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Made available in DSpace on 2021-06-25T10:46:23Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-01-01 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) The aim of this study is to evaluate whether the alterations in glucose metabolism and insulin resistance are mechanisms presented in cardiac remodelling induced by the toxicity of cigarette smoke. Male Wistar rats were assigned to the control group (C; n = 12) and the cigarette smoke-exposed group (exposed to cigarette smoke over 2 months) (CS; n = 12). Transthoracic echocardiography, blood pressure assessment, serum biochemical analyses for catecholamines and cotinine, energy metabolism enzymes activities assay; HOMA index (homeostatic model assessment); immunohistochemistry; and Western blot for proteins involved in energy metabolism were performed. The CS group presented concentric hypertrophy, systolic and diastolic dysfunction, and higher oxidative stress. It was observed changes in energy metabolism, characterized by a higher HOMA index, lower concentration of GLUT4 (glucose transporter 4) and lower 3-hydroxyl-CoA dehydrogenase activity, suggesting the presence of insulin resistance. Yet, the cardiac glycogen was depleted, phosphofructokinase (PFK) and lactate dehydrogenase (LDH) increased, with normal pyruvate dehydrogenase (PDH) activity. The activity of citrate synthase, mitochondrial complexes and ATP synthase (adenosine triphosphate synthase) decreased and the expression of Sirtuin 1 (SIRT1) increased. In conclusion, exposure to cigarette smoke induces cardiac remodelling and dysfunction. The mitochondrial dysfunction and heart damage induced by cigarette smoke exposure are associated with insulin resistance and glucose metabolism changes. Department of Internal Medicine Botucatu Medical School São Paulo State University-UNESP Faculty of Nutrition UFG – Univ Federal de Goiás Department of Chemical and Biological Sciences São Paulo State University-UNESP Department of Pathology and Legal Medicine Ribeirão Preto Medical School University of São Paulo Experimental Research Unit – UNIPEX Botucatu Medical School São Paulo State University-UNESP Department of Internal Medicine Botucatu Medical School São Paulo State University-UNESP Department of Chemical and Biological Sciences São Paulo State University-UNESP Experimental Research Unit – UNIPEX Botucatu Medical School São Paulo State University-UNESP CAPES: 001 FAPESP: 2014/24197-0 FAPESP: 2016/14547-0 FAPESP: 2016/25676-5

Made available in DSpace on 2020-12-12T02:08:48Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-07-01 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) The objective of this study was to evaluate Spondias mombin L. (SM) pulp and its influence on cardiac remodelling after myocardial infarction (MI). Male Wistar rats were assigned to four groups: a sham group (animals underwent simulated surgery) that received standard chow (S; n = 20), an infarcted group that received standard chow (MI; n = 24), an infarcted group supplemented with 100 mg of SM/kg bodyweight/d, (MIS100; n = 23) and an infarcted group supplemented with 250 mg of SM/kg bodyweight/d (MIS250; n = 22). After 3 months of treatment, morphological, functional and biochemical analyses were performed. MI induced structural and functional changes in the left ventricle with worsening systolic and diastolic function, and SM supplementation at different doses did not influence these variables as analysed by echocardiography and an isolated heart study (P >.05). However, SM supplementation attenuated cardiac remodelling after MI, reducing fibrosis (P =.047) and hypertrophy (P =.006). Biomarkers of oxidative stress, inflammatory processes and energy metabolism were further investigated in the myocardial tissue. SM supplementation improved the efficiency of energy metabolism and decreased lipid hydroperoxide in the myocardium [group S (n = 8): 267.26 ± 20.7; group MI (n = 8): 330.14 ± 47.3; group MIS100 (n = 8): 313.8 ± 46.2; group MIS250: 294.3 ± 38.0 nmol/mg tissue; P =.032], as well as decreased the activation of the inflammatory pathway after MI. In conclusion, SM supplementation attenuated cardiac remodelling processes after MI. We also found that energy metabolism, oxidative stress and inflammation are associated with this effect. In addition, SM supplementation at the highest dose is more effective. Internal Medicine Department Botucatu Medical School São Paulo State University (UNESP) School of Nutrition Sciences Faculty of Health Sciences University of Ottawa Chemistry and Biochemistry Department Institute of Biosciences São Paulo State University (UNESP) Internal Medicine Department Botucatu Medical School São Paulo State University (UNESP) Chemistry and Biochemistry Department Institute of Biosciences São Paulo State University (UNESP) FAPESP: 2014/23215-5 FAPESP: 2015/18502-8 FAPESP: 2018/03082-1

