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Exogenous Glucose (exogenous + glucose)

Distribution by Scientific Domains

Life Sciences	60%
Medical Sciences	40%

Selected Abstracts

A Metabolic Mechanism for the Detrimental Effect of Exogenous Glucose During Cardiac Storage

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 8 2003
Randy P. Pulis
The purpose of this study was to clarify the metabolic events that explain why supplemental glucose is detrimental during cardiac storage. Four solutions were used to flush and store porcine hearts: St. Thomas Hospital Solution (STHS), University of Wisconsin (UW) solution, and UW + 90 mM histidine, and UW + 90 mM histidine + 11 mM glucose. Despite equivalent increases in lactate in the two histidine-buffered groups throughout 10 h of storage, glycogen utilization was evident in the group without supplemental glucose. The presence of glucose resulted in a reduction in energy production, presumably mediated by direct inhibition of glycogenolysis. Furthermore, UW + histidine was the only group to show consistent improvements in ATP and total adenylates. It was concluded that inclusion of the buffering agent, histidine, to UW solution promotes anaerobic energy production as a result, in part, of preserved high levels of the regulatory control enzyme, phosphofructokinase. [source]

Acute effect of antidiabetic 1,4-dihydropyridine compound cerebrocrast on cardiac function and glucose metabolism in the isolated, perfused normal rat heart

CELL BIOCHEMISTRY AND FUNCTION, Issue 2 2008
Janina Briede
Abstract Diabetes mellitus (DM) is an important cardiovascular risk factor and is associated with abnormalities in endothelial and vascular smooth muscle cell function, evoked by chronic hyperglycemia and hyperlipidemia. Chronic insulin deficiency or resistance is marked by decreases in the intensity of glucose transport, glucose phosphorylation, and glucose oxidation, plus decreases in ATP levels in cardiac myocytes. It is important to search for new agents that promote glucose consumption in the heart and partially inhibit extensive fatty acid beta-oxidation observed in diabetic, ischemia. When the oxygen supply for myocardium is decreased, the heart accumulates potentially toxic intermediates of fatty acid beta-oxidation, that is, long-chain acylcarnitine and long-chain acyl-CoA metabolites. Exogenous glucose and heart glycogen become an important compensatory source of energy. Therefore we studied the effect of the antidiabetic 1,4-dihydropyridine compound cerebrocrast at concentrations from 10,10,M to 10,7,M on isolated rat hearts using the method of Langendorff, on physiological parameters and energy metabolism. Cerebrocrast at concentrations from 10,10,M to 10,7,M has a negative inotropic effect on the rat heart. It inhibits L -type Ca2+channels thereby diminishing the cellular Ca2+ supply, reducing contractile activity, and oxygen consumption, that normally favors enhanced glucose uptake, metabolism, and production of high-energy phosphates (ATP content) in myocardium. Cerebrocrast decreases heart rate and left ventricular (LV) systolic pressure; at concentrations of 10,10,M and 10,9,M it evokes short-term vasodilatation of coronary arteries. Increase of ATP content in the myocytes induced by cerebrocrast has a ubiquitous role. It can preserve the integrity of the cell plasma membranes, maintain normal cellular function, and inhibit release of lactate dehydrogenase (LDH) from cells that is associated with diabetes and heart ischemia. Administration of cerebrocrast together with insulin shows that both compounds only slightly enhance glucose uptake in myocardium, but significantly normalize the rate of contraction and relaxation (,±,dp/dt). The effect of insulin on coronary flow is more pronounced by administration of insulin together with cerebrocrast at a concentration of 10,7,M. Cerebrocrast may promote a shift of glucose consumption from aerobic to anerobic conditions (through the negative inotropic properties), and may be very significant in prevention of cardiac ischemic episodes. Copyright © 2007 John Wiley & Sons, Ltd. [source]

Glucose-induced release of tumour necrosis factor-alpha from human placental and adipose tissues in gestational diabetes mellitus

