Comparison of left ventricular mass and function in obese versus nonobese women &lt;40 years of age

Crisostomo, Lucı́ola Lopes; Araújo, Leila Maria Batista; Câmara, Edmundo José Nassri; Carvalho, Carlos Roberto; Silva, Fabrı́cio Afra; Vieira, Milene; Rabelo, Álvaro

doi:10.1016/s0002-9149(99)00519-6

Cited by 29 publications

(29 citation statements)

References 19 publications

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“…Heart weight is tightly coupled with body weight from infants to adults, and heart size is also extremely sensitive to nutritional status: Heart size is reduced in starved subjects or in patients with anorexia nervosa (Keys et al 1950;de Simone et al 1994), and increased in obese subjects without hypertension or other cardiovascular and/ or metabolic abnormalities (Crisostomo et al 1999). Consistently, cardiac Akt activity in mice is up-regulated during rapid postnatal growth, and down-regulated by overnight fasting .…”

Section: Insulin/igfmentioning

confidence: 96%

Regulation of cardiac growth and coronary angiogenesis by the Akt/PKB signaling pathway

Shiojima¹,

Walsh²

2006

Genes Dev.

323

260

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Postnatal growth of the heart is primarily achieved through hypertrophy of individual myocytes. Cardiac growth observed in athletes represents adaptive or physiological hypertrophy, whereas cardiac growth observed in patients with hypertension or valvular heart diseases is called maladaptive or pathological hypertrophy. These two types of hypertrophy are morphologically, functionally, and molecularly distinct from each other. The serine/threonine protein kinase Akt is activated by various extracellular stimuli in a phosphatidylinositol-3 kinasedependent manner and regulates multiple aspects of cellular functions including survival, growth and metabolism. In this review we will discuss the role of the Akt signaling pathway in the heart, focusing on the regulation of cardiac growth, contractile function, and coronary angiogenesis. How this signaling pathway contributes to the development of physiological/pathological hypertrophy and heart failure will also be discussed.Growth of the heart during embryonic development occurs primarily through proliferation of cardiac myocytes. However, cardiac myocytes withdraw from the cell cycle soon after birth, and subsequent growth of the heart during postnatal development is achieved predominantly through hypertrophy rather than hyperplasia of individual myocytes (Pasumarthi and Field 2002;Olson and Schneider 2003). In fact, there is almost a threefold increase in cardiac myocyte diameter in humans during development from infants to adults (Hudlicka and Brown 1996). Cardiac growth during normal postnatal development or the hypertrophy observed in trained athletes is referred to as "physiological," and it is characterized by normal or enhanced contractile function and normal architecture and organization of cardiac structure (Richey and Brown 1998). On the other hand, cardiac hypertrophy is also observed in patients with pathological conditions such as hypertension, myocardial infarction, and valvular heart diseases. This type of cardiac growth is called "pathological" hypertrophy, and is frequently associated with contractile dysfunction, interstitial fibrosis, and re-expression of fetal-type cardiac genes such as atrial natriuretic peptide and ␤-myosin heavy chain (Molkentin and Dorn 2001;Frey and Olson 2003). These data indicate that pathological cardiac hypertrophy is morphologically and molecularly distinct from physiological cardiac hypertrophy. The pathological form of cardiac hypertrophy is initially recognized as an adaptive response to increased external load, because increased wall stress induced by overload is attenuated by the increase in wall thickness. However, increased cardiac mass is clinically associated with increased morbidity and mortality (Levy et al. 1990), and a sustained overload eventually leads to contractile dysfunction and heart failure through poorly understood mechanisms (Molkentin and Dorn 2001;Frey and Olson 2003). In addition, hypertrophy of individual myocyte is a common feature of failing myocardium (Gerdes et al. 1992). Thus, pathological ...

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Section: Insulin/igfmentioning

confidence: 96%

Regulation of cardiac growth and coronary angiogenesis by the Akt/PKB signaling pathway

Shiojima¹,

Walsh²

2006

Genes Dev.

