scholarly journals Compartmentation of hexokinase in rat heart. A critical factor for tracer kinetic analysis of myocardial glucose metabolism.

1992 ◽  
Vol 90 (5) ◽  
pp. 1972-1977 ◽  
Author(s):  
R R Russell ◽  
J M Mrus ◽  
J I Mommessin ◽  
H Taegtmeyer
Keyword(s):  
Glucose Metabolism ◽  
Kinetic Analysis ◽  
Rat Heart ◽  
Critical Factor ◽  
Myocardial Glucose Metabolism ◽  
Tracer Kinetic

scholarly journals PET Measurements of Myocardial Glucose Metabolism with 1-11C-Glucose and Kinetic Modeling

2007 ◽  
Vol 48 (6) ◽  
pp. 955-964 ◽  
Author(s):  
P. Herrero ◽  
Z. Kisrieva-Ware ◽  
C. S. Dence ◽  
B. Patterson ◽  
A. R. Coggan ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Kinetic Modeling ◽  
Myocardial Glucose Metabolism

Abstract 1766: Diet-Induced Obesity Causes Inflammation by Activating Toll-Like Receptor 4 Signaling and Downregulates AMPK in Heart

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hwi Jin Ko ◽  
Dae Young Jung ◽  
Zhexi Ma ◽  
Jason K Kim
Keyword(s):  
Glucose Metabolism ◽  
Whole Body ◽  
Chow Diet ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Myocardial Glucose Metabolism ◽  
Cardiac Inflammation ◽  
Protein Levels ◽  
Diet Induced Obesity

Increasing evidence implicates the role of inflammation in diabetes and complications. Macrophages are shown to infiltrate adipose tissue in obesity, and inflammatory cytokines alter glucose metabolism in peripheral organs. Male C57BL/6 mice were fed high-fat diet (HFD; 55% fat by calories) or chow diet for 6 weeks, and heart samples were taken for analysis (n = 5~7). Chronic HFD increased whole body fat mass, measured by 1 H-MRS, by 3-fold, and elevated plasma IL-6 and TNF-α levels by 40%. Diet-induced obesity caused inflammation in heart and increased macrophage-specific CD68 levels by 5-fold (Fig. 1) (* P < 0.05 vs Chow). Diet-induced cardiac inflammation was associated with significant increases in toll-like receptor 4 (TLR4) and MyD88 levels in heart (Fig. 2). HFD also increased cardiomyocyte SOCS3 levels by more than 3-fold (Fig. 3). Myocardial glucose metabolism was measured using intravenous injection of 2-[ 14 C]deoxyglucose in awake mice (n = 6). Chronic HFD reduced myocardial glucose uptake by 50%, and this was associated with significant reductions in total GLUT4 and GLUT1 protein levels. Further, Thr 172 phosphorylation of AMPK, a critical regulator of energy balance, was markedly reduced in heart following HFD (Fig. 4). These results demonstrate that diet-induced obesity causes macrophage infiltration and inflammation in heart by increasing TLR4 signaling in cardiomyocytes. Similar to the effects of inflammation on peripheral glucose metabolism, diet-induced cardiac inflammation reduced myocardial glucose metabolism by downregulating AMPK and GLUT protein levels. Thus, our findings underscore an important role of inflammation in diabetic heart.

Temporal analysis of myocardial glucose metabolism by 2-[18F]fluoro-2-deoxy-D-glucose

1990 ◽  
Vol 259 (4) ◽  
pp. H1022-H1031 ◽  
Author(s):  
V. T. Nguyen ◽  
K. A. Mossberg ◽  
T. J. Tewson ◽  
W. H. Wong ◽  
R. W. Rowe ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Work Load ◽  
Temporal Analysis ◽  
Input Function ◽  
Graphical Analysis ◽  
Time Activity ◽  
Myocardial Glucose Metabolism ◽  
Fractional Rate ◽  
Endogenous Insulin

To assess kinetic changes of myocardial glucose metabolism after physiological interventions, we perfused isolated working rat hearts with glucose and 2-[18F]fluoro-2-deoxy-D-glucose (2-FDG). Tissue uptake of 2-FDG and the input function were measured on-line by external detection. The fractional rate of 2-FDG phosphorylation was determined by graphical analysis of time-activity curves. The steady-state uptake of 2-FDG was linear with time, and the tracer was retained predominantly in its phosphorylated form. Tissue accumulation of 2-FDG decreased with a reduction in work load and with the addition of competing substrates. Insulin caused a significant increase in 2-FDG accumulation in hearts from fasted but not from fed animals. We conclude that in the isolated working rat heart there is rapid adjustment of exogenous substrate utilization and that most interventions known to alter glucose metabolism induce parallel changes in 2-FDG uptake. Qualitative differences in the in vitro response to insulin may be affected by the presence of either endogenous insulin or glycogen.

scholarly journals The Endocannabinoid System Affects Myocardial Glucose Metabolism in the DOCA-Salt Model of Hypertension

2018 ◽  
Vol 46 (2) ◽  
pp. 727-739 ◽  
Author(s):  
Agnieszka Polak ◽  
Ewa Harasim-Symbor ◽  
Barbara Malinowska ◽  
Irena Kasacka ◽  
Alicja Lewandowska ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Glucose Metabolism ◽  
Antihypertensive Drugs ◽  
Fatty Acid Amide Hydrolase ◽  
Acid Amide ◽  
Colorimetric Method ◽  
Hypertensive Rats ◽  
Myocardial Glucose Metabolism ◽  
Amide Hydrolase ◽  
Fatty Acid Amide

