Increasing number of components of the metabolic syndrome and cardiac structural and functional abnormalities – cross-sectional study of the general population

Azevedo, Ana; Bettencourt, Paulo; Almeida, Pedro; Santos, Ana Cristina; Abreu-Lima, Cassiano; Hense, Hans‐Werner; Barros, Henrique

doi:10.1186/1471-2261-7-17

Cited by 53 publications

(65 citation statements)

References 38 publications

(25 reference statements)

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“…However, there is evidence that increasing the number of MetS components does contribute to the development of diabetes and CVD. 24,25 Thus, determining the number of components of MetS as an ordered variable is more appropriate to assess the graded association between MetS and depressive symptoms, since moving from one category to another may differ depending of number of components of MetS.…”

Section: Discussionmentioning

confidence: 99%

Components of the metabolic syndrome and depressive symptoms in community-dwelling older people: the Bambuí Cohort Aging Study

Ruas

Diniz

Firmo

et al. 2016

Rev. Bras. Psiquiatr.

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Objective: To investigate the moderating effect of an increasing number of clustered metabolic syndrome (MetS) components on the association between MetS and depressive symptoms in a population-based cohort of older adults in Brazil.Methods: This analysis used data from the Bambuí Cohort Aging Study. Participants in this cross-sectional study comprised 1,469 community-dwelling older people aged X 60 years. Analyses were performed to assess both the association between depressive symptoms and each individual MetS component and the association between depressive symptoms and clustering of an increasing number of MetS components.

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Section: Discussionmentioning

confidence: 99%

Components of the metabolic syndrome and depressive symptoms in community-dwelling older people: the Bambuí Cohort Aging Study

Ruas

Diniz

Firmo

et al. 2016

Rev. Bras. Psiquiatr.

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“…41 LV hypertrophy increases progressively as the number of metabolic syndrome risk factors increases. [40][41][42][43] Systolic and diastolic blood pressure and waist circumference are associated with LV hypertrophy. 44,45 However, stability in body weight is thought to be a preventive factor for diabetes, one of the components of metabolic syndrome.…”

Section: Rv Dysfunction In Pah and Its Importancementioning

confidence: 99%

Fatty Acid Metabolism in Pulmonary Arterial Hypertension: Role in Right Ventricular Dysfunction and Hypertrophy

Talati

Hemnes

2015

Pulm. circ.

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Pulmonary arterial hypertension (PAH) is a complex, multifactorial disease in which an increase in pulmonary vascular resistance leads to increased afterload on the right ventricle (RV), causing right heart failure and death. Our understanding of the pathophysiology of RV dysfunction in PAH is limited but is constantly improving. Increasing evidence suggests that in PAH RV dysfunction is associated with various components of metabolic syndrome, such as insulin resistance, hyperglycemia, and dyslipidemia. The relationship between RV dysfunction and fatty acid/glucose metabolites is multifaceted, and in PAH it is characterized by a shift in utilization of energy sources toward increased glucose utilization and reduced fatty acid consumption. RV dysfunction may be caused by maladaptive fatty acid metabolism resulting from an increase in fatty acid uptake by fatty acid transporter molecule CD36 and an imbalance between glucose and fatty acid oxidation in mitochondria. This leads to lipid accumulation in the form of triglycerides, diacylglycerol, and ceramides in the cytoplasm, hallmarks of lipotoxicity. Current interventions in animal models focus on improving RV dysfunction through altering fatty acid oxidation rates and limiting lipid accumulation, but more specific and effective therapies may be available in the coming years based on current research. In conclusion, a deeper understanding of the complex mechanisms of the metabolic remodeling of the RV will aid in the development of targeted treatments for RV failure in PAH.Keywords: pulmonary arterial hypertension, metabolic syndrome, fatty acid oxidation, glucose oxidation, right ventricle, fatty acid transporter (CD36), glucose transporters, insulin resistance, right ventricular lipotoxicity, lipotoxic cardiomyopathy. Pulmonary arterial hypertension (PAH) is a devastating disease characterized by progressive obliteration of the pulmonary vasculature, right heart failure, and death. The pathobiology of PAH is complex, and presently there is no curative treatment. Although PAH is classically thought to be a disease of the lungs, the role played by right ventricular (RV) hypertrophy and dysfunction that ultimately results in right heart failure and death is understudied. RV failure is the most common cause of death in PAH, 1 yet there are no specific therapies aimed at improving RV adaptation or function. However, it is well documented that pathological RV remodeling in PAH can be reversed with lung transplantation or with pulmonary thromboendarterectomy in chronic thromboembolic pulmonary hypertension (CTEPH). 2-9 The molecular mechanisms that mediate the transition from adaptive RV compensation to failure or that can promote reversible RV remodeling are presently unknown. Recently, our group and others have found evidence indicating that intracellular lipid accumulation and decreased fatty acid oxidation (FAO) may be features of RV failure related to PAH. [10][11][12][13] This raises a question: In PAH, can accumulation of fatty acids promote RV dysfun...

