Cardiac remodeling in a rat model of diet-induced obesity

Abstract

The mechanisms by which diet-induced obesity cause remodeling and cardiac dysfunction are still unknown. Interstitial collagen and myocardial ultrastructure are important in the development of left ventricular hypertrophy, and are essential to the adaptive and maladaptive changes associated with obesity. Thus, the accumulation of collagen and ultrastructural damage may contribute to cardiac dysfunction in obesity. The purpose of the present study was to investigate cardiac function in a rat model of diet-induced obesity and to test the hypothesis that cardiac dysfunction induced by obesity is related to myocardial collagen deposition and ultrastructural damage. Thirty-day-old male Wistar rats were fed standard (control [C]) and hypercaloric diets (obese [Ob]) for 15 weeks. Cardiac function was evaluated by echocardiogram and isolated left ventricle papillary muscle. Cardiac morphology was assessed by histology and electron microscopy. Compared with C rats, Ob rats had increased body fat, systolic blood pressure and area under the curve for glucose, leptin and insulin plasma concentrations. Echocardiographic indexes indicated that Ob rats had increased left ventricular mass, increased systolic stress and depressed systolic function. Analysis of the isolated papillary muscle was consistent with higher myocardial stiffness in Ob compared with C rats. The Ob rats had an increase in myocardial collagen and marked ultrastructural changes compared with C rats. Obesity promotes pathological cardiac remodeling with systolic dysfunction and an increase in myocardial stiffness, which, in turn, is probably related to afterload elevation and cardiac fibrosis. Obesity also causes damage to myocardial ultrastructure, but its effect on myocardial function needs to be further clarified.

Therapeutic Impact of Berries (Morus Alba and Morus Rubra) Fruit Extract in the Regression of High-Fat Diet-Induced Cardiac Dysfunction in Rats

“…The mechanisms underlying the accumulation of collagen in animals remain unknown; Leopoldo et al [30] proposed that the higher levels of collagen are associated with anomaly in insulin metabolism. Insulin growth factor induces transforming growth factor beta-1, which directly stimulates collagen expression.…”

Relationship of Left Ventricular Mass with BMI and Insulin Resistance in Normotensive Obese Women

“…Left ventricular filling is abnormal, peak atrial velocity is higher, and late diastolic flow rate is longer in the obese subjects. Left ventricular diastolic dysfunction and increased LVM may be related to collagen accumulation due to a volume overload in the left ventricle, myocyte hypertrophy, and interstitial fibrosis (16,17). Altered FGF23 levels may also contribute to cardiac remodeling (18).…”

Influência do tempo de exposição à obesidade sobre a função cardíaca de ratos

“…Como a obesidade pode acarretar remodelação cardíaca, (51)(52)(53)54,58,60) o coração foi analisado por meio de estudos estruturais e funcionais. A estrutura foi avaliada in vivo por meio do ecocardiograma e post mortem por análises macroscópicas e microscópicas.…”

“…(183) No entanto, segundo Okoshi, A análise da hipertrofia cardíaca também foi analisada pela mensuração da área seccional transversa do miócito (AST), corados com hematoxilina-eosina (HE). (121) Embora, a coloração com HE seja freqüentemente utilizada em diversos trabalhos experimentais, (51,53,60,121) em nosso estudo as lâminas de VE não apresentaram qualidade suficiente para leitura. A técnica de reticulina de Gomori foi utilizada, pela primeira vez, como alternativa para a mensuração da AST dos fragmentos do VE, embora a literatura não utilize esta técnica para a medida da AST.…”

“…(199) De acordo com inúmeros estudos, a angiotensina II também seria um dos agentes responsáveis pela fibrose intersticial secundária à obesidade, pois ativa o TGF-β. (97,119,199,200) (51,60,201) O estudo da função diastólica do VE é muito importante, tendo em vista que as alterações no enchimento desta cavidade podem anteceder a disfunção sistólica. (202) Neste estudo, a obesidade após 15 e 45 semanas não acarretou alterações nos índices que avaliam a diástole.…”