Made available in DSpace on 2013-08-12T18:57:41Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-07-01 Made available in DSpace on 2013-09-30T18:17:05Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-07-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:33:23Z No. of bitstreams: 0 Made available in DSpace on 2014-05-20T13:33:23Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-07-01 Heart failure is a frequent complication of myocardial infarction. Several factors, such as recurrent myocardial ischemia, infarct size, ventricular remodeling, stunned myocardium, mechanical complications, and hibernating myocardium influence the appearance of left ventricular systolic dysfunction after myocardial infarction. Importantly, its presence increases the risk of death by at least 3- to 4-fold. The knowledge of the mechanisms and clinical features are essential for the diagnosis and treatment of left ventricular dysfunction and heart failure after myocardial infarction. Therefore, this review will focus on the clinical implications and treatment of heart failure after myocardial infarction. UNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, Brazil UNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, Brazil

Heart failure is characterized by a decreased exercise capacity due to the early appearance of symptoms like dyspnoea and muscle fatigability. Although these symptoms can be caused by reduced cardiac output, there is no clear association between exercise intolerance and hemodynamic parameters (Mancini et al. 1992; Harrington et al. 2001). It has been suggested that intrinsic skeletal muscle abnormalities play a role in decreased exercise capacity and heart failure symptoms (Vescovo et al. 1998). Muscle wasting is common in chronic illnesses such as those associated with HIV infection, some types of cancer, and heart failure (Mancini et al. 1992; Gonzalez-Cadavid et al. 1998; Bruera & Sweeney 2000). The mechanisms responsible for muscle atrophy in heart failure are not clear. Myostatin, a recently identified member of the transforming growth factor beta (TGF-β) superfamily of secreted growth and differentiation factors, regulates muscle growth, acting as a negative regulator of skeletal muscle mass (McPherron et al. 1997; Lee 2004). Several studies have shown a negative correlation between myostatin expression and muscle mass. Mutations of myostatin gene in cattle are associated with muscle hypertrophy (McPherron & Lee 1997). Similarly, myostatin-null mice present increased muscle mass, resulting from both muscle fibre hyperplasia and hyperthrophy (McPherron et al. 1997). Pharmacological treatment with a myostatin antibody increased skeletal muscle mass and grip strength (Whittemore et al. 2003). Furthermore, systemic overexpression of myostatin in adult mice was found to induce profound muscle and fat loss (Zimmers et al. 2002). In a clinical setting, recent investigations have suggested that myostatin may be involved in the muscle mass reduction observed in AIDS and cancer patients (Gonzalez-Cadavid et al. 1998; Acharyya & Gutttridge 2007). In HIV-infected men, increased levels of myostatin immunoreactive material in serum and skeletal muscle appear to correlate with the presence of cachexia (Gonzalez-Cadavid et al. 1998). In heart failure, the role of myostatin on skeletal muscle wasting remains unclear. Recently, Lenk et al. (2009) reported that myostatin was up-regulated in cardiac and skeletal muscle during experimental heart failure. The aim of this study was to evaluate myostatin mRNA and protein expression and skeletal muscle trophism in rats with myocardial infarction-induced heart failure. As myostatin expression can be modulated by follistatin, an antagonistic protein, we also evaluated follistatin expression.