Background/Aims: Recent interest in the use of cannabinoids as therapeutic agents has revealed the involvement of the endogenous cannabinoid system (ECS) in the regulation of the cardiovascular system in hypertension. Abnormalities in glucose metabolism and insulin action are commonly detected in hypertensive animals. Thus, potential antihypertensive drugs should be investigated with respect to modulation of glucose homeostasis. Therefore, the aim of the present study was to evaluate the effects of the ECS activation after chronic fatty acid amide hydrolase inhibitor (URB597) administration on plasma glucose and insulin concentrations as well as parameters of myocardial glucose metabolism in the deoxycorticosterone acetate (DOCA)-salt hypertensive rats, an animal model of secondary hypertension. Methods: Hypertension was induced by DOCA (25mg/kg) injections and addition of 1% NaCl in the drinking water for six weeks. Chronic activation of the ECS was performed by URB597 (1mg/kg) injections for two weeks. We examined fasting plasma levels of insulin (ELISA), glucose and intramyocardial glycogen (colorimetric method). Expressions of glucose transporters (GLUT1, 4) and selected proteins engaged in GLUT translocation as well as glucose metabolism were determined using Western blotting. Results: Hypertension induced hypoinsulinemia with concomitant lack of significant changes in glycemia, reduced intramyocardial glycogen content and increased pyruvate dehydrogenase (PDH) expression in the cardiac muscle. Importantly, chronic URB597 administration in the hypertensive rats increased insulin concentration, elevated plasmalemmal GLUT1 and GLUT4 expression and concomitantly improved myocardial glycogen storage. Conclusion: Chronic administration of fatty acid amide hydrolase (FAAH) inhibitor has potential protective properties on myocardial glucose metabolism in hypertension.

Abstract 1209: Interleukin-6 Reduces Myocardial Glucose Metabolism by Altering AMPK, Insulin Signaling, and PKC-𝛉 in Mice

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Zhiyou Zhang ◽  
Hwi Jin Ko ◽  
Dae Young Jung ◽  
Zhexi Ma ◽  
Jason K Kim
Keyword(s):  
Glucose Metabolism ◽  
Insulin Signaling ◽  
Insulin Action ◽  
Cardiac Metabolism ◽  
Negative Regulator ◽  
Saline Control ◽  
Myocardial Glucose Metabolism ◽  
Peripheral Organs

Increasing evidence implicates the role of inflammation in the pathogenesis of diabetes and complications. Inflammatory cytokines (IL-6, TNF-α) are elevated in obese diabetic subjects, and are shown to modulate glucose metabolism in peripheral organs. In this report, we examined the effects of IL-6 on cardiac metabolism and insulin action in vivo. Male C57BL/6 mice were intravenously treated with IL-6 (16 ng/hr) or saline (control) for 2 hrs, and [ 14 C]2-deoxyglucose was intravenously injected in awake mice to measure myocardial glucose metabolism (n=9~10). Hyperinsulinemic-euglycemic clamps (2.5 mU/kg/min insulin infusion) were also performed in IL-6 or saline-treated mice (n=4~5) to measure cardiac insulin action. Acute treatment with IL-6 caused a 25% increase in myocardial STAT3 activity and significantly reduced basal myocardial glucose metabolism (Fig. 1 ; * P< 0.05). IL-6 treatment also reduced insulin-stimulated glucose uptake in heart, and these effects were associated with marked decreases in AMPK activity (Thr-phosphorylation of AMPK; Fig. 2 ) and IRS-1 tyrosine phosphorylation (Fig. 3 ). Acute IL-6 treatment increased myocardial expression of PKC-𝛉, which has been shown to mediate insulin resistance in peripheral organs (Fig. 4 ). These results indicate that IL-6 is a potent negative regulator of myocardial glucose metabolism and insulin action, and the underlying mechanism may involve IL-6 mediated activation of PKC-𝛉 and defects in AMPK and insulin signaling activity. Thus, our findings suggest a potential role of IL-6 in the pathogenesis of diabetic heart failure.

Tumour aggressiveness determined by kinetic analysis of glucose metabolism in meningiomas

1995 ◽  
pp. 177-179
Author(s):  
H. Shioya ◽  
K. Mineura ◽  
T. Sasajima ◽  
M. Kowada ◽  
H. Iida ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Kinetic Analysis

Malonate and fluoride effects on metabolism and contraction of electrically stimulated heart strips

1961 ◽  
Vol 200 (4) ◽  
pp. 727-731 ◽  
Author(s):  
Leslie I. Rice ◽  
David A. Berman
Keyword(s):  
Oxygen Consumption ◽  
Glucose Metabolism ◽  
Rat Heart ◽  
Contractile Activity ◽  
Simultaneous Recording ◽  
Force Of Contraction ◽  
Enzyme Systems ◽  
Pyruvate Oxidation ◽  
Oxidation Of Glucose ◽  
Stimulation Of

The effect of malonate and fluoride on the oxidation of C14-labeled substrates by electrically stimulated rat heart strips was investigated in an apparatus which permitted simultaneous recording of oxygen consumption and contractile activity. Malonate stimulated the force of contraction when glucose was the substrate, but not in the presence of pyruvate. Malonate had no significant effect on the rate of oxidation of glucose-1-C14, glucose-6-C14 or pyruvate-2-C14, indicating that its effect on contraction was not related to a) stimulation of glucose metabolism, b) inhibition of the Kreb's cycle, or c) stimulation of the phosphogluconate pathway. Malonate-2-C14 was oxidized by the ventricle strips, and the possibility exists that utilization of malonate as a substrate may account, at least in part, for its stimulation of contraction. The stimulation of contraction by fluoride was accompanied by significant alterations in metabolism. The oxidation of glucose and acetate was inhibited, whereas pyruvate oxidation was stimulated; these findings were interpreted in terms of known actions of fluoride on enzyme systems.

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