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

Abstract

Bouchard-Thomassin (LVH) can be affected by diet manipulation. Concentric LVH resulting from pressure overload can be worsened by feeding rats with a high-fructose diet. Eccentric LVH is a different type of hypertrophy and is associated with volume overload (VO) diseases. The impact of an abnormal diet on the development of eccentric LVH and on ventricular function in chronic VO is unknown. This study therefore examined the effects of a fructose-rich diet on LV eccentric hypertrophy, ventricular function, and myocardial metabolic enzymes in rats with chronic VO caused by severe aortic valve regurgitation (AR). Wistar rats were divided in four groups: sham-operated on control diet (SC; n ϭ 13) or fructose-rich diet (SF; n ϭ 13) and severe aortic regurgitation fed with the same diets [aortic regurgitation on control diet (ARC), n ϭ 16, and aortic regurgitation on fructose-rich diet (ARF), n ϭ 13]. Fructose-rich diet was started 1 wk before surgery, and the animals were euthanized 9 wk later. SF and ARF had high circulating triglycerides. ARC and ARF developed significant LV eccentric hypertrophy after 8 wk as expected. However, ARF developed more LVH than ARC. LV ejection fraction was slightly lower in the ARF compared with ARC. The increased LVH and decreased ejection fraction could not be explained by differences in hemodynamic load. SF, ARC, and ARF had lower phosphorylation levels of the AMP kinase compared with SC. A fructose-rich diet worsened LV eccentric hypertrophy and decreased LV function in a model of chronic VO caused by AR in rats. Normal animals fed the same diet did not develop these abnormalities. Hypertriglyceridemia may play a central role in this phenomenon as well as AMP kinase activity. cardiomyopathy; metabolic syndrome; heart hypertrophy; triglycerides; glucose; fatty acids CHRONIC LEFT VENTRICULAR VOLUME overload (VO) causes severe left ventricular dilatation and eccentric hypertrophy. This type of left ventricular hypertrophy is encountered mainly in patients with valvular diseases such as chronic mitral or aortic valve regurgitation (AR). AR is associated with a long asymptomatic period during which the left ventricle (LV) progressively dilates and hypertrophies. In parallel with the LV dilatation, systolic function slowly decreases and symptoms eventually appear (4, 5). Although it is not the most frequent valvular disease in Western countries, it has been estimated based on the Framingham study that 13% of the population suffer from AR of varying degrees of severity (40).No drug treatment has proved to be effective to decrease morbidity or mortality or delay the evolution toward heart failure or valve replacement surgery in patients with chronic VO from valve disease (5). The search for an effective treatment is still ongoing. Patient lifestyle has a significant impact on the evolution of many cardiac diseases. Whereas good habits such as exercising and eating low fat/low sugar diets seem beneficial, a lack of physical activity and eating imbalanced diets may act in the opposite way. ...

Atorvastatin Protects against Ischemia-Reperfusion Injury in Fructose-Induced Insulin Resistant Rats

“…The present study, however, supports the deleterious effect of long term high fructose feeding on ischemic-reperfusion injury, caused by impaired normal endothelial function, induction of oxidative stress and systemic inflammation [27,48,63,64]. The results obtained in the present study thus imply an important role of NOS in high fructose diet induced IRS [14,48] and also in atorvastatin mediated protection against ischemia-reperfusion injury.…”

Angiotensin II–Converting Enzyme Inhibition Improves Survival, Ventricular Remodeling, and Myocardial Energetics in Experimental Aortic Regurgitation

“…Although interstitial fibrosis is not an early feature of this animal model of eccentric LV remodeling, significant accumulation of collagen is present in later stages (≥6 months). 16,22 Our results suggest that the dilated hearts of Cpt-treated AR animals tolerated the abnormal hemodynamic overload and maintained a near normal myocardial metabolic profile. We previously showed that blood pressure in AR animals treated with Cpt is only slightly reduced and had similar findings in this protocol.…”

“…Enzymatic activities for hydroxyacyl-Coenzyme A dehydrogenase, hexokinase, and citrate synthase were determined as previously described. 16 Enzymatic activities for carnitine palmitoyl transferase and malonyl-CoA decarboxylase enzymatic activity determination were also previously described elsewhere.…”

Metformin Reduces Left Ventricular Eccentric Re-modeling In Experimental volume Overload in the Rat

“…Enzymatic activities for hydroxyacyl-Coenzyme A dehydrogenase (HADH), phosphofructokinase (PFK) and citrate synthase (CS) were determined as previously described [7].…”

“…Metformin is an AMPK activator widely used for the management of type 2 diabetes but its potential to help maintain normal myocardial metabolism and/or prevent LVH is not well understood [6]. We have previously demonstrated that LV volume overload caused by aortic valve regurgitation causes severe eccentric LVH and also significantly impairs myocardial metabolism [7].…”