Angiotensin‐Converting Enzyme Inhibition Reduces Lipid Deposits in Myocardium and Improves Left Ventricular Function of Obese Zucker Rats

Toblli, Jorge Eduardo; Cao, Gabriel; Rivas, Carlos; Derosa, G.; Domecq, P

doi:10.1038/oby.2006.183

Cited by 10 publications

(10 citation statements)

References 63 publications

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“…On the other hand, swimming training in obese rats improved this condition by lowering triglycerides and LDL cholesterol and augmenting HDL cholesterol. These changes are important, because these metabolic alterations can contribute to cardiac modifications [26], such as cardiac metabolic disorders and increased cardiac mass [27], as seen in the Zucker model [8], [10]. Likewise, in the untrained obese Zucker rats in this study, increased cardiac mass, measured by cardiac weight and echocardiography were found.…”

Section: Discussionsupporting

confidence: 58%

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Effects of Aerobic Exercise Training on Cardiac Renin-Angiotensin System in an Obese Zucker Rat Strain

et al. 2012

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ObjectiveObesity and renin angiotensin system (RAS) hyperactivity are profoundly involved in cardiovascular diseases, however aerobic exercise training (EXT) can prevent obesity and cardiac RAS activation. The study hypothesis was to investigate whether obesity and its association with EXT alter the systemic and cardiac RAS components in an obese Zucker rat strain.MethodsThe rats were divided into the following groups: Lean Zucker rats (LZR); lean Zucker rats plus EXT (LZR+EXT); obese Zucker rats (OZR) and obese Zucker rats plus EXT (OZR+EXT). EXT consisted of 10 weeks of 60-min swimming sessions, 5 days/week. At the end of the training protocol heart rate (HR), systolic blood pressure (SBP), cardiac hypertrophy (CH) and function, local and systemic components of RAS were evaluated. Also, systemic glucose, triglycerides, total cholesterol and its LDL and HDL fractions were measured.ResultsThe resting HR decreased (∼12%) for both LZR+EXT and OZR+EXT. However, only the LZR+EXT reached significance (p<0.05), while a tendency was found for OZR versus OZR+EXT (p = 0.07). In addition, exercise reduced (57%) triglycerides and (61%) LDL in the OZR+EXT. The systemic angiotensin I-converting enzyme (ACE) activity did not differ regardless of obesity and EXT, however, the OZR and OZR+EXT showed (66%) and (42%), respectively, less angiotensin II (Ang II) plasma concentration when compared with LZR. Furthermore, the results showed that EXT in the OZR prevented increase in CH, cardiac ACE activity, Ang II and AT2 receptor caused by obesity. In addition, exercise augmented cardiac ACE2 in both training groups.ConclusionDespite the unchanged ACE and lower systemic Ang II levels in obesity, the cardiac RAS was increased in OZR and EXT in obese Zucker rats reduced some of the cardiac RAS components and prevented obesity-related CH. These results show that EXT prevented the heart RAS hyperactivity and cardiac maladaptive morphological alterations in obese Zucker rats.

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Section: Discussionsupporting

confidence: 58%

“…Studies that used ACE inhibitors have suggested that the RAS seems to play a critical role in cardiac modifications [7], [27]. However, although some studies have shown that the RAS can participate in cardiac diseases related to obesity, they did not measure the cardiac RAS components [8], [27].…”

Section: Discussionmentioning

confidence: 99%

Effects of Aerobic Exercise Training on Cardiac Renin-Angiotensin System in an Obese Zucker Rat Strain

et al. 2012

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“…To our knowledge, however, no earlier studies have shown that a calcium channel blocker can regulate the expression of certain lipogenic gene and/or reduce tissue lipid content. Toblli et al 20 reported that renin angiotensin system inhibition, but not calcium channel blockade, suppressed lipid deposition in the heart 20 and liver 21 in obese Zucker rats.…”

Section: Discussionmentioning

confidence: 99%

Effects of the AT1 receptor blocker losartan and the calcium channel blocker benidipine on the accumulation of lipids in the kidney of a rat model of metabolic syndrome