To investigate the role of MMP-2 and MMP-9 in cardiac remodelling induced by tobacco smoke exposure in rats.Rats were allocated into two groups: C (n=9): control animals; ETS (n=9): exposed to tobacco smoke. After 4months, the animals underwent echocardiography, morphometric study and determination of MMP-2 and MMP-9 activity.ETS rats had larger diastolic (C=15.6 +/-1.2 mm/kg, ETS=18.0+/-0.9 mm/kg; p0.001) and systolic (C=7.3+/-1.2 mm/kg, ETS=9.2+/-0.9 mm/kg; p=0.001) ventricular diameters adjusted for body weight. Fractional shortening (C=53+/-4.8%, ETS=48+/- 3.3%; p=0.031) and ejection fraction (C=0.89+/-0.03, ETS=0.86+/-0.02; p=0.030) were smaller in the ETS group. Myocyte cross-sectional area (C=245+/-8 microm2, ETS=253+/-8 microm2; p=0.028) was higher in ETS rats. There were no differences in MMP-2 (C=50+/-14%; ETS=43+/-11%, p=0.228) or MMP-9 (C=0.36+/-0.3%; ETS=0.62+/-0.3%, p=0.630) activity between the groups.MMP-2 and MMP-9 did not participate in the remodelling process induced by tobacco smoke exposure.

Therefore The aim of this study is to investigate the cardiac glucose metabolism pathways in cardiac remodeling induced by TS . Methods 20 animals were allocated into 2 groups: group of animals exp...

Aim: To analyze the influence of rosemary (R) consumption on cardiac remodeling after myocardial infarction (MI). Material: Male Wistar rats were allocated into: 1) Sham group fed standard chow (SA...

Due to its antioxidant properties, tomato (Lycopersicon esculentum) and one of its primary constituents, lycopene have been evaluated in clinical and experimental studies. Our objective was to evaluate the influence of tomato and lycopene supplementation on the cardiac remodeling after acute myocardial infarction. Wistar rats were assigned to 6 groups: SHAM group, in which animals were submitted to simulated surgery (SHAM group; n=15); SHAM group that received lycopene 1mg/kg of body weight/day in the chow (SHAM-L group, n=9); SHAM group that received tomato in the chow (SHAM-T group, n=10); myocardial infarction (MI) group, in which animals were submitted to coronary artery ligation (MI group, n=16); MI group that received lycopene 1mg/kg of body weight/day in the chow (MI-L group, n=12); and MI group that received tomato in the chow (MI-T group, n=15). The amount of tomato supplemented had the same quantity of lycopene that was given for the groups supplemented only with this carotenoid. The rats were o...

Chronic inflammation presented in rheumatoid arthritis (RA) is associated with systemic manifestations, that include micronutrient deficiency, changes in body composition and cardiac morphofunctional alterations. The aim of this study is to evaluate the association of serum vitramin D and body composition with cardiac geometric pattern in patients with RA. Methods: 30 patients with RA were submitted to clinical, nutritional and biochemical evaluation. Bioimpedance analysis and dual-energy X-ray absorptiometry (DEXA) was performed to evaluate body composition. Transthoracic dopller- echocardiography was performed to evaluate left ventricle mass and relative wall thickness (RWT) in order to find cardiac geometry patterns. Patients were divided in Normal or abnormal pattern (concentric remodeling or concentric hypertrophy.) Results: The mean age was 53±9 years; 70% were woman, 43% presented with hypertension. All patients have been treated with methotrexate and a biological agent and presented with Disease a...

Echocardiogram period Sh-Sed Sh-Ex MI-Sed MI-Ex Diastolic Area (cm2) 0.55 ± 0.07 0.55 ± 0.10 1.06 ± 0.16* 0.96 ± 0.23# Systolic Area (cm2) 0.16 ± 0.04 0.16 ± 0.03 0.82 ± 0.15* 0.68 ± 0.18#† Δ Area (%) 70.1 ± 6.35 70.0 ± 5.69 22.8 ± 7.86* 29.7 ± 5.51#† LVDD (mm) 8.73 ± 0.66 9,17 ± 0,34 11,79 ± 1,03* 11,26 ± 1,20# LVDD/BW (mm/Kg) 16.8 ± 1.24 18.3 ± 1.43 22.2 ± 2.35* 22.5 ± 2.29# LA (mm) 6.41 ± 0.55 6.13 ± 0.53 8.58 ± 1.41* 8.15 ± 1,09# LA/BW (mm/Kg) 12.4 ± 1.72 12.2 ± 0.94 16.2 ± 2.98* 16.2 ± 1.85# PWSV (mm/s) 38.3 ± 3.07 36.4 ± 3.16 20.1 ± 5.33* 21.6 ± 4.91#