scholarly journals PO-233 The Neuroprotective Effects of Aerobic Exercise and Oral Resveratrol on Hippocampal Neurons in Diabetic Rats

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Han Li
Keyword(s):  
Protein Expression ◽  
Aerobic Exercise ◽  
Hippocampal Neurons ◽  
Escape Latency ◽  
Diabetic Rats ◽  
Aerobic Exercise Training ◽  
Sprague Dawley ◽  
Swimming Training ◽  
Neuroprotective Effects ◽  
Creb Protein

Objective The purpose of this study is to explore the effects of aerobic exercise combined with oral resveratrol on ethology and BDNF and CREB proteins of hippocampus neurons in diabetic rats, in order to provide a theoretical basis for revealing the neuroprotective mechanism of exercise and resveratrol. Methods 45 male Sprague Dawley rats, aged 8 weeks, were randomly divided into 5 groups: normal control (NC), diabetes control (DC), diabetes exercise (DE), diabetes resveratrol (DR) and diabetes exercise and resveratrol (DER). Exercise-related groups performed 8-week swimming training (60min/d，5d/week). Morris maze test, 7d. Escape latency time, strategy of finding platform performance, the protein expression of BDNF and CREB from hippocampus neurons were measured. Results 1）Compared with DM, DR and RE groups, the escape latency of DRE group was significantly shortened (p<0.01), and the strategy of finding platform performance was remarkably improved (p<0.05). 2) Compared with NC group, the protein expression of BDNF of DM group was obviously decreased (p <0.01), while in DRE group was improved significantly than that in DE group (p< 0.05). 3) The level of CREB expression in DM group clearly lower than in group NC (p<0.01), and the expression of CREB in DER and DE groups were remarkably increased (P <0.01) . Conclusions  Eight weeks of swimming training and/or oral resveratrol could increase the expression level of BDNF and CREB protein in the hippocampal neurons of diabetic rats, and improve the ability of spatial learning from behavioral study. It is suggested that the aerobic exercise training and the SIRT1 mechanism of resveratrol perhaps improve the situation of high glucose and indirectly stimulate the expression of BDNF and CREB protein. As a result,  that leads to improve the impair of learning and memory which caused by diabetes.  

scholarly journals Aerobic Exercise Training Decreases Hepatic Asprosin in Diabetic Rats

2019 ◽  
Vol 8 (5) ◽  
pp. 666 ◽  
Author(s):  
Jeong Rim Ko ◽  
Dae Yun Seo ◽  
Tae Nyun Kim ◽  
Se Hwan Park ◽  
Hyo-Bum Kwak ◽  
...  
Keyword(s):  
Exercise Training ◽  
Aerobic Exercise ◽  
Exercise Group ◽  
Diabetic Rats ◽  
Aerobic Exercise Training ◽  
Sprague Dawley ◽  
Protein Levels ◽  
Hepatic Glucose Metabolism ◽  
Sprague Dawley Rats ◽  
Hepatic Glucose

Asprosin, a novel hormone released from white adipose tissue, regulates hepatic glucose metabolism and is pathologically elevated in the presence of insulin resistance. It is unknown whether aerobic exercise training affects asprosin levels in type 1 diabetes mellitus (T1DM). The aim of this study was to determine whether (1) aerobic exercise training could decrease asprosin levels in the liver of streptozotocin (STZ)-induced diabetic rats and (2) the reduction in asprosin levels could induce asprosin-dependent downstream pathways. Five-week-old male Sprague–Dawley rats were randomly divided into control, STZ-induced diabetes (STZ), and STZ with aerobic exercise training groups (n = 6/group). T1DM was induced by a single dose of STZ (65 mg/kg intraperitoneally (i.p.)). The exercise group was made to run on a treadmill for 60 min at a speed of 20 m/min, 4 days per week for 8 weeks. Aerobic exercise training reduced the protein levels of asprosin, PKA, and TGF-β but increased those of AMPK, Akt, PGC-1β, and MnSOD. These results suggest that aerobic exercise training affects hepatic asprosin-dependent PKA/TGF-β and AMPK downstream pathways in T1DM.

