Physical training attenuates phosphocreatine and long-chain acyl-CoA alterations in diabetic rat heart

1993 ◽  
Vol 74 (4) ◽  
pp. 1785-1790 ◽  
Author(s):  
N. Mokhtar ◽  
S. Rousseau-Migneron ◽  
G. Tancrede ◽  
A. Nadeau
Keyword(s):  
Exercise Training ◽  
Training Program ◽  
Physical Training ◽  
High Energy ◽  
Heart Tissue ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Sedentary Control ◽  
Chain Acyl ◽  
Long Chain

This study was designed to assess the effect of physical training on high-energy phosphate levels in the heart of diabetic rats. Diabetes was induced with streptozocin (50 mg/kg), and exercise training was carried out on a treadmill with a progressive 10-wk program. Plasma glucose levels at the end of the training program showed only a small improvement of the diabetic state in trained animals (21.7 +/- 1.3 vs. 24.4 +/- 0.8 mmol/l; P < 0.05). The lower heart rate observed in sedentary diabetic rats (279 +/- 6 vs. 356 +/- 5 beats/min; P < 0.001) was improved by physical training (301 +/- 8 beats/min; P < 0.05 vs. sedentary diabetics). Significantly lower phosphocreatine levels were found in sedentary diabetic rats (12.0 +/- 0.7 mumol/g dry wt) than in sedentary control rats (15.0 +/- 0.9 mumol/g dry wt; P < 0.05) but not in trained diabetic rats (13.7 +/- 0.7 mumol/g dry wt). ATP levels were not affected by diabetes but were increased by training. The increased long-chain acyl-CoA levels in sedentary diabetic rats (146 +/- 7 vs. 119 +/- 8 mumol/g dry wt in sedentary control rats; P < 0.05) were improved by training (138 +/- 6 mumol/g dry wt; P > 0.05 vs. sedentary control rats). These data indicate that the diminution in phosphocreatine levels observed in the heart tissue of chronically diabetic rats can be attenuated by an exercise training program.

Metabolic effects of treadmill exercise training on the diabetic heart

1992 ◽  
Vol 73 (1) ◽  
pp. 265-271 ◽  
Author(s):  
D. J. Paulson ◽  
R. Mathews ◽  
J. Bowman ◽  
J. Zhao
Keyword(s):  
Exercise Training ◽  
Glucose Oxidation ◽  
Glucose Utilization ◽  
Plasma Lipids ◽  
High Energy ◽  
Diabetic Rats ◽  
Metabolic Effects ◽  
Sedentary Control ◽  
Oxidation Rates

This study determined whether exercise training in rats would prevent the accumulation of lipids and depressed glucose utilization found in hearts from diabetic rats. Diabetes was induced by intravenous streptozotocin (60 mg/kg). Trained diabetic rats were run on a treadmill for 60 min, 27 m/min, 10% grade, 6 days/wk for 10 wk. Training of diabetic rats had no effect on glycemic control but decreased plasma lipids. In vivo myocardial long-chain acylcarnitine, acyl-CoA, and high-energy phosphate levels were similar in sedentary control, sedentary diabetic, and trained diabetic groups. The levels of myocardial triacylglycerol were similar in sedentary control and diabetic rats but decreased in trained diabetic rats. Hearts were perfused with buffer containing diabetic concentrations of glucose (22 mM) and palmitate (1.2 mM). D-[U-14C] glucose oxidation rates (14CO2 production) were depressed in hearts from sedentary diabetic rats relative to sedentary control rats. Hearts from trained diabetic rats exhibited increased glucose oxidation relative to those of sedentary diabetic rats, but this improvement was below that of the sedentary control rats. [9,10(-3)H]palmitate oxidation rates (3H2O production) were identical in all three groups. These findings suggest that exercise training resulted in a partial normalization of myocardial glucose utilization in diabetic rats.

Exercise training alleviates MCT1 and MCT4 reductions in heart and skeletal muscles of STZ-induced diabetic rats

2003 ◽  
Vol 94 (6) ◽  
pp. 2433-2438 ◽  
Author(s):  
Taisuke Enoki ◽  
Yuko Yoshida ◽  
Hideo Hatta ◽  
Arend Bonen
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Skeletal Muscles ◽  
Diabetic Rats ◽  
Monocarboxylate Transporter ◽  
Sedentary Control ◽  
Monocarboxylate Transporter 1

