fructose/뇌졸중

BACKGROUND Feeding stroke-prone spontaneously hypertensive rats (SHRSP) a diet rich in fructose results in a profound glucose intolerance not observed in the normotensive Wistar Kyoto (WKY) strain. The aim of this study was to investigate the role of the liver in the underlying mechanisms in the

Diseases, disorders, and insults of aging are frequently studied in otherwise healthy animal models despite rampant co-morbidities and exposures among the human population. Stressor exposures can increase neuroinflammation and augment the inflammatory response following a challenge. The impact of

In vitro and in vivo studies suggest that fructose-1,6-diphosphate (FDP), an intermediary glycolytic pathway metabolite, ameliorates ischemic tissue injury through increased high-energy phosphate levels and may therefore have cardioprotective properties in patients undergoing coronary artery bypass

OBJECTIVE There is increasing interest into the potentially beneficial effects of galactose for obesity and type 2 diabetes management as it is a low-glycemic sugar reported to increase satiety and fat mobilization. However, fructose is also a low-glycemic sugar but with greater blood pressure

The purpose of the study was to investigate the dynamics of glucose and fructose concentrations in the blood changes and phosphohexose isomerase activity (PHI) in serum of unfed or after intravenous glucose injection patients, with acute cerebrovascular disease in the earliest period of illness. The

We compared the short-term hemodynamic effects of intravenous fructose 1,6-diphosphate (FDP) administration in patients with coronary artery disease. Hemodynamic measurements were performed before and after administration of FDP in two groups of patients: those with impaired left ventricular (LV)

Cell death after stroke involves apoptotic, autophagocytic and necrotic mechanisms which may cause the release of cytosolic proteins to the extracellular space. Aldolase C (AldC) is the brain specific isoform of the glycolytic enzyme fructose-1,6-bisphosphate aldolase. According to its

Despite intensive evaluation of acute stroke patients, perhaps only half of the attributable stroke risk is usually identified. In addition to traditional and non-traditional vascular risk factors-including most recently homocysteine, inflammation, and alterations of coagulation-a number of

BACKGROUND We hypothesized that the addition of fructose 1, 6-diphosphate (FDP) to a hypothermic heart preservation solution could improve metabolic recovery because it has several beneficial effects. METHODS Twenty adult Sprague-Dawley rats were used to study hypothermic heart preservation. The

The safety and tolerability of a free radical scavenger with Na+ channel blocking activity (dimethyl sulfoxide (DMSO)) combined with a glycolytic intermediate and high energy substrate (fructose 1,6-disphosphate (FDP)) were assessed in a mostly elderly patient group presenting with acute and

Ischaemia-related tissue injury is the leading cause of death in developed countries. Drugs that can reduce ischaemic injury would be beneficial in treatment of myocardial infarction (MI), surgical trauma and stroke. Fructose-1,6-diphosphate (FDP) is a key intermediate in anaerobic glycolysis and is

BACKGROUND Fructose-1,6-diphosphate (FDP) has been shown to protect tissue during hypoxia under various ischemic conditions, including isolated heart perfusion. We tested the hypothesis that adding FDP to St. Thomas solution can extend hypothermic heart preservation time. METHODS Sixteen adult

Objectives: Cerebral ischemia is caused by a reduction of the blood flow in a specific area in the brain, triggering cellular cascades in the tissue that result in neuronal death. This phenomenon leads to neurological decline in patients with stroke. The extent of the injury after stroke

Hypoxic stress is linked to various cardiovascular disorders (e.g., stroke, myocardial infarction), mediated, at least in part, by a reduction in ATP synthesis. Fructose-driven glycolysis is proposed as an alternative pathway capable of sustaining ATP production even under anoxic conditions. Here,

OBJECTIVE To observe abnormal metabolic changes caused by ischemic cerebral apoplexy and the regulating action of Tongsaimai pellets on abnormal metabolism by analyzing the change of small molecules in plasma of ischemic cerebral apoplexy rat. To find the potential biomarkers, and to explore