Influências de dietas ricas em ácidos graxos saturados e insaturados sobre o miocárdio de ratos

Pinotti, M.; Dal-Pai-Silva, Maeli; Sugizaki, Mário Mateus; Novelli, Yeda Santana Diniz; Sant'Ana, Léa Silvia; Aragon, Flávio Ferrari; Padovani, Carlos Roberto; Novelli, Ethel L. B.; Cicogna, Antônio Carlos

doi:10.1590/s0066-782x2007000300015

Cited by 3 publications

(4 citation statements)

References 20 publications

(47 reference statements)

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“…Regarding the occurrence of cardiac oxidative stress, studies by several authors have demonstrated the relationship between the consumption of hypercaloric diets and the increase in the production of free radicals, ROS and RNS [41,[47][48][49][50][51]. In our study, cardiac oxidative stress occurred markedly in the HF and HFS dietary interventions, promoting a substantial increase in protein carbonylation and lipid peroxidation.…”

Section: Discussionsupporting

confidence: 58%

High-Fat and Combined High-Fat and Sucrose Diets Promote Cardiac Oxidative Stress Independent of Nox2 Redox Regulation and Obesity in Rats

Gasparini

Matias

Torezani-Sales

et al. 2021

Cell Physiol Biochem

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BACKGROUND/AIMS: Oxidative stress is associated with cardiometabolic alterations, and the involvement of excess glucose and fatty acids has been demonstrated in this process. Thus, the aim of this study was to investigate the effects of different hypercaloric diets on cardiac oxidative stress. METHODS: Wistar rats were randomized into four groups: control (C), high-sucrose (HS), high-fat (HF), and high-fat with sucrose (HFS). Nutritional assessment, food profiles, histological analysis, comorbidities, and cardiovascular characteristics were determined. Cardiac oxidative stress was analyzed by malondialdehyde (MDA) and carbonylated proteins, and the cardiac protein expression levels of type 1 angiotensin receptor (AT-1), nicotinamide adenine dinucleotide phosphate oxidase 2 (Nox2), superoxide dismutase (SOD 1 e 2), glutathione peroxidase (GPX), and catalase (CAT) were determined by western blot. RESULTS: The HF group showed an increase in adiposity; however, it did not present adipocyte hypertrophy and comorbidities. Cardiac MDA and carbonylated protein levels were higher in the HF and HFS compared with the C group. The levels of oxidant and antioxidant proteins showed no difference between the groups. CONCLUSION: HF and HFS dietary interventions promoted cardiac oxidative stress, in the presence and absence of obesity, respectively. However, this process was neither mediated by the pro-oxidants AT1 and Nox2, nor by the quantitative reduction of antioxidant enzymes.

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Section: Discussionsupporting

confidence: 58%

High-Fat and Combined High-Fat and Sucrose Diets Promote Cardiac Oxidative Stress Independent of Nox2 Redox Regulation and Obesity in Rats

Gasparini

Matias

Torezani-Sales

et al. 2021

Cell Physiol Biochem

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“…The myocardial β-adrenergic mechanism is the main responsible by regulating the cardiac performance, especially by intracellular Ca 2+ handling [6,7]. Although functional studies using isolated papillary muscle have showed that obesity is able to lead to impairment in cardiac contractile [3,5,7], a small number of studies have evaluated the β-adrenergic response in high sugar-fat diet obesity-induced experimental models [29,45,46,47,48,49]. Our results demonstrated that the isoproterenol stimulation leaded to negative responses in both systolic (DT) and diastolic (−d T /d t ) response in the HSF group while the HSF + Ly group showed an improvement in the β-adrenergic response.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Tomato-Oleoresin Supplementation on Oxidative Injury Recoveries Cardiac Function by Improving β-Adrenergic Response in a Diet-Obesity Induced Model

