Cafeteria Diet Increases Fat Mass and Chronically Elevates Lumbar Sympathetic Nerve Activity in Rats

Obesity causes sympathetic activation that promotes atherosclerosis, end-organ damage, and hypertension. Because high-fat induced weight gain in rats elevates plasma leptin at 1 to 3 days after the onset of calorie-dense diets, we hypothesized that diet-induced overfeeding will increase sympathetic...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2012-12, Vol.60 (6), p.1498-1502
Main Authors: Muntzel, Martin S, Al-Naimi, Omar Ali S, Barclay, Alicia, Ajasin, David
Format: Article
Language:English
Subjects:
Adipose Tissue - physiopathology
Adiposity - physiology
Animals
Arterial hypertension. Arterial hypotension
Arterial Pressure - physiology
Biological and medical sciences
Blood and lymphatic vessels
Body Weight - physiology
Cardiology. Vascular system
Diet, High-Fat - adverse effects
Eating - physiology
Experimental diseases
Female
Heart Rate - physiology
Medical sciences
Obesity - etiology
Obesity - physiopathology
Rats
Rats, Wistar
Sympathetic Nervous System - physiopathology
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Summary:Obesity causes sympathetic activation that promotes atherosclerosis, end-organ damage, and hypertension. Because high-fat induced weight gain in rats elevates plasma leptin at 1 to 3 days after the onset of calorie-dense diets, we hypothesized that diet-induced overfeeding will increase sympathetic activity within 1 week after the onset of the regimen. To test this, we continuously measured sympathetic activity and blood pressure before and during the onset of diet-induced obesity using a high-calorie, cafeteria-style diet. Female Wistar rats, in which radiotelemeters had been implanted for continuous monitoring of lumbar sympathetic activity, mean arterial pressure, and heart rate, were randomly assigned to groups that received regular chow (control) or a cafeteria diet for a period of 15 days. This short-term, cafeteria-feeding regimen caused modest but nonsignificant increases in body weight (P=0.07) and a doubling of brown and white adipose tissue (P
ISSN:0194-911X
1524-4563
DOI:10.1161/HYPERTENSIONAHA.112.194886