We compared the changes in monocarboxylate transporter 1 (MCT1) and 4 (MCT4) proteins in heart and skeletal muscles in sedentary control and streptozotocin (STZ)-induced diabetic rats (3 wk) and in trained (3 wk) control and STZ-induced diabetic animals. In nondiabetic animals, training increased MCT1 in the plantaris (+51%; P < 0.01) but not in the soleus (+9%) or the heart (+14%). MCT4 was increased in the plantaris (+48%; P < 0.01) but not in the soleus muscles of trained nondiabetic animals. In sedentary diabetic animals, MCT1 was reduced in the heart (−30%), and in the plantaris (−31%; P < 0.01) and soleus (−26%) muscles. MCT4 content was also reduced in sedentary diabetic animals in the plantaris (−52%; P < 0.01) and soleus (−25%) muscles. In contrast, in trained diabetic animals, MCT1 and MCT4 in heart and/or muscle were similar to those of sedentary, nondiabetic animals ( P > 0.05) but were markedly greater than in the sedentary diabetic animals [MCT1: plantaris +63%, soleus +51%, heart +51% ( P > 0.05); MCT4: plantaris +107%, soleus +17% ( P > 0.05)]. These studies have shown that 1) with STZ-induced diabetes, MCT1 and MCT4 are reduced in skeletal muscle and/or the heart and 2) exercise training alleviated these diabetes-induced reductions.

scholarly journals Diet and Exercise Training Influence Skeletal Muscle Long-Chain acyl-CoA Synthetases

2020 ◽  
Vol 52 (3) ◽  
pp. 569-576 ◽  
Author(s):  
HARRISON D. STIERWALT ◽  
SARAH E. EHRLICHER ◽  
MATTHEW M. ROBINSON ◽  
SEAN A. NEWSOM
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Diet And Exercise ◽  
Chain Acyl ◽  
Long Chain

scholarly journals Physical training reverses changes in hepatic mitochondrial diameter of Alloxan-induced diabetic rats

2018 ◽  
Vol 16 (3) ◽  
Author(s):  
Gabriel Keine Kuga ◽  
Rafael Calais Gaspar ◽  
Vitor Rosetto Muñoz ◽  
Susana Castelo Branco Ramos Nakandakari ◽  
Leonardo Breda ◽  
...  
Keyword(s):  
Body Weight ◽  
Physical Training ◽  
Hepatic Metabolism ◽  
Liver Glycogen ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Hepatic Glycogen ◽  
Sedentary Control ◽  
Exercise Protocol ◽  
Training Protocol

ABSTRACT Objective To investigate the effects of physical training on metabolic and morphological parameters of diabetic rats. Methods Wistar rats were randomized into four groups: sedentary control, trained control, sedentary diabetic and trained diabetic. Diabetes mellitus was induced by Alloxan (35mg/kg) administration for sedentary diabetic and Trained Diabetic Groups. The exercise protocol consisted of swimming with a load of 2.5% of body weight for 60 minutes per day (5 days per week) for the trained control and Trained Diabetic Groups, during 6 weeks. At the end of the experiment, the rats were sacrificed and blood was collected for determinations of serum glucose, insulin, albumin and total protein. Liver samples were extracted for measurements of glycogen, protein, DNA and mitochondrial diameter determination. Results The sedentary diabetic animals presented decreased body weight, blood insulin, and hepatic glycogen, as well as increased glycemia and mitochondrial diameter. The physical training protocol in diabetic animals was efficient to recovery body weight and liver glycogen, and to decrease the hepatic mitochondrial diameter. Conclusion Physical training ameliorated hepatic metabolism and promoted important morphologic adaptations as mitochondrial diameter in liver of the diabetic rats.

Exercise training increases sarcolemmal GLUT-4 protein and mRNA content in diabetic heart

1997 ◽  
Vol 82 (3) ◽  
pp. 828-834 ◽  
Author(s):  
Brett A. Osborn ◽  
June T. Daar ◽  
Richard A. Laddaga ◽  
Fred D. Romano ◽  
Dennis J. Paulson
Keyword(s):  
Exercise Training ◽  
Diabetic Rats ◽  
Cardiac Performance ◽  
Diabetic Heart ◽  
Sedentary Control ◽  
Protein Levels ◽  
Glut 4 ◽  
Mrna Content ◽  
Significant Depression ◽  
Glucose Transport Protein

Osborn, Brett A., June T. Daar, Richard A. Laddaga, Fred D. Romano, and Dennis J. Paulson. Exercise training increases sarcolemmal GLUT-4 protein and mRNA content in diabetic heart. J. Appl. Physiol. 82(3): 828–834, 1997.—This study determined whether dynamic exercise training of diabetic rats would increase the expression of the GLUT-4 glucose transport protein in prepared cardiac sarcolemmal membranes. Four groups were compared: sedentary control, sedentary diabetic, trained control, and trained diabetic. Diabetes was induced by intravenous streptozotocin (60 mg/kg). Trained control and diabetic rats were run on a treadmill for 60 min, 27 m/min, 10% grade, 6 days/wk for 10 wk. Sarcolemmal membranes were isolated by using differential centrifugation, and the activity of sarcolemmal K+- p-nitrophenylphosphatase ( pNPPase; an indicator of Na+-K+-adenosinetriphosphatase activity) was quantified. Hearts from the sedentary diabetic group exhibited a significant depression of sarcolemmal pNPPase activity. Exercise training did not significantly alter pNPPase activity. Sedentary diabetic rats exhibited an 84 and 58% decrease in GLUT-4 protein and mRNA, respectively, relative to control rats. In the trained diabetic animals, sarcolemmal GLUT-4 protein levels were only reduced by 50% relative to control values, whereas GLUT-4 mRNA were returned to control levels. The increase in myocardial sarcolemmal GLUT-4 may be beneficial to the diabetic heart by enhancing myocardial glucose oxidation and cardiac performance

