Glucose for the Heart

Depré, Christophe; Vanoverschelde, J.-L.; Taegtmeyer, Heinrich

doi:10.1161/01.cir.99.4.578

Cited by 377 publications

(284 citation statements)

References 185 publications

(171 reference statements)

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“…Consistent with this notion, heart function under ischemic condition is greater when the heart is oxidizing glucose than fatty acids (Stanley et al 2005). Furthermore, there is a crossregulatory mechanism between glucose/lactate oxidation and fatty acid oxidation, where glucose/lactate oxidation inhibits fatty acid oxidation and vice versa (Depre et al 1999). Therefore, stimulation of glucose oxidation may be beneficial under ischemic conditions, and the cardioprotective effects of glucose-insulin-potassium (GIK) therapy or fatty acid oxidation inhibitors shown in clinical trials support this notion (Wolff et al 2002).…”

Section: Regulation Of Camentioning

confidence: 74%

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

Shiojima¹,

Walsh²

2006

Genes Dev.

322

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: Regulation Of Camentioning

confidence: 74%

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

Shiojima¹,

Walsh²

2006

Genes Dev.

322

260

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“…[41][42][43]. Evidence exists to suggest that this is an adaptive response that protects the heart from further damage (e.g., ref.…”

Section: Discussionmentioning

confidence: 99%

Transverse aortic constriction leads to accelerated heart failure in mice lacking PPAR-γ coactivator 1α

Arany

Новиков

Chin

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

342

297

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Heart failure is accompanied by important defects in metabolism. The transcriptional coactivator peroxisome proliferator-activated receptor-␥ coactivator 1␣ (PGC-1␣) is a powerful regulator of mitochondrial biology and metabolism. PGC-1␣ and numerous genes regulated by PGC-1␣ are repressed in models of cardiac stress, such as that generated by transverse aortic constriction (TAC). This finding has suggested that PGC-1␣ repression may contribute to the maladaptive response of the heart to chronic hemodynamic loads. We show here that TAC in mice genetically engineered to lack PGC-1␣ leads to accelerated cardiac dysfunction, which is accompanied by signs of significant clinical heart failure. Treating cardiac cells in tissue culture with the catecholamine epinephrine leads to repression of PGC-1␣ and many of its target genes, recapitulating the findings in vivo in response to TAC. Importantly, introduction of ectopic PGC-1␣ can reverse the repression of most of these genes by epinephrine. Together, these data indicate that endogenous PGC-1␣ serves a cardioprotective function and suggest that repression of PGC-1␣ significantly contributes to the development of heart failure. Moreover, the data suggest that elevating PGC-1␣ activity may have therapeutic potential in the treatment of heart failure.cardiac metabolism ͉ mitochondria ͉ transcription

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“…These metabolic alterations may impair the energetic and functional adaptation of the heart to ischemia or hemodynamic overload (36,37). In addition, insulin has putative direct cell survival effects during AMI and other critical illness (38).…”

Section: Mechanism Of Stress Hyperglycemiamentioning

confidence: 99%

Fasting Glucose in Acute Myocardial Infarction

et al. 2007

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OBJECTIVE -Elevation of blood glucose is a common metabolic disorder among patients with acute myocardial infarction (AMI) and is associated with adverse prognosis. However, few data are available concerning the long-term prognostic value of elevated fasting glucose during the acute phase of infarction.RESEARCH DESIGN AND METHODS -We prospectively studied the relationship between fasting glucose and long-term mortality in patients with AMI. Fasting glucose was determined after an Ն8 h fast within 24 h of admission. The median duration of follow-up was 24 months (range 6 -48). All multivariable Cox models were adjusted for the Global Registry of Acute Coronary Events (GRACE) risk score.RESULTS -In nondiabetic patients (n ϭ 1,101), compared with patients with normal fasting glucose (Ͻ100 mg/dl), the adjusted hazard ratio for mortality progressively increased with higher tertiles of elevated fasting glucose (first tertile 1.5 [95% CI 0.8 -2.9], P ϭ 0.19; second tertile 3.2 [1.9 -5.5], P Ͻ 0.0001; third tertile 5.7 [3.5-9.3], P Ͻ 0.0001). The c statistic of the model containing the GRACE risk score increased when fasting glucose data were added (0.8 Ϯ 0.02-0.85 Ϯ 0.02, P ϭ 0.004). Fasting glucose remained an independent predictor of mortality after further adjustment for ejection fraction. Elevated fasting glucose did not predict mortality in patients with diabetes (n ϭ 462).CONCLUSIONS -Fasting glucose is a simple robust tool for predicting long-term mortality in nondiabetic patients with AMI. Fasting glucose provides incremental prognostic information when added to the GRACE risk score and left ventricular ejection fraction. Fasting glucose is not a useful prognostic marker in patients with diabetes. Diabetes Care 30:960 -966, 2007R ecent studies have emphasized the prognostic value of high blood glucose levels in patients with acute myocardial infarction (AMI) (1-6). Previous investigations focused on the relationship between random blood glucose on admission and outcome. We have previously shown that elevated fasting glucose concentrations are superior to admission glucose levels in predicting 30-day mortality in patients with AMI (7). However, few data on the relationship between fasting glucose and long-term outcome are available.Knowledge of mortality predictors in AMI can be used to generate predictive models that can aid clinicians' decisions making, in particular in identifying patients who are at high or low risk of death (8). Such risk assessment methods have been developed for acute coronary syndromes (9 -11). Whether glucose levels can be used to improve the predictive ability of such risk models is not known.Heart failure has been shown to promote insulin resistance and glucose intolerance (12,13), raising the possibility that the association between stress hyperglycemia and adverse outcome is partly mediated through the acute reduction in left ventricular systolic performance. However, the relationship between infarct size or left ventricular dysfunction and the degree of stress hyperglycemia remains...

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Glucose for the Heart

Cited by 377 publications

References 185 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

Transverse aortic constriction leads to accelerated heart failure in mice lacking PPAR-γ coactivator 1α

Fasting Glucose in Acute Myocardial Infarction

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