High Fat/Low Carbohydrate Feeding Prevents Cardiac Hypertrophy, LV Remodeling and ANF Gene Induction, Independent of Hypertension

Abstract

Chronic hypertension (HTN) causes left ventricular hypertrophy (LVH) and dilation, which leads to heart failure. Diets high in fat and low in carbohydrate are recommended to patients at risk, but their impact on LV adaptations to HTN are unknown. Male Dahl salt sensitive rats were fed for 12 wk with either 1) low fat (10% kcal fat), 2) low fat/high salt (6% NaCl), or 3) high fat/high salt (60% kcal fat, 67% saturated, 33% unsaturated; 6% NaCl) (n=10/group). Tail cuff blood pressure (BP) measurements and echocardiographic assessment of LV dimensions were performed before & after 11wks on diets. There were no differences in these parameters between groups prior to feeding, and body mass was not different among groups. BP increased with salt feeding, with no differences between low fat & high fat groups (P<0.05, 126±2, 201±3 and 193±3 mmHg respectively). Compared to the low fat/low salt group, HTN lead to an increase in LV mass (3.38±0.19 vs 2.13±0.05 g/kg) and end diastolic area (EDA; 0.80±0.03 vs 0.66±0.02 cm2), which corresponded with an 11-fold induction of atrial natriuretic factor (ANF) mRNA expression (10.7±0.2 vs 1.0±0.1%) in the low fat/high salt group. In contrast, despite similar elevations in BP, the high fat/high salt group had significantly reduced LV mass (2.74±0.11 g/kg), LV EDA (0.66±0.03), and ANF expression (3.8±0.1%) compared to the low fat/high salt group. Conclusion High fat low carbohydrate feeding prevented HTN induced LVH and LV remodeling. We speculate that the mechanism for this dramatic effect may be reduced cardiac protein synthesis secondary to a reduction in plasma insulin associated with chronic low carbohydrate/high fat diets.