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High fat diet induced hypertension and impaired glucose tolerance in the Obesity‐Prone Sprague Dawley rat: Effect of increased salt intake and renal denervation
Author(s) -
Han Ruijun,
Banek Christopher T,
AsirvathamJeyaraj Ninitha,
Wang Xinying,
Osborn John
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1006.10
Subject(s) - medicine , endocrinology , denervation , blood pressure , impaired glucose tolerance , obesity , sodium , kidney , insulin resistance , chemistry , organic chemistry
Cardiovascular disease, including hypertension (HTN), remains a leading cause of morbidity and mortality worldwide. Indeed, high fat (HFD) and high salt (HSD) diets are closely linked to HTN development, but the mechanisms remain undefined. Moreover, HTN in these models is widely attributed to an increase in sympathetic nerve activity, particularly to the kidney, which is attenuated renal denervation (RDNX). This study was designed to elucidate the combined effects HFD and HSD in the development of HTN. Further, we hypothesized that HTN and impaired glucose tolerance commonly induced by a HFD would be exacerbated by increased salt intake. In addition, we predicted these effects would be attenuated or reversed by RDNX. To test this hypothesis, obesity prone Sprague Dawley male rats were fed with either a low fat diet (LFD; 10 KCal% fat, n=12) or a high fat diet (HFD; 45 KCal% fat, n=12) for 8 weeks, then switched to either a low (0.26% sodium chloride, LSD, n=5) or high sodium (4% sodium chloride, HSD, n=7) diet for an additional 6 weeks. Mean arterial pressure (MAP) was measured by radiotelemetry, and bodyweight and glucose clearance were also measured. At study termination, tissues and plasma were collected for further analysis. HFD rats exhibited increased body weight, and impaired glucose tolerance compared to LFD rats. Addition of HSD feeding had no additional effect on bodyweight or glucose tolerance. MAP in HFD rats was higher (123±2 mmHg) compared to LFD rats (114±2mmHg). HSD had no further hypertensive effect in HFD‐treated animals. RDNX normalized MAP in HFD fed rats and HFD+HSD fed rats, but had no effect on the bodyweight or glucose tolerance. Assessment of renal and peripheral inflammation is currently underway. Together, these findings indicate that addition of a HSD to obese hypertensive rats does not exacerbate HTN and or impaired glucose tolerance. Further study of these intriguing effects in experimental and clinical models is necessary to accurately assess the dietary contribution to cardiovascular and metabolic disease. Support or Funding Information Supported by RO1HL116476