Influence of physical training on insulin release and glucose utilization by islet cells and liver glucokinase activity in the rat

1982 ◽  
Vol 243 (6) ◽  
pp. E464-E469 ◽  
Author(s):  
W. Zawalich ◽  
S. Maturo ◽  
P. Felig
Keyword(s):  
Exercise Training ◽  
Insulin Release ◽  
Physical Training ◽  
Glucose Utilization ◽  
Islet Cells ◽  
Sedentary Control ◽  
The Face ◽  
Glucose Phosphorylation ◽  
Liver Homogenates ◽  
Perifused Islets

The effect of physical training on insulin release and glucose utilization by perifused islets and on liver glucokinase activity was examined in rats that exercised spontaneously by running (in wheel cage) up to 4-6 mi/day for 36 +/- 4 days and in sedentary controls kept in standard cages. Perifusion of islets with 4 mM glucose resulted in comparable rates of insulin release from islets obtained from trained and sedentary control rats. In contrast, when the perifusion glucose concentration was raised to 10 mM, the biphasic increase in insulin release was 40-50% lower in the trained rats as compared with untrained rats. This decrease in glucose-stimulated insulin release occurred in the face of comparable rates of glucose utilization by islets from control and trained rats. Glucose phosphorylation by liver homogenates from trained rats was reduced at all concentrations of glucose examined (0.5-100 mM). The calculated glucokinase activity was diminished by 40%, whereas hexokinase activity was decreased by 15% in the livers from trained rats. We conclude that 1) hypoinsulinemia induced by exercise training is due to decreased sensitivity of the beta-cell to the stimulant action of glucose independent of changes in islet cell utilization of glucose, and 2) exercise training results in a diminution of liver glucokinase activity that may be a consequence of the hypoinsulinemia.

Lack of effect of thyroid hormone on diabetic rat heart function and biochemistry

1984 ◽  
Vol 62 (6) ◽  
pp. 617-621 ◽  
Author(s):  
Arun G. Tahiliani ◽  
John H. McNeill
Keyword(s):  
Heart Function ◽  
Myocardial Dysfunction ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Diabetic Rat ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Chain Acyl ◽  
Uptake Activity ◽  
Streptozotocin Diabetic Rats ◽  
Developed Pressure

Cardiac functional abnormalities are frequently seen in diabetics and diabetes is also known to produce a state of mild hypothyroidism. To study the degree of involvement of diabetes-induced hypothyroidism on altered myocardial function, thyroid replacement therapy was carried out in streptozotocin-diabetic rats. Triiodothyronine (T3) treatment was initiated 3 days after the rats were made diabetic and was carried out for 6 weeks thereafter. Isolated perfused hearts from diabetic rats exhibited a depression in left ventricular developed pressure and positive and negative dP/dt at higher filling pressures as compared with controls. The depression could not be prevented by thyroid treatment. Calcium uptake activity in the cardiac sarcoplasmic reticulum (SR) was also depressed as a result of diabetes and this depression also was not prevented by thyroid treatment. Long chain acyl carnitine levels were found to be elevated in diabetic cardiac SR and could not be lowered by T3 treatment. The results indicate that the myocardial dysfunction observed in diabetic rats is due to factors other than the induced hypothyroidism.

scholarly journals Reduced Na-K pump but increased Na-K-2Cl cotransporter in aorta of streptozotocin-induced diabetic rat

2001 ◽  
Vol 280 (2) ◽  
pp. H851-H858 ◽  
Author(s):  
Luis Michea ◽  
Verónica Irribarra ◽  
I. Annelise Goecke ◽  
Elisa T. Marusic
Keyword(s):  
Skeletal Muscle ◽  
Atpase Activity ◽  
Heart Tissue ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
K Uptake ◽  
Control Value ◽  
Protein Levels ◽  
Paired Control ◽  
And Function

