scholarly journals Oxytocin Increases Glucose Uptake in Neonatal Rat Cardiomyocytes

Endocrinology ◽  
2010 ◽  
Vol 151 (2) ◽  
pp. 482-491 ◽  
Author(s):  
Maria Florian ◽  
Marek Jankowski ◽  
Jolanta Gutkowska
Keyword(s):  
Glucose Uptake ◽  
Glucose Transporter ◽  
Primary Cultures ◽  
Metabolic Stress ◽  
Neonatal Rat ◽  
Stem Cell Marker ◽  
Rat Cardiomyocytes ◽  
Myocardial Glucose Uptake ◽  
Neonatal Rat Cardiomyocytes ◽  
Basal Glucose Uptake

We have recently shown that an entire oxytocin (OT) system, a peptide and its cognate receptors, is synthesized in the heart. In fetal and newborn hearts, OT exists in its extended three-amino acid form, OT-Gly-Lys-Arg (OT-GKR). OT translocates glucose transporter type 4 to the plasma membrane in human endothelial cells. Therefore, we hypothesized that the cardiac OT/OT-GKR system may be involved in the regulation of myocardial glucose uptake in physiological conditions and during metabolic stress such as hypoxia. Primary cultures of neonatal rat cardiomyocytes (CM) and cardiac progenitor cells expressing ATP-binding cassette efflux transporter G2 transporter (stem cell marker) were studied. OT (10 nm) increased basal glucose uptake in CM to 4.0 ± 0.2 fmol/mg protein, with OT-GKR (10 nm) elevating it to 5.3 ± 0.4 fmol/mg protein (P < 0.001) in comparison with 2.2 fmol/mg in control cells. OT had a moderate synergistic effect with 0.1 mm 2,4-dinitrophenol, augmenting basal glucose uptake to 5.5 ± 0.5 fmol/mg. OT-GKR (10 nm) was even more potent in combination with 2,4-dinitrophenol, increasing glucose uptake to 9.0 ± 1.0 fmol/mg. Wortmannin (0.1 μm), an inhibitor of phosphatidylinositol-3-kinase, significantly suppressed the effect of OT and insulin (10 nm) (P < 0.001), indicating common pathways. Our data suggest that OT and OT-GKR influence glucose uptake in neonatal rat CM and may thus play a role in the maintenance of cardiac function and cell survival during metabolic stress.

Active uptake of hydrophilic copper complex Cu(ii)–TETA in primary cultures of neonatal rat cardiomyocytes

Metallomics ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 565-575 ◽  
Author(s):  
Chunyan Fu ◽  
Junhong Lizhao ◽  
Zhenghui Luo ◽  
Tao Wang ◽  
Craig A. Grapperhaus ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Copper Complex ◽  
Primary Cultures ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Active Uptake ◽  
Neonatal Rat Cardiomyocytes ◽  
Independent Process

Cu(ii)–TETA is transported across the cell membrane via an unknown ATP-dependent and CTR1-independent process.

scholarly journals Curcumin Protects Neonatal Rat Cardiomyocytes against High Glucose-Induced Apoptosis via PI3K/Akt Signalling Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Wei Yu ◽  
Wenliang Zha ◽  
Zhiqiang Ke ◽  
Qing Min ◽  
Cairong Li ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
High Glucose ◽  
Primary Cultures ◽  
Signalling Pathway ◽  
Neonatal Rat ◽  
Curcumin Treatment ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Enhanced Expression ◽  
Induced Apoptosis

