Reduced high-energy phosphate levels in rat hearts. I. Effects of alloxan diabetes

Tb, Allison; Bruttig, SP; Mf, Crass; Rs, Eliot; Shipp, J C

doi:10.1152/ajplegacy.1976.230.6.1744

Cited by 49 publications

(21 citation statements)

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“…[32][33][34] The mechanisms by which IP inhibits reperfusion arrhythmias may involve the reduction of Ca 2+ overload due to the inhibition of production of [H + ] and lactate [35][36][37] and the opening of sarcolemmal and/or mitochondrial K ATP channels. [38][39][40][41][42][43][44] However, the details of the mechanisms have not been clarified. In control rats, the incidence and the duration of RVT in CIP(+) were significantly lower than in CIP(-)(P < 0.05).…”

Section: Discussionmentioning

confidence: 99%

The Insulin Sensitizer Pioglitazone Improves the Deterioration of Ischemic Preconditioning in Type 2 Diabetes Mellitus Rats

et al. 2007

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SUMMARYWe investigated the effects of ischemic preconditioning (IP) on reperfusion arrhythmias in type 2 diabetic rats as well as the effects of the insulin sensitizer pioglitazone. Thirty-week-old OLETF rats with or without pioglitazone (10 mg/kgBW, orally) were used as a model for type 2 diabetes. LETO rats served as controls. The incidences and durations of reperfusion ventricular tachyarrhythmias (RVT) were evaluated using a working heart method. After 5 minutes of initial perfusion, the rats were divided into the following groups: 1) control rats without IP (CIP(-)), 2) control rats with IP (CIP(+)), 3) diabetic rats without IP (DIP(-)), 4) diabetic rats with IP (DIP(+)), 5) pioglitazone-treated diabetic rats without IP (TDIP(-)), and 6) pioglitazone-treated diabetic rats with IP (TDIP(+)). Three 2-minute cycles of global diastolic ischemia and 5 minutes of reperfusion before long ischemia were performed as IP. The incidence and duration of RVT in CIP(+) were significantly lower than in CIP(-). There was no significant difference in the duration of RVT between DIP(+) and DIP(-). However, the duration of RVT in TDIP(+) was significantly shorter than TDIP(-). These results suggested that the effects of IP on reperfusion arrhythmias are deteriorated in type 2 diabetic rats. The insulin sensitizer pioglitazone can improve the deterioration of IP against reperfusion arrhythmias in type 2 diabetic rats. (Int Heart J 2007; 48: 623-635)

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Section: Discussionmentioning

confidence: 99%

The Insulin Sensitizer Pioglitazone Improves the Deterioration of Ischemic Preconditioning in Type 2 Diabetes Mellitus Rats

et al. 2007

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“…In metabolic abnormalities related to insulin deficiency, glucose oxidation is suppressed by the lowered activities of enzymes in glycolysis, resulting in a decrease in Pyr production and the sequential reduction of ATP. [21][22][23][24] In addition, it has also been suggested that alterations in contractile proteins and abnormalities in calcium transients induce myocardial dysfunction in diabetes mellitus. 22) To prepare the experimental animals reflecting diabetes mellitus, it is established that STZ provides a permanent diabetes equivalent to clinically type I diabetes mellitus, which causes β-cell necrosis selectively in the pancreas.…”

Section: Discussionmentioning

confidence: 99%

“…[21][22][23][24] The lack of insulin is known to inhibit enzymes involved in glycolysis in type I diabetes mellitus, 23) in addition to elevating the level of intracellular glucose following hyperglycemia. 28) However, the oral administration of vanadate significantly increased the myocardial contents of Pyr and Lac over the baseline values obtained from group C and inhibited decreases in ATP, P-Cr, and cytosolic phosphorylation potential in diabetic rat hearts.…”

Section: Discussionmentioning

confidence: 99%

Vanadate Improves Cardiac Function and Myocardial Energy Metabolism in Diabetic Rat Hearts

et al. 2003

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SUMMARYVanadium mimicking the metabolic effects of insulin is known to decrease serum glucose levels and to influence glucose metabolism in diabetes mellitus. However, it is unclear whether vanadium ameliorates the metabolic disorder in diabetic hearts causing myocardial dysfunction. The purpose of this study was to assess the effects of vanadium on cardiac performance and energy metabolism in diabetic rat hearts. Four groups of Wistar rats were studied: untreated control rats (group C, n = 8), vanadate-treated rats (group V, n = 10), untreated diabetic rats (group DM, n = 9) induced by streptozotocin, and vanadate-treated diabetic rats (group DMV, n = 8). Vanadate-treated rats drank a 1.5 mM sodium orthovanadate (Na 3 VO 4 ) solution during a 4 week diabetic condition. Hearts were perfused with Krebs-Henseleit buffer after the diabetic duration. After the maximum left ventricular dP/dt and cardiac efficiency were calculated, the myocardial contents of ATP and creatine phosphate (P-Cr) and myocardial energy metabolism were assessed by cytosolic phosphorylation potential. Peak positive and negative dP/dt, and cardiac efficiency decreased significantly in group DM compared with group C, while there were no significant differences between groups C and DMV. The myocardial contents of ATP (µmol/g wet heart) and P-Cr (µmol/g wet heart), and cytosolic phosphorylation potential (M -1 ) increased from 2.72 ± 0.46, 1.45 ± 0.58, and 3,530 ± 1,220 in group DM to 3.88 ± 0.76, 3.81 ± 1.36, and 11,200 ± 2,400 in group DMV, respectively. It is concluded that vanadium restored the production of high energy phosphates in the myocardium and improved myocardial dysfunction by regulating metabolic processes in diabetic rat hearts. (Jpn Heart J 2003; 44: 745-757)