DIABETIC MEDICINE, Issue 11 2001
M. T. Coughlan
Abstract Aims, The cytokine tumour necrosis factor-alpha (TNF-,) has been implicated in the pathogenesis of insulin resistance in Type 2 diabetes mellitus, but limited data are available in relation to gestational diabetes mellitus (GDM), a disease in which similar biochemical abnormalities exist. We investigated the effect of exogenous glucose on the release of TNF-, from placental and adipose (omental and subcutaneous) tissue obtained from normal pregnant women, and women with GDM. Methods, Human tissue explants were incubated for up to 24 h and TNF-, concentration in the incubation medium quantified by ELISA. The effect of normal (5 mmol/l) and high (15 and 25 mmol/l) glucose concentrations on the release of TNF-, was assessed. Results, In placental and subcutaneous adipose tissues obtained from women with GDM (n = 6), TNF-, release was significantly greater under conditions of high glucose compared with normal glucose (placenta, 25 mmol/l 5915.7 ± 2579.6 and 15 mmol/l 4547.1 ± 2039.1 vs. 5 mmol/l 1897.1 ± 545.5; subcutaneous adipose tissue, 25 mmol/l 423.5 ± 207.0 and 15 mmol/l 278.5 ± 138.7 vs. 5 mmol/l 65.3 ± 28.5 pg/mg protein; P < 0.05). In contrast, there was no stimulatory effect of high glucose on TNF-, release by tissues obtained from normal pregnant women (n = 6) (placenta, 25 mmol/l 1542.1 ± 486.2 and 15 mmol/l 4263.3 ± 2737.7 vs. 5 mmol/l 5422.4 ± 1599.0; subcutaneous adipose tissue, 25 mmol/l 189.8 ± 120.4 and 15 mmol/l 124.5 ± 32.3 vs. 5 mmol/l 217.9 ± 103.5 pg/mg protein). Conclusions, These observations suggest that tissues from patients with GDM release greater amounts of TNF-, in response to high glucose. As TNF-, has been previously implicated in the regulation of glucose and lipid metabolism, and of insulin resistance, these data are consistent with the hypothesis that TNF-, may be involved in the pathogenesis and/or progression of GDM. Diabet. Med. 18, 921,927 (2001) [source]

Advances in Campylobacter biology and implications for biotechnological applications

MICROBIAL BIOTECHNOLOGY, Issue 3 2010
Byeonghwa Jeon
Summary Campylobacter jejuni is a major foodborne pathogen of animal origin and a leading cause of bacterial gastroenteritis in humans. During the past decade, especially since the publication of the first C. jejuni genome sequence, major advances have been made in understanding the pathobiology and physiology of this organism. It is apparent that C. jejuni utilizes sophisticated mechanisms for effective colonization of the intestinal tracts in various animal species. Although Campylobacter is fragile in the environment and requires fastidious growth conditions, it exhibits great flexibility in the adaptation to various habitats including the gastrointestinal tract. This high adaptability is attributable to its genetically, metabolically and phenotypically diverse population structure and its ability to change in response to various challenges. Unlike other enteric pathogens, such as Escherichia coli and Salmonella, Campylobacter is unable to utilize exogenous glucose and mainly depends on the catabolism of amino acids as a carbon source. Campylobacter proves highly mutable in response to antibiotic treatments and possesses eukaryote-like dual protein glycosylation systems, which modify flagella and other surface proteins with specific sugar structures. In this review we will summarize the distinct biological traits of Campylobacter and discuss the potential biotechnological approaches that can be developed to control this enteric pathogen. [source]

Effects of exogenous glucose on carotenoid accumulation in tomato leaves

PHYSIOLOGIA PLANTARUM, Issue 2 2008
Anne Mortain-Bertrand
To investigate the effect of carbohydrate on carotenoid accumulation in leaves, excised plants of tomato (Lycopersicum esculentum var. cerasiformae, wva 106) were supplied with glucose through the transpiration stream for 48 h. We report here that sugar accumulation in leaves led to a decrease of carotenoid content, which was related to the reduction of Chl. The decrease in carotenoid amount correlated with a sugar-induced repression of genes encoding enzymes of the carotenoid and of the Rohmer pathways. The lower 1-deoxy- d -xylulose-5-phosphate synthase transcript level probably leads to a decreased metabolic flux through the methylerythritol pathway and subsequently to a lower amount of substrate available for plastidic isoprenoid synthesis. Differences between responses of young (sink) and mature (source) leaves to carbohydrate accumulation are discussed. [source]