Perfil nutricional e cardiovascular de ratos normotensos e hipertensos sob dieta hiperlipídica

Júnior, Silvio A. Oliveira; Okoshi, Katashi; Leopoldo, André Soares; Campos, Dijon; Martinez, Paula Felippe; Okoshi, Marina Politi; Padovani, Carlos Roberto; Dal-Pai-Silva, Maeli; Cicogna, Antônio Carlos

doi:10.1590/s0066-782x2009001100014

Cited by 15 publications

(10 citation statements)

References 39 publications

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“…These results are consistent with studies on the effects of combined hypertension and DM in mice [10] and SHR [52]. It should be pointed out that, although we found no significant differences in collagen content between SHR and SHR-DM, both groups presented increased myocardial fibrosis against literature data from normotensive rats [18,53,54]. Therefore, we can conclude that additional fibrosis is not involved in diabetes-induced impaired cardiac function in SHR.…”

Section: Discussionsupporting

confidence: 92%

Diabetes mellitus activates fetal gene program and intensifies cardiac remodeling and oxidative stress in aged spontaneously hypertensive rats

Rosa

Xavier

Campos

et al. 2013

Cardiovasc Diabetol

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BackgroundThe combination of systemic arterial hypertension and diabetes mellitus (DM) induces greater cardiac remodeling than either condition alone. However, this association has been poorly addressed in senescent rats. Therefore, this study aimed to analyze the influence of streptozotocin-induced DM on ventricular remodeling and oxidative stress in aged spontaneously hypertensive rats (SHR).MethodsFifty 18 month old male SHR were divided into two groups: control (SHR, n = 25) and diabetic (SHR-DM, n = 25). DM was induced by streptozotocin (40 mg/kg, i.p.). After nine weeks, the rats underwent echocardiography and myocardial functional study in left ventricular (LV) isolated papillary muscle preparations. LV samples were obtained to measure myocyte diameters, interstitial collagen fraction, and hydroxyproline concentration. Gene expression of atrial natriuretic peptide (ANP) and α- and β-myosin heavy chain (MyHC) isoforms was evaluated by RT-PCR. Serum oxidative stress was assessed by measuring lipid hydroperoxide concentration and superoxide dismutase and glutathione peroxidase activities. Statistics: Student’s t test or Mann-Whitney test, p < 0.05.ResultsSHR-DM presented higher blood glucose (487 ± 29 vs. 89.1 ± 21.1 mg/dL) and lower body weight (277 ± 26 vs. 339 ± 38 g). Systolic blood pressure did not differ between groups. Echocardiography showed LV and left atrial dilation, LV diastolic and relative wall thickness decrease, and LV systolic and diastolic function impairment in SHR-DM. Papillary muscle study showed decreased myocardial contractility and contractile reserve in SHR-DM. Myocyte diameters and myocardial interstitial collagen fraction and hydroxyproline concentration did not differ between groups. Increased serum pro-oxidant activity and gene expression of ANP and β/α-MyHC ratio were observed in DM.ConclusionDiabetes mellitus induces cardiac dilation and functional impairment, increases oxidative stress and activates fetal gene program in aged spontaneously hypertensive rats.

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Section: Discussionsupporting

confidence: 92%

Diabetes mellitus activates fetal gene program and intensifies cardiac remodeling and oxidative stress in aged spontaneously hypertensive rats

Rosa

Xavier

Campos

et al. 2013

Cardiovasc Diabetol

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“…Within these studies, the data collectively suggest that Wistar and SD rats have distinct lipid metabolism,[20] and Wistars may develop myocardial pathology with shorter dietary interventions [70], [76]. Additional strain differences in metabolic and myocardial responses to high-fat feeding have been demonstrated [77]. Our findings provide evidence for a strain effect on feed efficiency, body weight, heart rate and serum adiponectin and the myocardial FA profile.…”

