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ischemia/obesidad

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Effect of chronic CPT-1 inhibition on myocardial ischemia-reperfusion injury (I/R) in a model of diet-induced obesity.

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OBJECTIVE By increasing circulating free fatty acids and the rate of fatty acid oxidation, obesity decreases glucose oxidation and myocardial tolerance to ischemia. Partial inhibition of fatty acid oxidation may improve myocardial tolerance to ischemia/reperfusion (I/R) in obesity. We assessed the

Ischemia-related changes of fat-mass and obesity-associated protein expression in the gerbil hippocampus.

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Fat-mass and obesity-associated protein (Fto) plays important roles in energy metabolism. It also acts as a demethylase and is most abundantly found in the brain. In the present study, we examined the spatial and temporal changes of Fto immunoreactivity after five minutes of transient forebrain

The obesity paradox in the stress echo lab: fat is better for hearts with ischemia or coronary microvascular dysfunction

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Background: Obesity is an independent risk factor for coronary artery disease (CAD), but once CAD has developed it has been associated with improved survival ("obesity paradox"). Aim:

Impaired myocardial MIF/AMPK activation aggravates myocardial ischemia reperfusion injury in high-fat diet-induced obesity.

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Backgound: Obese patients are more sensitive to myocardial ischemia, which has been linked with high mortality rates. The following study investigates the effects of impaired macrophage migration inhibitory factor (MIF)/AMP-activated protein kinase (AMPK) activation on increased

Differential PI3K signal transduction in obesity-associated cardiac hypertrophy and response to ischemia.

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OBJECTIVE Elevated insulin and inflammatory cytokine levels in obesity may chronically activate signaling pathways regulating cardiac growth and contractility. Our aim was to examine the effect of obesity on cardiac PI3K isoform and Akt activation during left ventricular (LV) hypertrophy and heart

Obesity induced-insulin resistance causes endothelial dysfunction without reducing the vascular response to hindlimb ischemia.

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Impairment of vascular growth is a hallmark of diabetic complications, but the progression and mechanisms are poorly understood. To determine whether obesity and early diabetes impair endothelium-dependent vasodilatation and vascular response to ischemia, microvascular function as well as angiogenic

Developmental programming resulting from maternal obesity in mice: effects on myocardial ischaemia-reperfusion injury.

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A comprehensive number of epidemiological and animal studies suggest that prenatal and early life events are important determinants for disorders later in life. Among them, prenatal stress (i.e. stress experienced by the pregnant mother with impact on the fetal ontogeny) has clear programming

Evaluation of ischaemia in obese patients: feasibility and accuracy of a low-dose protocol with a cadmium-zinc telluride camera.

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OBJECTIVE Obesity is a significant and independent risk factor for cardiovascular disease, and assessing ischaemia in obese patients is clinically important but sometimes difficult because of imaging artefacts. The aim of this study was to evaluate the feasibility and diagnostic accuracy of
We studied the effect of combined antimicrobial therapy with amoxicillin, metronidazole, and clarithromycin on the severity of ischemia/reperfusion myocardial injury in Wistar rats with alimentary obesity and acute inflammation of the large intestine. General ischemia/reperfusion was reproduced on

Myocutaneous revascularization following graded ischemia in lean and obese mice.

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BACKGROUND Murine models of diabetes and obesity have provided insight into the pathogenesis of impaired epithelialization of excisional skin wounds. However, knowledge of postischemic myocutaneous revascularization in these models is limited. METHODS A myocutaneous flap was created on the dorsum of

Discordant signaling and autophagy response to fasting in hearts of obese mice: Implications for ischemia tolerance.

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Autophagy is regulated by nutrient and energy status and plays an adaptive role during nutrient deprivation and ischemic stress. Metabolic syndrome (MetS) is a hypernutritive state characterized by obesity, dyslipidemia, elevated fasting blood glucose levels, and insulin resistance. It has also been

Assessment of Myocardial Ischemia in Obese Individuals Undergoing Physical Stress Echocardiography (PSE).

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BACKGROUND Physical stress echocardiography is an established methodology for diagnosis and risk stratification of coronary artery disease in patients with physical capacity. In obese (body mass index ≥ 30 kg/m2) the usefulness of pharmacological stress echocardiography has been demonstrated;

Systemic administration of ghrelin did not restore angiogenesis in hindlimb ischemia in control and diet-induced obese mice.

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BACKGROUND Ghrelin is a novel growth hormone releasing peptide that mainly regulates food intake and energy homeostasis, however, recently, it is indicated that it may be closely related with physiological and/or pathological angiogenesis. OBJECTIVE The objective of the present study was to evaluate
Peripheral artery disease (PAD) is defined as peripheral blood flow impairment, especially in the legs, caused by atherosclerotic stenosis. The disease decreases quality of life because of intermittent claudication or necrosis of the leg. The hindlimb ischemia model, in which ischemia is induced by
BACKGROUND Obesity and the metabolic syndrome frequently coexist. Both are associated with cardiovascular disease (CVD). However, the contribution of obesity to cardiovascular risk, independent of the presence of the metabolic syndrome, remains controversial. RESULTS From the WISE study, 780 women
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