Effect of feeding with bilberry fruit on the expression pattern of αCaMKII in hippocampal neurons in normal and diabetic rats

2017 ◽  
Vol 20 (2) ◽  
pp. 313-319 ◽  
Author(s):  
M. Matysek ◽  
S. Mozel ◽  
R. Szalak ◽  
A. Zacharko-Siembida ◽  
K. Obszańska ◽  
...  
Keyword(s):  
Cognitive Processes ◽  
Hippocampal Neurons ◽  
Negative Impact ◽  
Expression Patterns ◽  
Memory Loss ◽  
Diabetic Rats ◽  
Control Group ◽  
Neuroprotective Effects ◽  
The Central Nervous System ◽  
And Control

Abstract αCaMKII, widely occurring in the central nervous system, plays a significant role in cognitive processes. It is well known that diabetes is a risk factor that may trigger brain atrophy, cognitive dysfunction and finally lead to memory loss. Antioxidants richly present in bilberry fruits are believed to have significant effects on diabetes-related brain dysfunctions mainly due to their abilities to modulate neurotransmitter release that lead to reduction of the negative impact of free radicals on cognitive processes. The aim of the present research was to immunohistochemically investigate the expression patterns of αCaMKII in hippocampal neurons from non-diabetic, diabetic and diabetic rats fed with an extract of bilberry fruit. The obtained results show that in comparison to the control group, in diabetic rats hippocampal neurons immunoreactive (ir) to αCaMKII were swollen and the lengths of the neuronal fibres were reduced. Further study shows that in diabetic rats fed with bilberry fruit, αCaMKII-positive nerve fibres were significantly longer when compared to the groups of diabetic and control rats. Additionally, we observed statistically significant changes in the average larger diameter of αCaMKII-ir hippocampal neurons between groups of diabetic rats (with vs. without supplement of bilberry fruit). The results of the present work suggest that antioxidants present in bilberry fruits influence the morphology of and possibly exhibit beneficial and neuroprotective effects on hippocampal neurons during diabetes. It is likely that changes in the appearance of αCaMKII-expressed hippocampal neurons may reflect the diabetes-evoked rise in Ca2+ level in the cerebral nerve terminals. The present research extends our knowledge of preventive mechanisms for cognitive dysfunctions occurring in the brain during diabetes.

scholarly journals Physical activity as a non-pharmacological and useful strategy in controlling of the apoptotic symptoms in diabetic model rats

2021 ◽  
Vol 16 (8) ◽  
pp. 602-606
Author(s):  
M. Bostani ◽  
S.A. Noaein
Keyword(s):  
Aerobic Exercise ◽  
Pancreatic Beta Cells ◽  
Diabetic Control ◽  
Pancreatic Tissue ◽  
Diabetic Rats ◽  
Aerobic Exercise Training ◽  
Bax Protein ◽  
Male Wistar Rats ◽  
Healthy Control ◽  
Induced Apoptosis

Background. In recent years, diabetes has become a global health problem. Apoptosis of pancreatic beta cells plays an important role in the pathogenesis of type 1 diabetes. Exercise as a non-pharmacological strategy to reduce the diabetic-induced complications has always been of interest to researchers. Therefore, the purpose of this study was to investigate the effect of aerobic exercise on levels of Bax, Bcl-2 and Bax/Bcl-2 ratio in pan­creatic tissue of streptozotocin (STZ)-induced diabetic rats. Materials and methods. A total number of 40 male Wistar rats (10 weeks old, 200–250 gr weight) were randomly divided into healthy control (HC), healthy trained (HT), diabetic control (DC), and diabetic trained (DT) groups. Diabetes was also induced by a single intraperitoneally injection of streptozocin (45 mg/kg). The training groups performed the exercise on the treadmill for five consecutive days within six weeks. The pancreatic tissue levels of the Bax and the Bcl-2 proteins were further determined via ELISA method. Results. The results showed that the induction of diabetes had significantly decreased the levels of Bcl-2 protein and increased the levels of Bax protein and Bax/Bcl-2 ratio in the pancreatic tissue (p < 0.05). As well, the findings showed that six weeks of aerobic exercise training had significantly increased the levels of Bcl-2 and significantly decreased the levels of Bax protein in DT group. Also, the Bax/Bcl-2 ratio reduced significantly in DT group (p < 0.05). The increase in displacement and transmission of apoptosis inducing factor (AIF) that have seen in oxidative stress status, is reduced in the tissues of trained individuals which indica­ting of the inhibition in the apoptotic signaling. Conclusions. According to the results of this study, exercise can be considered as an effective strategy to reduce the rate of diabetic-induced apoptosis and control its complications.

scholarly journals Nicotinamide Mononucleotide Administration Prevents Experimental Diabetes-Induced Cognitive Impairment and Loss of Hippocampal Neurons

2020 ◽  
Vol 21 (11) ◽  
pp. 3756
Author(s):  
Krish Chandrasekaran ◽  
Joungil Choi ◽  
Muhammed Ikbal Arvas ◽  
Mohammad Salimian ◽  
Sujal Singh ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Neuronal Loss ◽  
Memory Deficits ◽  
Diabetic Rats ◽  
Resonance Spectroscopy ◽  
Gamma Aminobutyric Acid ◽  
Sprague Dawley ◽  
Protein Levels ◽  
Nicotinamide Mononucleotide