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“…As the number of disease components in metabolic syndrome increases in a patient, the structure and function of the heart becomes more compromised. 1) For example, metabolic syndrome increases the risk of atrial enlargement and fibrillation 2,3) and left ventricular hypertrophy and diastolic dysfunction. 1,4) These structural and functional abnormalities are considered to contribute to the increased cardiovascular morbidity and mortality associated with metabolic syndrome.…”

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confidence: 99%

Characterization of Cardiac Size and Function in SHRSP.Z-Leprfa/IzmDmcr Rats, a New Animal Model of Metabolic Syndrome

Tada

Kagota

Matsumoto

et al. 2010

Biological & Pharmaceutical Bulletin

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Lifestyle-related diseases-visceral obesity, hypertension, dyslipidemia and glucose intolerance-are known to appear in a cluster referred to as metabolic syndrome. As the number of disease components in metabolic syndrome increases in a patient, the structure and function of the heart becomes more compromised. 1) For example, metabolic syndrome increases the risk of atrial enlargement and fibrillation 2,3) and left ventricular hypertrophy and diastolic dysfunction. 1,4) These structural and functional abnormalities are considered to contribute to the increased cardiovascular morbidity and mortality associated with metabolic syndrome. However, the mechanisms underlying these abnormalities are not well understood.SHRSP.Z-Lepr fa /IzmDmcr rats (SHRSP-fatty) were established by crossing stroke-prone SHR (SHRSP/Izm) with Zucker obese rats to create a new animal model of metabolic syndrome.5) These rats develop spontaneous severe hypertension and obesity, and exhibit metabolic abnormalities (dyslipidemia, hyperinsulinemia and hyperglycemia), which are similar to those found in human metabolic syndrome. To date SHRSP-fatty have been used in studies that evaluated dysfunction of vasodilation mechanisms, cardiovascular remodeling, and atherogenic dyslipidemia in metabolic syndrome. [6][7][8] The aim of the present study was to characterize the cardiac structure and function in SHRSP-fatty. Increased cardiac stiffness induced by disturbed myocardial collagen turnover is suggested as one of the mechanisms of cardiac abnormalities in hypertension and diabetes.9,10) Therefore, as structural parameters, heart weight and a major myocardial collagen, collagen type I, as an index of fibrosis, were measured. Additionally, collagen type III, which contributes to tissue elasticity, was measured and the ratio of type I to type III was calculated as an index of myocardial stiffness. To assess cardiac function in SHRSP-fatty, heart rate, systolic blood pressure, cardiac output, blood flow and stroke volume were measured by tail-cuff and plethysmography, and compared to those in hypertensive lean SHRSP and normotensive lean WistarKyoto rats (WKY). Systolic and diastolic cardiac functions were also determined by echocardiography. The results may inform us whether this model would be a useful animal model to evaluate cardiac complications of metabolic syndrome. MATERIALS AND METHODS Experimental AnimalsMale SHRSP-fatty (nϭ18), SHRSP (nϭ18) and normotensive control WKY (nϭ18) were purchased at 16 weeks of age from Japan SLC, Inc. (Hamamatsu, Japan). The rats were established by the Disease Model Cooperative Research Association (Hamamatsu, Japan). Standard chow (CE-2; Clea Japan Inc., Tokyo, Japan) and water were available ad libitum during the experimental period. The study protocols were performed according to the Guideline for the Care and Use of Laboratory Animals approved by Mukogawa Women's University.Tail-Cuff Method and Plethysmography Systolic blood pressure and heart rate of conscious rats were meas- Cardiac structural and funct...

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Increasing number of components of the metabolic syndrome and cardiac structural and functional abnormalities – cross-sectional study of the general population

Abstract: Background: We aimed to assess whether we could identify a graded association between increasing number of components of the metabolic syndrome and cardiac structural and functional abnormalities independently of predicted risk of coronary heart disease by the Framingham risk score.

Cited by 53 publications

References 38 publications

Components of the metabolic syndrome and depressive symptoms in community-dwelling older people: the Bambuí Cohort Aging Study

Components of the metabolic syndrome and depressive symptoms in community-dwelling older people: the Bambuí Cohort Aging Study

Fatty Acid Metabolism in Pulmonary Arterial Hypertension: Role in Right Ventricular Dysfunction and Hypertrophy

Characterization of Cardiac Size and Function in SHRSP.Z-Leprfa/IzmDmcr Rats, a New Animal Model of Metabolic Syndrome

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