The activities of Na-K-ATPase and Na-K-2Cl cotransporter (NKCC1) were studied in the aorta, heart, and skeletal muscle of streptozotocin (STZ)-induced diabetic rats and control rats. In the aortic rings of STZ rats, the Na-K-ATPase-dependent 86Rb/K uptake was reduced to 60.0 ± 5.5% of the control value ( P < 0.01). However, Na-K-ATPase activity in soleus skeletal muscle fibers of STZ rats and paired control rats was similar, showing that the reduction of Na-K-ATPase activity in aortas of STZ rats is tissue specific. To functionally distinguish the contributions of ouabain-resistant (α1) and ouabain-sensitive (α2 and α3) isoforms to the Na-K-ATPase activity in aortic rings, we used either a high (10−3 M) or a low (10−5M) ouabain concentration during 86Rb/K uptake. We found that the reduction in total Na-K-ATPase activity resulted from a dramatic decrement in ouabain-sensitive mediated 86Rb/K uptake (26.0 ± 3.9% of control, P < 0.01). Western blot analysis of membrane fractions from aortas of STZ rats demonstrated a significant reduction in protein levels of α1- and α2-catalytic isoforms (α1 = 71.3 ± 9.8% of control values, P < 0.05; α2 = 44.5 ± 11.3% of control, P < 0.01). In contrast, aortic rings from the STZ rats demonstrated an increase in NKCC1 activity (172.5 ± 9.5%, P < 0.01); however, in heart tissue no difference in NKCC1 activity was seen between control and diabetic animals. Transport studies of endothelium-denuded or intact aortic rings demonstrated that the endothelium stimulates both Na-K-ATPase and Na-K-2Cl dependent 86Rb/K uptake. The endothelium-dependent stimulation of Na-K-ATPase and Na-K-2Cl was not hampered by diabetes. We conclude that abnormal vascular vessel tone and function, reported in STZ-induced diabetic rats, may be related to ion transport abnormalities caused by changes in Na-K-ATPase and Na-K-2Cl activities.

Acyl-CoA inhibition of adenine nucleotide translocation in ischemic myocardium

1975 ◽  
Vol 228 (3) ◽  
pp. 689-692 ◽  
Author(s):  
AL Shug ◽  
E Shrago ◽  
N Bittar ◽  
JD Folts ◽  
Koke
Keyword(s):  
Myocardial Ischemia ◽  
Tissue Concentration ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Energy Charge ◽  
Heart Tissue ◽  
Acid Oxidation ◽  
Inner Mitochondrial Membrane ◽  
Chain Acyl ◽  
Long Chain

The translocation of adenine nucleotides across the inner mitochondrial membrane and the tissue concentration of long-chain acyl-CoA esters were studied in dog heart after experimental myocardial ischemia. Ligation of the anterior coronary artery initiated events leading to an early decrease in adenine nucleotide translocase activity. A reciprocal increase in the concentration of heart tissue long-chain acyl-CoA esters was also observed. Adjacent nonischemic tissue showed changes intermediate between that of ischemic and normal heart tissue. It is postulated that a decrease in fatty acid oxidation after myocardial ischemia would lead to an accumulation of long-chain acyl-CoA esters, which in turn would inhibit adenine nucleotide translocation. The net result would be a lowering of the energy charge of the cell, adversely affecting muscle contraction and electrical conduction.

scholarly journals A mitochondrial long-chain fatty acid oxidation defect leads to uncharged tRNA accumulation and activation of the integrated stress response in the mouse heart

2021 ◽  
Author(s):  
Pablo Ranea-Robles ◽  
Natalya N Pavlova ◽  
Aaron Bender ◽  
Brandon Stauffer ◽  
Chunli Yu ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Stress Response ◽  
High Energy ◽  
Acid Oxidation ◽  
Mouse Heart ◽  
Integrated Stress Response ◽  
Mitochondrial Fatty Acid ◽  
Short Period ◽  
Chain Acyl ◽  
Long Chain

The heart relies mainly on mitochondrial fatty acid β-oxidation (FAO) for its high energy requirements. Cardiomyopathy and arrhythmias can be severe complications in patients with inherited defects in mitochondrial long-chain FAO, reinforcing the importance of FAO for cardiac health. However, the pathophysiological mechanisms that underlie the cardiac abnormalities in long-chain FAO disorders remain largely unknown. Here, we investigated the cardiac transcriptional adaptations to the FAO defect in the long-chain acyl-CoA dehydrogenase (LCAD) knockout (KO) mouse. We found a prominent activation of the integrated stress response (ISR) mediated by the eIF2α/ATF4 axis in both fed and fasted states, accompanied by a reduction in cardiac protein synthesis during a short period of food withdrawal. Notably, we found an accumulation of uncharged tRNAs in LCAD KO hearts, consistent with a reduced availability of cardiac amino acids, in particular, glutamine. Our results show that perturbations in amino acid metabolism caused by long-chain FAO deficiency impact cardiac metabolic signaling, in particular the ISR, and may play a role in the associated cardiac pathology

Sign in / Sign up

Export Citation Format

Share Document