323

260

View full text Add to dashboard Cite

show abstract

“…Heart size is markedly reduced in patients with anorexia nervosa (7), and modest weight reduction in normotensive obese subjects is associated with reduced heart size in the absence of changes in blood pressure or other hemodynamic parameters (8). Conversely, heart size is increased in obese subjects without hypertension or other cardiovascular and/or metabolic abnormalities (9). Thus, it is likely that mechanisms exist that couple heart size to nutrient-dependent changes in body size (10).…”

mentioning

confidence: 99%

Akt Signaling Mediates Postnatal Heart Growth in Response to Insulin and Nutritional Status

Shiojima

Yefremashvili

Luo

et al. 2002

Journal of Biological Chemistry

206

182

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Akt is a serine-threonine kinase that mediates a variety of cellular responses to external stimuli. During postnatal development, Akt signaling in the heart was up-regulated when the heart was rapidly growing and was down-regulated by caloric restriction, suggesting a role of Akt in nutrient-dependent regulation of cardiac growth. Consistent with this notion, reductions in Akt, 70-kDa S6 kinase 1, and eukaryotic initiation factor 4E-binding protein 1 phosphorylation were observed in mice with cardiac-specific deletion of insulin receptor gene, which exhibit a small heart phenotype. In contrast to wild type animals, caloric restriction in these mice had little effect on Akt phosphorylation in the heart. Furthermore, forced expression of Akt1 in these hearts restored 70-kDa S6 kinase 1 and eukaryotic initiation factor 4E-binding protein 1 phosphorylation to normal levels and rescued the small heart phenotype. Collectively, these results indicate that Akt signaling mediates insulin-dependent physiological heart growth during postnatal development and suggest a mechanism by which heart size is coordinated with overall body size as the nutritional status of the organism is varied.

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“…(23)(24)(25) Embora a obesidade possa acarretar falência cardíaca, existem informações controversas, principalmente, sobre a função sistólica em humanos obesos na presença (26)(27)(28)(29)(30) ou ausência de comorbidades. (5,23,(31)(32)(33)(34)(35)(36)(37)(38)(39)(40) As pesquisas clínicas, realizadas por ecocardiograma, mostram que indivíduos obesos apresentam disfunção diastólica do ventrículo esquerdo (VE). (5,(26)(27)(28)32,(34)(35)(36)38,39) Apenas um trabalho encontrou função diastólica preservada no VE, verificando alteração no desempenho diastólico somente no ventrículo direito.…”

Section: Introductionunclassified

“…(5,23,(31)(32)(33)(34)(35)(36)(37)(38)(39)(40) As pesquisas clínicas, realizadas por ecocardiograma, mostram que indivíduos obesos apresentam disfunção diastólica do ventrículo esquerdo (VE). (5,(26)(27)(28)32,(34)(35)(36)38,39) Apenas um trabalho encontrou função diastólica preservada no VE, verificando alteração no desempenho diastólico somente no ventrículo direito. (33) Os estudos que avaliaram a performance sistólica na obesidade mostram desempenho preservado, (30,31,33,36,37) aumentado (32,34,35,38) ou diminuído; (5,27,29,39,40) a razão para esta discrepância, provavelmente, está relacionada às técnicas utilizadas para avaliar a função sistólica.…”

Section: Introductionunclassified

“…(5,(26)(27)(28)32,(34)(35)(36)38,39) Apenas um trabalho encontrou função diastólica preservada no VE, verificando alteração no desempenho diastólico somente no ventrículo direito. (33) Os estudos que avaliaram a performance sistólica na obesidade mostram desempenho preservado, (30,31,33,36,37) aumentado (32,34,35,38) ou diminuído; (5,27,29,39,40) a razão para esta discrepância, provavelmente, está relacionada às técnicas utilizadas para avaliar a função sistólica. (5) Outro fator que poderia interferir nos resultados seria a intensidade da obesidade;…”

Section: Introductionunclassified

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

Leopoldo¹

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Comparison of left ventricular mass and function in obese versus nonobese women <40 years of age

Cited by 29 publications

References 19 publications

Regulation of cardiac growth and coronary angiogenesis by the Akt/PKB signaling pathway

Regulation of cardiac growth and coronary angiogenesis by the Akt/PKB signaling pathway

Akt Signaling Mediates Postnatal Heart Growth in Response to Insulin and Nutritional Status

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

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