Postprandial Myocardial Perfusion in Healthy Subjects and in Type 2 Diabetic Patients

Scognamiglio, R; Negut, Christian; Kreutzenberg, Saula Vigili de; Tiengo, Antonio; Avogaro, Angelo

doi:10.1161/circulationaha.104.495127

Cited by 139 publications

(44 citation statements)

References 44 publications

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“…These observations suggest coupling between the metabolic and coronary vascular actions of INS metabolic signaling in the heart. These beneficial cardiac effects of INS metabolic signaling are decreased in states of INS resistance [37,38,39,40,41,42,43,44]. We have observed ANG II-induced inhibition of NO production can be reversed by inhibition of mTOR/S6K1 in endothelial cells.…”

Section: Effects Of Overnutrition and Raas (Mtor/s6k1)-mediated Inmentioning

confidence: 83%

“…2). INS metabolic signaling increases coronary vessel NO production which, in turn, contributes to the beneficial effects of INS on glucose uptake, coronary blood flow, and diastolic relaxation [36,37,38,39,40,41]. These observations suggest coupling between the metabolic and coronary vascular actions of INS metabolic signaling in the heart.…”

Section: Effects Of Overnutrition and Raas (Mtor/s6k1)-mediated Inmentioning

confidence: 99%

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The Impact of Overnutrition on Insulin Metabolic Signaling in the Heart and the Kidney

Pulakat¹,

DeMarco²,

Whaley‐Connell³

et al. 2011

Cardiorenal Med

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Overnutrition characterized by overconsumption of food rich in fat and carbohydrates is a significant contributor to hypertension, type 2 diabetes, and the cardiorenal syndrome. Overnutrition activates the renin-angiotensin-aldosterone system (RAAS) and causes chronic exposure of cardiovascular and renal tissue to increased circulating nutrients, insulin (INS), and angiotensin II (ANG II). Emerging evidence suggests that overnutrition, aldosterone, and ANG II promote INS resistance, a chronic condition that underlies these co-morbidities, through activation of the mammalian target of the rapamycin (mTOR)/S6 kinase 1 (S6K1) signaling pathway in cardiovascular tissue and the kidney. However, a novel ANG II type 2 receptor (AT₂R)-mediated cross talk between the RAAS and mTOR pathways ameliorates overnutrition-induced activation of mTOR/S6K1 signaling in cardiovascular tissue of rats, mice, and humans and confers cardioprotection.

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Section: Effects Of Overnutrition and Raas (Mtor/s6k1)-mediated Inmentioning

confidence: 83%

Section: Effects Of Overnutrition and Raas (Mtor/s6k1)-mediated Inmentioning

confidence: 99%

The Impact of Overnutrition on Insulin Metabolic Signaling in the Heart and the Kidney

Pulakat¹,

DeMarco²,

Whaley‐Connell³

et al. 2011

Cardiorenal Med

View full text Add to dashboard Cite

show abstract

“…This implies that even low-level activation of the microvascular endothelium could have a large net effect in vivo [18]. Of note in the context of this hypothesis, it has been postulated that defects in post-prandial myocardial microvascular perfusion, assessed using myocardial contrast echocardiography, might be an early indicator of coronary artery disease in patients with type 2 diabetes [30]. …”

Section: Shared Mechanisms Of Vascular Damage Affecting Small and Larmentioning

confidence: 99%

Vascular Disease in the Metabolic Syndrome: Do We Need to Target the Microcirculation to Treat Large Vessel Disease?

Krentz

Clough

Byrne³

2009

J Vasc Res

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The metabolic syndrome of vascular risk is threatening large numbers of ever-younger people. To date, the syndrome has been chiefly viewed as a potential risk marker that confers a heightened probability of developing type 2 diabetes and occlusive atherothrombotic disease of large- and medium-sized arteries. Accumulating evidence suggests that the components of the metabolic syndrome may also adversely affect the microvasculature through several inter-related mechanisms. These include the following observations: classic risk factors for macrovascular disease such as high blood pressure and dyslipidaemia also accelerate microvascular complications of diabetes, lesser disturbances of glucose metabolism (i.e. impaired glucose tolerance) may be associated with some forms of microvascular dysfunction, non-glucose intermediary metabolites may promote renovascular hypertension thereby damaging the microvasculature, and insulin resistance appears to be directly associated with microvascular dysfunction. In turn, microvascular complications such as nephropathy and autonomic neuropathy may promote the development and progression of atherosclerosis. We argue that the vascular implications of the metabolic syndrome should be broadened to include the microvasculature. The hypothesis that vascular events can be prevented, or at least deferred, through earlier therapeutic intervention in pre-diabetic subjects with glucose intolerance is amenable to testing in clinical trials.

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“…These overweight-/obesity-related comorbidities appear to be driven, in part, by decreases in insulin metabolic signaling in cardiac and renal tissue (fig. 1) [12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50]. In addition to insulin resistance, several other mechanisms, such as enhanced activation of the renin-angiotensin-aldosterone system (RAAS), inflammation and oxidative stress, may help explain the linkage between overnutrition and heart and kidney disease.…”

Section: Introductionmentioning

confidence: 99%

Overnutrition and the Cardiorenal Syndrome: Use of a Rodent Model to Examine Mechanisms

Whaley‐Connell

Pulakat²,

DeMarco

et al. 2011

Cardiorenal Med

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Obesity has reached epidemic proportions with far-reaching health care and economic implications. Overnutrition, characterized by excess intake of carbohydrates and fats, has been associated with end-organ damage in several tissues, including the heart and the kidney. Furthermore, overnutrition is one of the most important modifiable and preventable causes of morbidity and mortality associated with cardiovascular and kidney diseases. Insulin resistance and compensatory hyperinsulinemia as well as associated mechanisms, including enhanced renin-angiotensin-aldosterone system activity, inflammation, and oxidative stress, have been implicated in obesity-related cardiorenal injury. In this review, the effect of overnutrition on heart and kidney disease is assessed in a rodent model of overnutrition and obesity, the Zucker obese rat.

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Postprandial Myocardial Perfusion in Healthy Subjects and in Type 2 Diabetic Patients

Cited by 139 publications

References 44 publications

The Impact of Overnutrition on Insulin Metabolic Signaling in the Heart and the Kidney

The Impact of Overnutrition on Insulin Metabolic Signaling in the Heart and the Kidney

Vascular Disease in the Metabolic Syndrome: Do We Need to Target the Microcirculation to Treat Large Vessel Disease?

Overnutrition and the Cardiorenal Syndrome: Use of a Rodent Model to Examine Mechanisms

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