Diabetes predisposes to cognitive decline leading to dementia and is associated with decreased brain NAD+ levels. This has triggered an intense interest in boosting nicotinamide adenine dinucleotide (NAD+) levels to prevent dementia. We tested if the administration of the precursor of NAD+, nicotinamide mononucleotide (NMN), can prevent diabetes-induced memory deficits. Diabetes was induced in Sprague-Dawley rats by the administration of streptozotocin (STZ). After 3 months of diabetes, hippocampal NAD+ levels were decreased (p = 0.011). In vivo localized high-resolution proton magnetic resonance spectroscopy (MRS) of the hippocampus showed an increase in the levels of glucose (p < 0.001), glutamate (p < 0.001), gamma aminobutyric acid (p = 0.018), myo-inositol (p = 0.018), and taurine (p < 0.001) and decreased levels of N-acetyl aspartate (p = 0.002) and glutathione (p < 0.001). There was a significant decrease in hippocampal CA1 neuronal volume (p < 0.001) and neuronal number (p < 0.001) in the Diabetic rats. Diabetic rats showed hippocampal related memory deficits. Intraperitoneal NMN (100 mg/kg) was given after induction and confirmation of diabetes and was provided on alternate days for 3 months. NMN increased brain NAD+ levels, normalized the levels of glutamate, taurine, N-acetyl aspartate (NAA), and glutathione. NMN-treatment prevented the loss of CA1 neurons and rescued the memory deficits despite having no significant effect on hyperglycemic or lipidemic control. In hippocampal protein extracts from Diabetic rats, SIRT1 and PGC-1α protein levels were decreased, and acetylation of proteins increased. NMN treatment prevented the diabetes-induced decrease in both SIRT1 and PGC-1α and promoted deacetylation of proteins. Our results indicate that NMN increased brain NAD+, activated the SIRT1 pathway, preserved mitochondrial oxidative phosphorylation (OXPHOS) function, prevented neuronal loss, and preserved cognition in Diabetic rats.

Effect of the Joint Administration of Selenium and Vitamin E in Combination with Regular Aerobic Exercise on Markers of Lipid Peroxidation and Glutathione Peroxidase in Diabetic Rats

2005 ◽  
Vol 15 (3) ◽  
pp. 266-278 ◽  
Author(s):  
Hyun-Tae Kim
Keyword(s):  
Vitamin E ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Acute Effect ◽  
Exercise Group ◽  
Diabetic Rats ◽  
Aerobic Exercise Training ◽  
Long Term Treatment

We investigated the effect of long-term treatment (6 wk) with selenium and vitamin E, in combination with aerobic exercise training, on malondialdehyde (MDA), oxidized low-density lipoprotein (ox-LDL), and glutathione peroxi-dase (GPx) in STZ-induced diabetic rats. The rats were assigned randomly to one of three treatment groups (n = 12 per group): 1) exercise group (EX), 2) selenium/vitamin E/exercise group (SVE), and 3) selenium/vitamin E group (SV). To estimate the acute effect of exercise, a 30-min endurance exercise was used. The MDA concentration was significantly lower in the SVE. The ox-LDL was significantly lower in the SVE and SV. The hepatic concentrations of selenium and vitamin E were significantly higher in the SVE. These results indicate that the increase in MDA is mildly attenuated in rats that were aerobically trained. Moreover, the joint administration of selenium and vitamin E with or without exercise training reduces the levels of ox-LDL.

Aerobic exercise training improves skeletal muscle function and Ca2+ handling-related protein expression in sympathetic hyperactivity-induced heart failure

2010 ◽  
Vol 109 (3) ◽  
pp. 702-709 ◽  
Author(s):  
C. R. Bueno ◽  
J. C. B. Ferreira ◽  
M. G. Pereira ◽  
A. V. N. Bacurau ◽  
P. C. Brum
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Protein Expression ◽  
Aerobic Exercise ◽  
Muscle Function ◽  
Exercise Tolerance ◽  
Aerobic Exercise Training ◽  
Related Protein ◽  
Skeletal Muscle Function ◽  
Related Proteins