The function of curcumin on NADPH oxidase-related ROS production and cardiac apoptosis, together with the modulation of protein signalling pathways, was investigated in cardiomyocytes. Primary cultures of neonatal rat cardiomyocytes were exposed to 30 mmol/L high glucose with or without curcumin. Cell viability, apoptosis, superoxide formation, the expression of NADPH oxidase subunits, and potential regulatory molecules, Akt and GSK-3β, were assessed in cardiomyocytes. Cardiomyocytes exposure to high glucose led to an increase in both cell apoptosis and intracellular ROS levels, which were strongly prevented by curcumin treatment (10 μM). In addition, treatment with curcumin remarkably suppressed the increased activity of Rac1, as well as the enhanced expression ofgp91phoxandp47phoxinduced by high glucose. Lipid peroxidation and SOD were reversed in the presence of curcumin. Furthermore, curcumin treatment markedly inhibited the reduced Bcl-2/Bax ratio elicited by high glucose exposure. Moreover, curcumin significantly increased Akt and GSK-3βphosphorylation in cardiomyocytes treated with high glucose. In addition, LY294002 blocked the effects of curcumin on cardiomyocytes exposure to high glucose. In conclusion, these results demonstrated that curcumin attenuated high glucose-induced cardiomyocyte apoptosis by inhibiting NADPH-mediated oxidative stress and this protective effect is most likely mediated by PI3K/Akt-related signalling pathway.

Chemical Hypoxia-induced Glucose Transporter-4 Translocation in Neonatal Rat Cardiomyocytes

2008 ◽  
Vol 39 (1) ◽  
pp. 52-60 ◽  
Author(s):  
Fu Guan ◽  
Bo Yu ◽  
Guo-xian Qi ◽  
Jian Hu ◽  
Ding-yin Zeng ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Neonatal Rat ◽  
Glucose Transporter 4 ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Chemical Hypoxia

scholarly journals Anti-hypoxic effect of ginsenoside Rbl on neonatal rat cardiomyocytes is mediated through the specific activation of glucose transporter-4 ex vivo

2009 ◽  
Vol 30 (4) ◽  
pp. 396-403 ◽  
Author(s):  
Hong-liang Kong ◽  
Jian-ping Wang ◽  
Zhan-quan Li ◽  
Shu-mei Zhao ◽  
Jing Dong ◽  
...  
Keyword(s):  
Glucose Transporter ◽  
Ex Vivo ◽  
Neonatal Rat ◽  
Glucose Transporter 4 ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Endothelin-stimulated glucose uptake: effects of intracellular Ca2+, cAMP and glucosamine

2002 ◽  
Vol 103 (s2002) ◽  
pp. 418S-423S ◽  
Author(s):  
Jinshyun R. WU-WONG ◽  
Cathleen E. BERG ◽  
Brian D. DAYTON
Keyword(s):  
Glucose Uptake ◽  
Biosynthetic Pathway ◽  
Neonatal Rat ◽  
Intracellular Camp ◽  
Acetoxymethyl Ester ◽  
Hexosamine Biosynthetic Pathway ◽  
Rat Cardiomyocytes ◽  
Amino Acid Peptide ◽  
Neonatal Rat Cardiomyocytes ◽  
Camp Levels

Endothelin-1 (ET-1) is a 21-amino-acid peptide that binds to G-protein-coupled receptors to evoke biological responses. Previously we have shown that ET-1 stimulates glucose uptake in 3T3-L1 adipocytes and neonatal rat cardiomyocytes, but the mechanism is not completely understood. ET-1 is known to modulate intracellular Ca2+ and cAMP levels. Depletion of intracellular Ca2+ by treating 3T3-L1 adipocytes with EDTA and 1,2-bis(2-amino-5-methylphenoxy)ethane-N,N,N´,N´-tetra-acetic acid tetra-acetoxymethyl ester (MAPTAM) did not have a significant effect on ET-1-induced glucose uptake. Forskolin, a potent stimulator which stimulates adenylate cyclase and increases the intracellular cAMP level, partially inhibited insulin-stimulated glucose uptake in 3T3-L1 cells, but had no significant impact on the effect of ET-1. Forskolin also did not show an effect on the tyrosine phosphorylation of a 75kDa protein induced by ET-1. Glucosamine treatment causes insulin resistance in cells, possibly by entering the hexosamine biosynthetic pathway. In neonatal rat cardiomyocytes, glucosamine treatment blocked both insulin and ET-1-stimulated glucose uptake and also eliminated the translocation of IRAP, an aminopeptidase in GLUT4-containing vesicles, from the cytoplasm to the plasma membrane. These results suggest that ET-1-induced glucose uptake is independent of its effects on modulating intracellular Ca2+ and cAMP levels, but is likely linked to the hexosamine biosynthetic pathway.

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