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“…50,16 An involvement of the uncoupling proteins has been hypothesized in the uncoupling effect of heart muscle mitochondria by high NEFA concentrations, 17,18 that could decrease the ATP formation and the heart work efficiency in the diabetic rat. 51 More recently, however, the putative uncoupling effect of these proteins has been questioned. In fact UCP homologs were found to be upregulated in several different metabolic conditions characterized by increased NEFA availability, such as lipid infusion, food deprivation and streptozotocin-induced diabetes.…”

Section: Nefa and Gene Expression In Rat Heartmentioning

confidence: 99%

“…19 UCP3 is predominantly expressed in skeletal muscles and only slightly detectable in rat heart muscle. 20 -22 In the diabetic rat heart, in spite of a reported increased NEFA oxidation, the intracellular concentration of ATP was reported to be low, 23 resulting from an uncoupling of oxidative phosphorylation that has been hypothesized to be linked to an increased gene expression of UCP3. 24 The aim of the present study was therefore to investigate the effects of an increased availability of NEFA on heart insulin-dependent glucose metabolism and on GLUT4 mRNA.…”

Section: Introductionmentioning

confidence: 99%

Changes in FAT/CD36, UCP2, UCP3 and GLUT4 gene expression during lipid infusion in rat skeletal and heart muscle

et al. 2002

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OBJECTIVE: It has been reported that an increased availability of free fatty acids (NEFA) not only interferes with glucose utilization in insulin-dependent tissues, but may also result in an uncoupling effect of heart metabolism. We aimed therefore to investigate the effect of an increased availability of NEFA on gene expression of proteins involved in transmembrane fatty acid (FAT=CD36) and glucose (GLUT4) transport and of the uncoupling proteins UCP2 and 3 at the heart and skeletal muscle level. STUDY DESIGN: Euglycemic hyperinsulinemic clamp was performed after 24 h Intralipid 1 plus heparin or saline infusion in lean Zucker rats. Skeletal and heart muscle glucose utilization was calculated by 2-deoxy-[1-3 H]-D-glucose technique. Quantification of FAT=CD36, GLUT4, UCP2 and UCP3 mRNAs was obtained by Northern blot analysis or RT-PCR. RESULTS: In Intralipid 1 plus heparin infused animals a significant decrease in insulin-mediated glucose uptake was observed both in the heart (22.62 AE 2.04 vs 10.37 AE 2.33 ng=mg=min; P < 0.01) and in soleus muscle (13.46 AE 1.53 vs 6.84 AE 2.58 ng=mg=min; P < 0.05). FAT=CD36 mRNA was significantly increased in skeletal muscle tissue ( þ 117.4 AE 16.3%, P < 0.05), while no differences were found at the heart level in respect to saline infused rats. A clear decrease of GLUT4 mRNA was observed in both tissues. The 24 h infusion of fat emulsion resulted in a clear enhancement of UCP2 and UCP3 mRNA levels in the heart (99.5 AE 15.3 and 80 AE 4%) and in the skeletal muscle (291.5 AE 24.7 and 146.9 AE 12.7%). CONCLUSIONS: As a result of the increased availability of NEFA, FAT=CD36 gene expression increases in skeletal muscle, but not at the heart level. The augmented lipid fuel supply is responsible for the depression of insulin-mediated glucose transport and for the increase of UCP2 and 3 gene expression in both skeletal and heart muscle.

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Reduced high-energy phosphate levels in rat hearts. I. Effects of alloxan diabetes

Cited by 49 publications

References 0 publications

The Insulin Sensitizer Pioglitazone Improves the Deterioration of Ischemic Preconditioning in Type 2 Diabetes Mellitus Rats

The Insulin Sensitizer Pioglitazone Improves the Deterioration of Ischemic Preconditioning in Type 2 Diabetes Mellitus Rats

Vanadate Improves Cardiac Function and Myocardial Energy Metabolism in Diabetic Rat Hearts

Changes in FAT/CD36, UCP2, UCP3 and GLUT4 gene expression during lipid infusion in rat skeletal and heart muscle

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