The cellular mechanisms of positive effects associated with aerobic exercise training on overall intrinsic skeletal muscle changes in heart failure (HF) remain unclear. We investigated potential Ca2+ abnormalities in skeletal muscles comprising different fiber compositions and investigated whether aerobic exercise training would improve muscle function in a genetic model of sympathetic hyperactivity-induced HF. A cohort of male 5-mo-old wild-type (WT) and congenic α2A/α2C adrenoceptor knockout (ARKO) mice in a C57BL/6J genetic background were randomly assigned into untrained and trained groups. Exercise training consisted of a 8-wk running session of 60 min, 5 days/wk (from 5 to 7 mo of age). After completion of the exercise training protocol, exercise tolerance was determined by graded treadmill exercise test, muscle function test by Rotarod, ambulation and resistance to inclination tests, cardiac function by echocardiography, and Ca2+ handling-related protein expression by Western blot. α2A/α2CARKO mice displayed decreased ventricular function, exercise intolerance, and muscle weakness paralleled by decreased expression of sarcoplasmic Ca2+ release-related proteins [α1-, α2-, and β1-subunits of dihydropyridine receptor (DHPR) and ryanodine receptor (RyR)] and Ca2+ reuptake-related proteins [sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)1/2 and Na+/Ca2+ exchanger (NCX)] in soleus and plantaris. Aerobic exercise training significantly improved exercise tolerance and muscle function and reestablished the expression of proteins involved in sarcoplasmic Ca2+ handling toward WT levels. We provide evidence that Ca2+ handling-related protein expression is decreased in this HF model and that exercise training improves skeletal muscle function associated with changes in the net balance of skeletal muscle Ca2+ handling proteins.

Effect of combination of chlorella intake and aerobic exercise training on glycemic control in type 2 diabetic rats

Nutrition ◽  
2019 ◽  
Vol 63-64 ◽  
pp. 45-50 ◽  
Author(s):  
Naoki Horii ◽  
Natsuki Hasegawa ◽  
Shumpei Fujie ◽  
Masataka Uchida ◽  
Keiko Iemitsu ◽  
...  
Keyword(s):  
Glycemic Control ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Diabetic Rats ◽  
Aerobic Exercise Training ◽  
Type 2 Diabetic

Chronic tempol treatment attenuates the renal hemodynamic effects induced by a heme oxygenase inhibitor in streptozotocin diabetic rats

2011 ◽  
Vol 301 (5) ◽  
pp. R1540-R1548 ◽  
Author(s):  
Francisca Rodriguez ◽  
Bernardo Lopez ◽  
Cayetano Perez ◽  
Francisco J. Fenoy ◽  
Isabel Hernandez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Heme Oxygenase ◽  
Oral Treatment ◽  
Diabetic Rats ◽  
Renal Hemodynamics ◽  
Heme Oxygenase 1 ◽  
Acute Administration ◽  
Sprague Dawley

Heme oxygenase-1 (HO-1) is induced by oxidative stress and plays an important role in protecting the kidney from oxidant-mediated damage in the streptozotocin (STZ) rat model of type-1 diabetes mellitus (DM-1). HO-derived metabolites, presumably carbon monoxide (CO), mediate vasodilatory influences in the renal circulation, particularly in conditions linked to elevated HO-1 protein expression or diminished nitric oxide (NO) levels. We tested the hypothesis that diabetes increases oxidative stress and induces HO-1 protein expression, which contributes to regulate renal hemodynamics in conditions of low NO bioavailability. Two weeks after the induction of diabetes with STZ (65 mg/kg iv), Sprague-Dawley rats exhibited higher renal HO-1 protein expression, hyperglycemia, and elevated renal nitrotyrosine levels than control normoglycemic animals. In anesthetized diabetic rats, renal vascular resistance (RVR) was increased, and in vivo cortical NO levels were reduced ( P < 0.05) compared with control animals. Acute administration of the HO inhibitor Stannous mesoporphyrin (SnMP; 40 μmol/kg iv) did not alter renal hemodynamics in control rats, but greatly decreased glomerular filtration rate and renal blood flow, markedly increasing RVR in hyperglycemic diabetic rats. Chronic oral treatment with the SOD mimetic tempol prevented the elevation of nitrotyrosine, the HO-1 protein induction, and the increases in RVR induced by SnMP in the diabetic group, without altering basal NO concentrations or RVR. Increasing concentrations of a CO donor (CO-releasing molecule-A1) on pressurized renal interlobar arteries elicited a comparable relaxation in vessels taken from control or diabetic animals. These results suggest that oxidative stress-induced HO-1 exerts vasodilatory actions that partially maintain renal hemodynamics in uncontrolled DM-1.

scholarly journals Metabolomic Response of Skeletal Muscle to Aerobic Exercise Training in Insulin Resistant Type 1 Diabetic Rats

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Michelle S. Dotzert ◽  
Michael R. Murray ◽  
Matthew W. McDonald ◽  
T. Dylan Olver ◽  
Thomas J. Velenosi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Diabetic Rats ◽  
Aerobic Exercise Training ◽  
Insulin Resistant
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