Section: Discussionsupporting

confidence: 52%

Docosahexaenoic Acid Supplementation Does Not Improve Western Diet-Induced Cardiomyopathy in Rats

et al. 2012

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Obesity increases risk for cardiomyopathy in the absence of hypertension, diabetes or ischemia. The fatty acid milieu, modulated by diet, may modify myocardial structure and function, lending partial explanation for the array of cardiomyopathic phenotypy. We sought to identify gross, cellular and ultrastructural myocardial changes associated with Western diet intake, and subsequent modification with docosahexaenoic acid (DHA) supplementation. Wistar and Sprague-Dawley (SD) rats received 1 of 3 diets: control (CON); Western (WES); Western + DHA (WES+DHA). After 12 weeks of treatment, echocardiography was performed and myocardial adiponectin, fatty acids, collagen, area occupied by lipid and myocytes, and ultrastructure were determined. Strain effects included higher serum adiponectin in Wistar rats, and differences in myocardial fatty acid composition. Diet effects were evident in that both WES and WES+DHA feeding were associated with similarly increased left ventricular (LV) diastolic cranial wall thickness (LVWcr/d) and decreased diastolic internal diameter (LVIDd), compared to CON. Unexpectedly, WES+DHA feeding was associated additionally with increased thickness of the LV cranial wall during systole (LVWcr/s) and the caudal wall during diastole (LVWca/d) compared to CON; this was observed concomitantly with increased serum and myocardial adiponectin. Diastolic dysfunction was present in WES+DHA rats compared to both WES and CON. Myocyte cross sectional area (CSA) was greater in WES compared to CON rats. In both fat-fed groups, transmission electron microscopy (TEM) revealed myofibril degeneration, disorganized mitochondrial cristae, lipid inclusions and vacuolation. In the absence of hypertension and whole body insulin resistance, WES+DHA intake was associated with more global LV thickening and with diastolic dysfunction, compared to WES feeding alone. Myocyte hypertrophy, possibly related to subcellular injury, is an early change that may contribute to gross hypertrophy. Strain differences in adipokines and myocardial fatty acid accretion may underlie heterogeneous data from rodent studies.

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“…In contrast, Carroll et al 9 , found no change in the fraction of total collagen in obese rats subjected to a high-fat diet for 12 weeks. Previous studies carried out in our laboratory showed that Wistar rats made obese by a 15-week high fat diet 10 and Wistar-Kyoto rats made obese by 20-week high fat and carbohydrate diet 11 showed increased myocardial total collagen. In these studies, however, the fractions of collagen types I and III were not evaluated.…”

Section: Introductionmentioning

confidence: 71%

Influence of Term of Exposure to High-Fat Diet-Induced Obesity on Myocardial Collagen Type I and III

Silva

Leopoldo

Campos

et al. 2013

Arquivos Brasileiros De Cardiologia

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Background Obesity is a risk factor for many medical complications; medical research has shown that hemodynamic, morphological and functional abnormalities are correlated with the duration and severity of obesity. Objective Present study determined the influence of term of exposure to high-fat diet-induced obesity on myocardial collagen type I and III. Methods Thirty-day-old male Wistar rats were randomly distributed into two groups: a control (C) group fed a standard rat chow and an obese (Ob) group alternately fed one of four palatable high-fat diets. Each diet was changed daily, and the rats were maintained on their respective diets for 15 (C15 and Ob15) and 30 (C30 and Ob30) consecutive weeks. Obesity was determined by adiposity index. Results The Ob15 group was similar to the C15 group regarding the expression of myocardial collagen type I; however, expression in the Ob30 group was less than C30 group. The time of exposure to obesity was associated with a reduction in collagen type I in Ob30 when compared with Ob15. Obesity did not affect collagen type III expression. Conclusion This study showed that the time of exposure to obesity for 30 weeks induced by unsaturated high-fat diet caused a reduction in myocardial collagen type I expression in the obese rats. However, no effect was seen on myocardial collagen type III expression.

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Perfil nutricional e cardiovascular de ratos normotensos e hipertensos sob dieta hiperlipídica

Cited by 15 publications

References 39 publications

Diabetes mellitus activates fetal gene program and intensifies cardiac remodeling and oxidative stress in aged spontaneously hypertensive rats

Diabetes mellitus activates fetal gene program and intensifies cardiac remodeling and oxidative stress in aged spontaneously hypertensive rats

Docosahexaenoic Acid Supplementation Does Not Improve Western Diet-Induced Cardiomyopathy in Rats

Influence of Term of Exposure to High-Fat Diet-Induced Obesity on Myocardial Collagen Type I and III

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