D009765:Obesity / Q000178:diet therapy* / Q000503:physiopathology*; D017207:Rats, Sprague-Dawley; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology
chemical_list: D001337:Autonomic Agents; D005765:Gastrointestinal Agents; D020738:Leptin; D002766:Cholecystokinin
keywords: cholecystokinin; hypertension; leptin; obesity; sympathetic nerve