et al. 2019

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The system redox imbalance is one of the pathways related to obesity-related cardiac dysfunction. Lycopene is considered one of the best antioxidants. The aim of this study was to test if the tomato-oleoresin would be able to recovery cardiac function by improving β-adrenergic response due its antioxidant effect. A total of 40 animals were randomly divided into two experimental groups to receive either the control diet (Control, n = 20) or a high sugar-fat diet (HSF, n = 20) for 20 weeks. Once cardiac dysfunction was detected by echocardiogram in the HSF group, animals were re- divided to begin the treatment with Tomato-oleoresin or vehicle, performing four groups: Control (n = 6); (Control + Ly, n = 6); HSF (n = 6) and (HSF + Ly, n = 6). Tomato oleoresin (10 mg lycopene/kg body weight (BW) per day) was given orally every morning for a 10-week period. The analysis included nutritional and plasma biochemical parameters, systolic blood pressure, oxidative parameters in plasma, heart, and cardiac analyses in vivo and in vitro. A comparison among the groups was performed by two-way analysis of variance (ANOVA). Results: The HSF diet was able to induce obesity, insulin-resistance, cardiac dysfunction, and oxidative damage. However, the tomato-oleoresin supplementation improved insulin-resistance, cardiac remodeling, and dysfunction by improving the β-adrenergic response. It is possible to conclude that tomato-oleoresin is able to reduce the oxidative damage by improving the system’s β-adrenergic response, thus recovering cardiac function.

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“…In the current literature, few studies have evaluated the βA components in experimental models of obesity induced by high-fat diet [ 34 , 35 , 73 – 76 ]. Some studies have shown that cardiac function impairment is related to βA system changes [ 35 , 73 , 74 ], while others researchers have not reported reduced βA response [ 34 , 49 , 75 , 76 ]. One explanation for these discrepancies and divergent data existing literature about obesity and βA system may be related to leptin levels, type of diet, animal model utilized and catecholamine levels [ 49 , 73 – 75 , 77 , 78 ].…”

Section: Discussionmentioning

confidence: 99%

“…Some studies have shown that cardiac function impairment is related to βA system changes [ 35 , 73 , 74 ], while others researchers have not reported reduced βA response [ 34 , 49 , 75 , 76 ]. One explanation for these discrepancies and divergent data existing literature about obesity and βA system may be related to leptin levels, type of diet, animal model utilized and catecholamine levels [ 49 , 73 – 75 , 77 , 78 ]. Meanwhile, it is still unclear whether obesity induced by high-fat diets leads to a reduction in the number of β-adrenergic receptors and/or defects of other components of the β-adrenergic pathway, resulting in cardiac impairment.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Dysfunction Induced by Obesity Is Not Related to β-Adrenergic System Impairment at the Receptor-Signalling Pathway

et al. 2015

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Obesity has been shown to impair myocardial performance. Some factors have been suggested as responsible for possible cardiac abnormalities in models of obesity, among them beta-adrenergic (βA) system, an important mechanism of regulation of myocardial contraction and relaxation. The objective of present study was to evaluate the involvement of βA system components in myocardial dysfunction induced by obesity. Thirty-day-old male Wistar rats were distributed in control (C, n = 25) and obese (Ob, n = 25) groups. The C group was fed a standard diet and Ob group was fed four unsaturated high-fat diets for 15 weeks. Cardiac function was evaluated by isolated papillary muscle preparation and βA system evaluated by using cumulative concentrations of isoproterenol and Western blot. After 15 weeks, the Ob rats developed higher adiposity index than C rats and several comorbidities; however, were not associated with changes in systolic blood pressure. Obesity caused structural changes and the myocardial responsiveness to post-rest contraction stimulus and increased extracellular calcium (Ca2+) was compromised. There were no changes in cardiac function between groups after βA stimulation. The obesity was not accompanied by changes in protein expression of G protein subunit alpha (Gsα) and βA receptors (β1AR and β2AR). In conclusion, the myocardial dysfunction caused by unsaturated high-fat diet-induced obesity, after 15 weeks, is not related to βAR system impairment at the receptor-signalling pathway.

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Influências de dietas ricas em ácidos graxos saturados e insaturados sobre o miocárdio de ratos

Cited by 3 publications

References 20 publications

High-Fat and Combined High-Fat and Sucrose Diets Promote Cardiac Oxidative Stress Independent of Nox2 Redox Regulation and Obesity in Rats

High-Fat and Combined High-Fat and Sucrose Diets Promote Cardiac Oxidative Stress Independent of Nox2 Redox Regulation and Obesity in Rats

Protective Effect of Tomato-Oleoresin Supplementation on Oxidative Injury Recoveries Cardiac Function by Improving β-Adrenergic Response in a Diet-Obesity Induced Model

Cardiac Dysfunction Induced by Obesity Is Not Related to β-Adrenergic System Impairment at the Receptor-Signalling Pathway

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