Effect of Eight Weeks of Exercise Training on the Hippocampal Tissue in Streptozotocin-Induced Diabetic Rats: A Histological Study

Context. Nigella sativa seeds are usually used as traditional medicine for a wide range of therapeutic purposes. Objective. To investigate the subacute toxicity of NS aqueous extract and select its lowest dose to study its antidiabetic effect. Methods. 5 AqE.NS doses (2, 6.4, 21, 33, and 60 g/Kg) were daily administered to mice by gavage. Biochemical parameters measurements and histological study of the liver and the kidney were performed after 6 weeks of supplementation. Thereafter, and after inducing diabetes by alloxan, rats were treated by 2 g/Kg of AqE.NS during 8 weeks. Metabolic parameters were measured on sera. A horizontal electrophoresis of plasmatic lipoprotein was conducted. Glycogen, total lipids, and triglycerides were measured in the liver. TBARS were evaluated on adipose tissue, liver, and pancreas. Results. AqE.NS showed no variation in urea and albumin at the 5 doses, but hepatotoxicity from 21 g/Kg was confirmed by histopathological observations of the liver. In diabetic rats, AqE.NS significantly decreased glycemia, TG, T-cholesterol, LDL-c, and TBARS and showed a restored insulinemia and a significant increase in HDL-c. Results on the liver indicated a decrease in lipids and a possible glycogenogenesis. Conclusion. AqE.NS showed its safety at low doses and its evident antihyperglycemic, antihyperlipidemic, and antioxidant effect.

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TREADMILL EXERCISE TRAINING PROTECTS AGAINST METABOLIC DYSFUNCTION AND DIAPHRAGM WEAKNESS IN OBESE DIABETIC RATS

The FASEB Journal ◽

10.1096/fasebj.2018.32.1_supplement.588.26 ◽

2018 ◽

Vol 32 (S1) ◽

Author(s):

Noriko Ichinoseki‐Sekine ◽

Takamasa Tsuzuki ◽

Matthew J. Hinkley ◽

Toshinori Yoshihara ◽

Hiroyuki Kobayashi ◽

...

Keyword(s):

Exercise Training ◽

Treadmill Exercise ◽

Diabetic Rats ◽

Metabolic Dysfunction ◽

Obese Diabetic Rats ◽

Diaphragm Weakness

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Influence of exercise training on ischemic brain injury in type 1 diabetic rats

Journal of Applied Physiology ◽

10.1152/japplphysiol.00437.2012 ◽

2012 ◽

Vol 113 (7) ◽

pp. 1121-1127 ◽

Cited By ~ 16

Author(s):

Denise M. Arrick ◽

Hong Sun ◽

William G. Mayhan

Keyword(s):

Brain Injury ◽

Exercise Training ◽

Vascular Function ◽

Ischemia Reperfusion ◽

Diabetic Rats ◽

Ischemic Brain Injury ◽

Ischemic Brain ◽

Cerebrovascular Function ◽

Pial Arterioles

While exercise training (ExT) appears to influence cerebrovascular function during type 1 diabetes (T1D), it is not clear whether this beneficial effect extends to protecting the brain from ischemia-induced brain injury. Thus our goal was to examine whether modest ExT could influence transient focal ischemia-induced brain injury along with nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during T1D. Sprague-Dawley rats were divided into four groups: nondiabetic sedentary, nondiabetic ExT, diabetic (streptozotocin; 50 mg/kg ip) sedentary, and diabetic ExT. In the first series of studies, we measured infarct volume in all groups of rats following right MCA occlusion for 2 h, followed by 24 h of reperfusion. In a second series of studies, a craniotomy was performed over the parietal cortex, and we measured responses of pial arterioles to an endothelial NOS (eNOS)-dependent, a neuronal NOS (nNOS)-dependent, and a NOS-independent agonist in all groups of rats. We found that sedentary diabetic rats had significantly larger total, cortical, and subcortical infarct volumes following ischemia-reperfusion than sedentary nondiabetic, nondiabetic ExT, and diabetic ExT rats. Infarct volumes were similar in sedentary nondiabetic, ExT nondiabetic, and ExT diabetic rats. In contrast, ExT did not alter infarct size in nondiabetic compared with sedentary nondiabetic rats. In addition, ExT diabetic rats had impaired eNOS- and nNOS-dependent, but not NOS-independent, vasodilation that was restored by ExT. Thus ExT of T1D rats lessened ischemic brain injury following middle cerebral artery occlusion and restored impaired eNOS- and nNOS-dependent vascular function. Since the incidence of ischemic stroke is increased during T1D, we suggest that our finding are significant in that modest ExT may be a viable preventative therapeutic approach to lessen ischemia-induced brain injury that may occur in T1D subjects.