et al. 2010

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Unfavorable lipid accumulation may occur in the kidneys in the presence of metabolic syndrome and diabetes. The aim of this study was to investigate whether excess lipids would accumulate in the kidneys of Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an animal model of metabolic syndrome. From 34 weeks of age, OLETF rats were treated orally with a calcium channel blocker, benidipine (3 mg kg À1 per day), or an AT1 receptor blocker, losartan (25 mg kg À1 per day), for 8 weeks. Blood pressure was slightly but significantly higher in the untreated OLETF rats (149±4 mm Hg) than in Long-Evans Tokushima Otsuka (LETO) rats (136 ± 2 mm Hg), and both losartan (135 ± 3 mm Hg) and benidipine (138 ± 3 mm Hg) reduced blood pressure in OLETF rats to a level comparable to that in LETO rats. Tissue content of triglycerides (TG) was greater in OLETF rats than in LETO rats (6.24±3.77 and 2.85±1.32 lg mg À1 . tissue, respectively), and both losartan and benidipine reduced these values. Histological analysis showed lipid droplets in tubular cells in which increased dihydroethidium fluorescence was present. Expression of peroxisome proliferator-activated receptor-a, PGC-1a and uncoupling protein-2 was found to be higher in OLETF rats than in LETO rats; however, the expression of these genes was not altered by treatment with either antihypertensive drug. In contrast, both losartan and benidipine increased the amount of total and phosphorylated forms of AMP kinase and the expression of carnitine palmitoyltransferase-1 (CPT-1). In conclusion, treatment of OLETF rats with losartan and benidipine reduced the tissue content of TG, decreased the production of superoxide and regulated the expression of genes related to fatty acid oxidation such as AMP-activated protein kinase and CPT-1 in the kidneys.

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“…Vários mecanismos têm sido discutidos para explicar essa correlação, incluindo alterações hemodinâmicas com sobrecarga cardíaca e remodelamento ventricular, entretanto estes mecanismos não explicam completamente o desenvolvimento da disfunção cardíaca em indivíduos obesos (KENCHAIAH, EVANS, LEVY, WILSON, BENJAMIN, LARSON, KANNEL & VASAN, 2002). Estudos com ratos Zucker obesos demonstram que a disfunção diastólica pode ser ocasionada pelo acúmulo de lipídios e fi brose cardíaca (TOBLLI, CAO, DEROSA & FORCADA, 2005;TOBLLI, CAO, RIVAS, DEROSA & DOMECQ, 2006). Além disso, essas alterações morfológicas e estruturais são acompanhadas por alterações moleculares no padrão de expressão gênica dos marcadores de hipertrofi a cardíaca patológica, como o aparecimento da alfa…”

Section: Introductionunclassified

“…Ratos Zucker obesos apresentam aumento de fi brose cardíaca (TOBLLI et al, 2005(TOBLLI et al, , 2006 e da expressão da βMCP, sem alterações da αMCP (GOLFMAN et al, 2005). Estas alterações determinam modifi cações na capacidade contrátil do miocárdio, o que pode levar à diminuição na velocidade de encurtamento dos sarcômeros e causar disfunção cardíaca (IZUMO et al, 1988;SWYNGHEDAUW, 2006).…”

Section: Introductionunclassified

Treinamento físico aeróbio previne à hipertrofia cardíaca patológica e melhora a função diastólica em ratos Zucker obesos

Barretti

Carmo

Rosa

et al. 2011

Rev. bras. educ. fís. esporte

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A obesidade é uma patologia diretamente relacionada com o desenvolvimento de doenças cardiovasculares. Por outro lado, o treinamento físico aeróbio atenua o desenvolvimento da obesidade e promove benefícios cardíacos em obesos. Dessa forma, nosso objetivo foi investigar se a obesidade altera a função cardíaca e se sua associação com o treinamento físico aeróbio promove melhora na função cardíaca em ratos Zucker obesos. Os ratos Zucker foram divididos da seguinte forma: grupo magro (GM), grupo obeso (GO), grupo magro treinado (GMTR) e grupo obeso treinado (GOTR). O protocolo de treinamento aeróbio de natação foi realizado por um período de 10 semanas com cinco sessões semanais de 60 minutos de duração. A frequência cardíaca de repouso, a pressão arterial sistólica, a hipertrofia e função cardíaca foram avaliadas no final do período de treinamento físico. Ambos os grupos treinados apresentaram uma queda de 12% da frequência cardíaca de repouso, quando comparado com seus respectivos controles. Ainda, nossos resultados demonstraram que o treinamento aeróbio reduziu o aumento da massa cardíaca em 13% e melhorou a função diastólica na obesidade em 43%. Em conclusão, nossos dados demonstraram que o treinamento físico aeróbio reverteu os prejuízos cardíacos causados pela obesidade.

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Angiotensin‐Converting Enzyme Inhibition Reduces Lipid Deposits in Myocardium and Improves Left Ventricular Function of Obese Zucker Rats

Abstract: TOBLLI, JORGE EDUARDO,

Cited by 10 publications

References 63 publications

Effects of Aerobic Exercise Training on Cardiac Renin-Angiotensin System in an Obese Zucker Rat Strain

Effects of Aerobic Exercise Training on Cardiac Renin-Angiotensin System in an Obese Zucker Rat Strain

Effects of the AT1 receptor blocker losartan and the calcium channel blocker benidipine on the accumulation of lipids in the kidney of a rat model of metabolic syndrome

Treinamento físico aeróbio previne à hipertrofia cardíaca patológica e melhora a função diastólica em ratos Zucker obesos

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