Cellular and Molecular Mechanisms Contributing to Cardiac Hypertrophy in Obesity and Obesity-Related Hypertension

Gómez-Viquez, Norma Leticia; Mailloux-Salinas, Patrick; Molina-Muñoz, Tzindilú; Guevara, Rodrigo; Bravo, Gerardo Ferrando; Carvajal, Karla

doi:10.1007/978-3-030-47336-5_9

Cited by 1 publication

(5 citation statements)

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“…( 8 ) In this sense, the role of CaMKII δ in the development of CH has been well established in several cardiomyopathies. ( 1 , 11 – 14 ) Accordingly, our data in SHR rats showed that three sugar diets (S, F, or S + F) cause a significant increase in the level of ox-CaMKII δ ( Fig. 2 C and D), that was not accompanied by a change in the expression of this kinase in any of the experimental groups ( Fig.…”

Section: Discussionmentioning

confidence: 63%

“…OS in the heart has been related with the development of CH and HF. ( 1 ) In a previous study, we reported that consumption of S and F induces CH by a mechanism that involves both the development of OS and activation of CaMKII δ due to an increase in oxidation level of this kinase. ( 8 ) In this sense, the role of CaMKII δ in the development of CH has been well established in several cardiomyopathies.…”

Section: Discussionmentioning

confidence: 96%

“…Pressure overload during AH has been widely reported to induce CH. ( 1 , 39 , 41 ) In SHR animals, the development of AH has been described as early as 3 months of age with respect to control rats. ( 38 ) Genetic predisposition and unhealthy lifestyle support the hypothesis that from early ages, subjects who develop obesity could develop AH and have a high probability of developing CH and later HF.…”

Section: Discussionmentioning

confidence: 99%

“…Arterial hypertension (AH) and obesity are independent risk factors for cardiac disease (CD) and mortality. ( 1 , 2 ) AH is a complex disease that arises from both genetic predisposition and exposure to environmental factors. ( 3 ) It has been reported that early AH is mostly due to genetic predisposition, but the increase in unhealthy lifestyle has favored its prevalence in young adults (<45 years), and notably, in children and adolescents.…”

Section: Introductionmentioning

confidence: 99%

“…To this end, we evaluated the effects of S, F, and S + F on IR, OS markers and cardiac structure in freshly weaned male spontaneous hypertensive rats (SHR). Moreover, we assessed the oxidation state of Ca 2+ /calmodulin-dependent protein kinase II isoform delta (CaMKII δ ) since the oxidation state of this protein is susceptible to OS and is related with an overactivation of this protein, ( 1 , 11 ) which in turn has been associated with the development, progression, and severity of CD in different cardiomyopathies, including hypertensive and obesity cardiomyopathies. ( 1 , 11 – 14 )…”

Section: Introductionmentioning

confidence: 99%

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Combined fructose and sucrose consumption from an early age aggravates cardiac oxidative damage and causes a dilated cardiomyopathy in ‍SHR rats

Arias-Chávez

Mailloux-Salinas

Aparicio

et al. 2023

J. Clin. Biochem. Nutr.

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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.

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