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Influence of training on skeletal muscle enzymatic adaptations in normal and diabetic rats

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1985.249.4.e360 ◽

1985 ◽

Vol 249 (4) ◽

pp. E360-E365 ◽

Cited By ~ 2

Author(s):

E. G. Noble ◽

C. D. Ianuzzo

Keyword(s):

Skeletal Muscle ◽

Exercise Training ◽

Citrate Synthase ◽

Diabetic Rats ◽

Muscle Fiber Types ◽

Fiber Types ◽

Marker Enzymes ◽

Oxidative Potential ◽

Hydroxyacyl Coa Dehydrogenase ◽

Fast Twitch

Muscle homogenates representing slow-twitch oxidative, fast-twitch oxidative-glycolytic, fast-twitch glycolytic, and mixed fiber types were prepared from normal, diabetic, and insulin-treated diabetic rats. Diabetes was induced by injection of 80 mg . kg-1 of streptozotocin. The activities of citrate synthase, succinate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase were employed as markers of oxidative potential, whereas phosphorylase, hexokinase, and phosphofructokinase activities were used as an indication of glycolytic capacity. Diabetes was associated with a general decrement in the activity of oxidative marker enzymes for all fiber types except the fast-twitch glycolytic fiber. In contrast, the fast-twitch glycolytic fibers demonstrated the greatest decline in glycolytic enzymatic activity. Insulin-treated animals, either trained or untrained, exhibited enzyme activities similar to their normal counterparts. Exercise training of diabetic rats mimicked the effect of insulin treatment and caused a near normalization of the activity of the marker enzymes. These findings suggest that the enzymatic potential of all skeletal muscle fiber types of diabetic rats may be normalized by exercise training even in the absence of significant amounts of insulin.

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

Journal of Applied Physiology ◽

10.1152/japplphysiol.01155.2002 ◽

2003 ◽

Vol 94 (6) ◽

pp. 2433-2438 ◽

Cited By ~ 29

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.

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Effect of Exercise Training on Endogenous Stem Cells Activation in Ischemia Reperfusion Induced Skeletal Muscle Injury: A Physio- Histological Study

Journal of Cytology & Histology ◽

10.4172/2157-7099.1000339 ◽

2015 ◽

Vol 06 (04) ◽

Author(s):

Mira Farouk Youssef

Keyword(s):

Skeletal Muscle ◽

Stem Cells ◽

Exercise Training ◽

Muscle Injury ◽

Ischemia Reperfusion ◽

Histological Study ◽

Skeletal Muscle Injury

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Effect of Exercise Training on the Expression of p53 and iNOS in the Cardiac Muscle of Type I Diabetic Rats

Journal of Endocrinology and Metabolism ◽

10.4021/jem123e ◽

2012 ◽

Cited By ~ 1

Author(s):

Al-Jarrah

Keyword(s):

Exercise Training ◽

Cardiac Muscle ◽

Diabetic Rats ◽

Type I

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Moderate exercise training reduces kidney oxidative stress and mortality of hypertensive diabetic rats

The FASEB Journal ◽

10.1096/fasebj.22.1_supplement.753.4 ◽

2008 ◽

Vol 22 (S1) ◽

Author(s):

Tatiana Sousa Cunha ◽

Roberta Hack Mendes ◽

Mariane Bertagnolli ◽

Vinícius Viegas ◽

Cristiano Teixeira Mostarda ◽

...

Keyword(s):

Oxidative Stress ◽

Exercise Training ◽

Diabetic Rats ◽

Moderate Exercise ◽

Moderate Exercise Training

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Effect of exercise training on glucose homeostasis in normal and insulin-deficient diabetic rats

Journal of Applied Physiology ◽

10.1152/jappl.1988.65.2.844 ◽

1988 ◽

Vol 65 (2) ◽

pp. 844-851 ◽

Cited By ~ 26

Author(s):

L. J. Goodyear ◽

M. F. Hirshman ◽

S. M. Knutson ◽

E. D. Horton ◽

E. S. Horton

Keyword(s):

Skeletal Muscle ◽

Exercise Training ◽

Glucose Tolerance ◽

Glucose Uptake ◽

Glucose Homeostasis ◽

Plasma Glucose ◽

Citrate Synthase ◽

Diabetic Rats ◽

Oral Glucose ◽

Oral Glucose Tolerance

The effect of 8-wk of treadmill training on plasma glucose, insulin, and lipid concentrations, oral glucose tolerance, and glucose uptake in the perfused hindquarter of normal and streptozocin-treated, diabetic Sprague-Dawley rats was studied. Diabetic rats with initial plasma glucose concentrations of 200-450 mg/dl and control rats were divided into trained and sedentary subgroups. Training resulted in lower plasma free fatty acid concentrations and increased triceps muscle citrate synthase activity in both the control and diabetic rats; triglyceride concentrations were lowered by training only in the diabetic animals. Oral glucose tolerance and both basal and insulin-stimulated glucose uptake in hindquarter skeletal muscle were impaired in the diabetic rats, and plasma glucose concentrations (measured weekly) gradually increased during the experiment. Training did not improve the hyperglycemia, impaired glucose tolerance, or decreased skeletal muscle glucose uptake in the diabetic rats, nor did it alter these parameters in the normal control animals. In considering our results and those of previous studies in diabetic rats, we propose that exercise training may improve glucose homeostasis in animals with milder degrees of diabetes but fails to cause improvement in the more severely insulin-deficient, diabetic rat.

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