Dietas hipercalóricas-hiperlipídicas associadas à ingestão aquosa de frutose induzem obesidade e hipertrofia ventricular esquerda, quando administradas em ratos logo após o desmame

• Ano de defesa: 2019
• Autor(a) principal: Silva, Franciely Alves da
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Mato Grosso; Brasil; Faculdade de Nutrição (FANUT); UFMT CUC - Cuiabá; Programa de Pós-Graduação em Nutrição, Alimentos e Metabolismo
• Palavras-chave em Português: Dietas obesogênicas; Frutose; Remodelagem cardíaca; Obesidade; Ventrículo esquerdo; CNPQ::CIENCIAS DA SAUDE::NUTRICAO; Obesogenic diets; Fructose; Heart remodeling; Obesity; Left ventricl
• Link de acesso: http://ri.ufmt.br/handle/1/2838

The objective of this study was to verify if the hypercaloric-hyperlipidic diets lead to left ventricular hypertrophy in recently weaned male rats. The animals were divided into 3 groups: Group C (Control), treated with a balanced diet for growing rats with 7% lipid (D7; 3,857.5 kcal); Group OB1 treated with diet containing 45% lipids (D45; 4,707.5 Kcal) and Group OB2 treated with diet containing 60% lipids (D60; 5,270.4 kcal). Group OB1 and OB2 received 10% fructose and group C received water. All groups were treated for 70 days. The initial body mass (IBM) and final body mass (FBM), food intake (FI) and water intake (WI), adiposity index (AI), masses of white adipose tissue (WAT) retroperitoneal (RAT), perrienal (PAT), omental (OAT) and epididimal (EAT) were obtained during this period. The mass (g) of the heart (HE), left ventricle (LV) and right ventricle (RV) and the relation of these values to tibial (TB) length (mm) as a marker for cardiac hypertrophy. Commercial kits (Bioclin®) determined serum levels (mg/dL) of glucose, triacylglycerol (TAG), total cholesterol (TC), HDL-c, LDL-c and creatine kinase MB fraction (CK-MB). Commercial kits (Millipore®) determined concentrations (pg/ml) of TNF-α, IL6 and Leptin. The protein content of signaling pathways: i) Leptin-STAT3/pSTAT3; ii) amino-terminal c-jun kinases (JNK) and p38 MAPK in the LV were determined by Western blotting. Data are expressed as mean ± standard error of the mean (SEM) (One way ANOVA; p <0.05). There was an increase in WI of OB1 and OB2 animals in relation to group C, accompanied with higher final body mass, increased adiposity and masses of WATs (RAT, PAT). Only OB1 group showed differences in WAT, OAT and EAT masses when compared to group C. AI of OB1 and OB2 were similar, although increased masses of evaluated WATs were observed only in OB1. We observed hypertrophy of HE, LV and RV in OB1 and OB2 compared to C group, with increased ratio of HE/TB and LV/TB. The data shows increased ratio of RV/TB only in OB1 group, in relation to C group. TC and HDL-c were higher in OB1 compared to C group, with no difference between OB1 and OB2. Both groups had increased levels of TAG and lower LDL when compared to group C. The CK-MB was higher in OB1 and OB2 than in C group. TNF-α and IL6 levels were lower in OB1 and OB2 when compared to group C, whereas leptin increased only in OB1. In addition, there was a positive correlation between Leptin levels and LV mass in OB1 and OB2 groups. There was a reduction of protein content only in STAT3 of OB1 and OB2 in relation to C group. The introduction of hypercaloric diets (45% and 60% of fat) associated with 10% fructose introduced in recently weaned male rats produced a model similar to human obesity and with hypertrophy of left ventricle (HLV). The data also suggest that impairment in leptin signaling with reduction in STAT3 content can be associated to hyperleptinemia and HLV.