The prevalence of the metabolic syndrome (MetS) and its cardiac comorbidities as cardiac hypertrophy (CH) have increased considerably due to the high consumption of carbohydrates, such as sucrose and/or fructose. We compared the effects of sucrose (S), fructose (F) and their combination (S + F) on the development of MetS in weaned male Wistar rats and established the relationship between the consumption of these sugars and the degree of cardiac CH development, oxidative stress (OS) and Calcium/calmodulin-dependent protein kinase type II subunit delta oxidation (ox-CaMKII δ ). 12 weeks after the beginning of treatments with S, F or S + F, arterial pressure (AP) was measured and 8 weeks later (to complete 20 weeks) the animals were sacri ced and blood samples, visceral adipose tissue and hearts were obtained. Biochemical parameters were determined in serum and cardiac tissue to evaluate the development of MetS and OS. To evaluate CH, atrial natriuretic peptide (ANP), CaMKII δ and ox-CaMKII δ were determined by western blot and histological studies were performed in cardiac tissue. Our data showed that chronic consumption of S + F exacerbates MetS-induced CH which is related with a higher OS and ox-CaMKII δ .

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BACKGROUND The aim of this study was to evaluate the effects of capsaicin (Cap), moderate exercise (Ex), and their combination on arterial blood pressure (BP) and metabolic complications in hypoestrogenic (HE) obese (HEOb) rats. Female Wistar rats were ovariectomized and given 300 g L−1 sucrose solution (HEOb), or purified water (HE) ad libitum, for 28 weeks. After shaving the abdominal skin, cold cream vehicle was applied to sedentary (Sed) and exercise (Ex) groups, and 0.75 g kg−1 Cap cream was applied to Ex groups. Ex groups ran on a treadmill every day for 20 min at speeds from 0.15 to 0.3 m s−1. For combination groups (Cap + Ex), topical Cap was applied 90 min before Ex. The treatments were performed for 6 weeks, and BP was recorded before and at the end of the experimental protocol. The animals were killed by decapitation, and blood and tissues were obtained to perform oxidative profile, as well as to undertake biochemical and histologic studies. RESULTS Compared with individual treatments, the combined therapy (Cap + Ex) in HEOb rats caused a higher reduction in the caloric intake, body weight, abdominal fat percentage, oxidative stress, and hepatic steatosis. In HEOb groups, Cap was the only treatment that reduced BP and prevented dyslipidemia and oxidative stress. CONCLUSION The present data show that Cap improves the metabolic alterations induced by obesity and hypoestrogenism, suggesting that Cap can be considered as an excellent candidate for therapy of these clinical conditions. © 2020 Society of Chemical Industry

The prevalence of the metabolic syndrome (MetS) and its cardiac comorbidities as cardiac hypertrophy (CH) have increased considerably due to the high consumption of carbohydrates, such as sucrose and/or fructose. We compared the effects of sucrose (S), fructose (F) and their combination (S + F) on the development of MetS in weaned male Wistar rats and established the relationship between the consumption of these sugars and the degree of cardiac CH development, oxidative stress (OS) and Calcium/calmodulin-dependent protein kinase type II subunit delta oxidation (ox-CaMKIIδ). 12 weeks after the beginning of treatments with S, F or S + F, arterial pressure (AP) was measured and 8 weeks later (to complete 20 weeks) the animals were sacrificed and blood samples, visceral adipose tissue and hearts were obtained. Biochemical parameters were determined in serum and cardiac tissue to evaluate the development of MetS and OS. To evaluate CH, atrial natriuretic peptide (ANP), CaMKIIδ and ox-CaMKIIδ were determined by western blot and histological studies were performed in cardiac tissue. Our data showed that chronic consumption of S + F exacerbates MetS-induced CH which is related with a higher OS and ox-CaMKIIδ.

Obesity increases the risk of arterial hypertension in young adults and favors an early-onset cardiomyopathy by generating oxidative stress. In this sense, indiscriminate consumption of sucrose and fructose sweetened beverages from early ages causes obesity, however its consequences on the heart when there is a genetic predisposition to develop hypertension are not clear. We compared the effects of sucrose, fructose, and their combination in weanling male spontaneously hypertensive rats to determine the relationship between genetic hypertension, obesity, and consumption of these sugars on the degree of cardiac hypertrophy, oxidative stress and Ca 2+ /calmodulin dependent protein kinase II delta oxidation. Histological, biochemical, and Western blot studies were performed 12 weeks after treatment initiation. We found that chronic consumption of sucrose or fructose leads to obesity, exacerbates genetic arterial hypertension-induced metabolic alterations, and increases cardiac oxidative stress, Ca 2+ /calmodulin dependent protein kinase II delta oxidation and cardiac hypertrophy. Nonetheless, when sucrose and fructose are consumed together, metabolic alterations worsen and are accompanied by dilated cardiomyopathy. These data suggest that sucrose and fructose combined consumption starting from maternal weaning in rats with genetic predisposition to arterial hypertension accelerates the progression of cardiomyopathy resulting in an early dilated cardiomyopathy.