High-sugar diets increase cardiac dysfunction and mortality in hypertension compared to low-carbohydrate or high-starch diets

Abstract

Objective Sugar consumption affects insulin release and, in hypertension, may stimulate cardiac signaling mechanisms that accelerate left ventricular hypertrophy and the development of heart failure. We investigated the effects of high-fructose or sucrose diets on ventricular function and mortality in hypertensive Dahl salt-sensitive rats. Methods Rats were fed chows that were either high starch (70% starch, 10% fat by energy), high fat (20% carbohydrates, 60% fat), high fructose (61% fructose, 9% starch, 10% fat), or high sucrose (61% sucrose, 9% starch, 10% fat). Hypertension was induced by adding 6% salt to the chow (n = 8–11/group). Results After 8 weeks of treatment, systolic blood pressure and left ventricular mass were similarly increased in all rats that were fed high-salt diets. Hypertension caused a switch in mRNA myosin heavy chain isoform from α to β, and this effect was greater in the high-salt sucrose and fructose groups than in starch and fat groups. The cardiac mRNA for atrial natriuretic factor was also increased in all high-salt groups compared to respective controls, with the increase being significantly greater in the hypertensive sucrose fed group. Mortality was greater in the sucrose group (44%) compared to all the other hypertensive groups (12–18%), as was cardiomyocyte apoptosis. Left ventricular ejection fraction was lower in the high-salt sucrose group, which was due to an increase in end-systolic volume, and not increased end-diastolic volume. Conclusion Diets high in sugar accelerated cardiac systolic dysfunction and mortality in hypertension compared to either a low-carbohydrate/high-fat or high-starch diet.

Left Ventricular Mass and Function With Reduced-Fat or Reduced-Carbohydrate Hypocaloric Diets in Overweight and Obese Subjects

“…We suggest that the limited impact of macronutrient composition on LV mass in patients may be explained by the modest carbohydrate or fat restriction compared to dietary manipulations in rodents. 12,13,16 Species differences in the susceptibility to dietary interventions also may be involved.…”

“…9 In animals, high-fat feeding attenuated cardiac hypertrophy and remodeling, 10,11 whereas high-carbohydrate feeding accelerated the process. 12 Excessive simple sugars and saturated fatty acid ingestion worsened cardiac structure and function. 13,14 In contrast, n-3 polyunsaturated fatty acid supplementation attenuated cardiac hypertrophy and fibrosis in rats.…”

Fructose diet treatment in mice induces fundamental disturbance of cardiomyocyte Ca2+handling and myofilament responsiveness

“…In this study, the MHC isoform shift was characterized at the mRNA level. This approach has been previously validated in a rodent model of hypertensive cardiopathology (43). A more detailed dissection of the contribution of MHC isoform switch to myofilament Ca 2ϩ responsiveness, including analysis of MHC protein content and activity, is now warranted.…”

A high-fructose diet worsens eccentric left ventricular hypertrophy in experimental volume overload

“…Previous studies have reported that a fructose-rich diet fed to rats will eventually lead to the development of metabolic abnormalities sharing many similarities with the human metabolic syndrome (12,27). This type of diet has also been shown to increase cardiac dysfunction and mortality in an animal model of LV pressure overload with concentric left ventricular hypertrophy (8,27,37,38). The potential impact of a high-fructose diet on the progression of VO cardiomyopathy has never been explored.…”