scholarly journals Role of Hyperketonemia in Inducing Oxidative Stress and Cellular Damage in Cultured Hepatocytes and Type 1 Diabetic Rat Liver

2015 ◽  
Vol 37 (6) ◽  
pp. 2160-2170 ◽  
Author(s):  
Preeti Kanikarla-Marie ◽  
Sushil K. Jain
Keyword(s):  
Oxidative Stress ◽  
Liver Damage ◽  
Diabetic Control ◽  
Diabetic Rats ◽  
Cellular Damage ◽  
Diabetic Rat ◽  
Blood Levels ◽  
Per Se ◽  
Rat Livers

Background/Aims: Type 1 diabetic (T1D) patients have a higher incidence of liver disease. T1D patients frequently experience elevated plasma ketone levels along with hyperglycemia. However, no study has examined whether hyperketonemia per se has any role in excess liver damage in T1D. This study investigates the hypothesis that hyperketonemia can induce oxidative stress and cellular dysfunction. Methods: STZ treated diabetic rats, FL83B hepatocytes, and GCLC knocked down (GSH deficient) hepatocytes were used. Results: The blood levels of ALT and AST, biomarkers of liver damage, and ketones were elevated in T1D rats. An increase in NOX4 and ROS along with a reduction in GSH and GCLC levels was observed in T1D rat livers in comparison to those seen in non-diabetic control or type 2 diabetic rats. MCP-1 and ICAM-1 were also elevated in T1D rat livers and ketone treated hepatocytes. Macrophage markers CCR2 and CD11A that interact with MCP-1, and ICAM-1 respectively, were also elevated in the T1D liver, indicating macrophage infiltration. Additionally, activated macrophages increased hepatocyte damage with ketone treatment, which was similar to that seen in GCLC knockdown hepatocytes without ketones. Conclusion: Hyperketonemia per se can induce macrophage mediated damage to hepatocytes and the liver, caused by GSH depletion and oxidative stress up regulation in T1D.

scholarly journals Curcumin attenuates oxidative stress in liver in Type 1 diabetic rats

2017 ◽  
Vol 12 (1) ◽  
pp. 452-459 ◽  
Author(s):  
Zhenglu Xie ◽  
Xinqi Zeng ◽  
Xiaqing Li ◽  
Binbin Wu ◽  
Guozhi Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Polyol Pathway ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Curcumin Treatment ◽  
Kinase C ◽  
Diabetic Model ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Plasma Malondialdehyde

AbstractWe investigated the effect of curcumin on liver anti-oxidative stress in the type 1 diabetic rat model induced by streptozotocin (STZ). Experimental diabetic rats were induced by STZ intraperitoneally. All rats were fed for 21 days including three groups of control (NC), diabetic model (DC) and curcumin-treated (Cur, 1.5 g/kg by gavage). The results showed that curcumin-treatment significantly decreased the blood glucose and plasma malondialdehyde levels, but significantly increased the plasma superoxide dismutase, glutathione peroxidase and reduced glutathione levels. Curcumin treatment decreased the activity of aldose reductase, but increased the plasma glucose-6-phosphate dehydrogenase, glucose synthetase and glucose-polymerizing activities. Curcumin treatment significantly decreased the protein of protein kinase C (PKC) and poly ADP ribose polymerase (PARP) expression in the Cur group compared with the DC group. Moreover, the sorbitol dehydrogenase activity was significantly decreased and deterred glucose enters into the polyol pathway leading to an increased NADPH content in the Cur group compared with the DC group. Our data provides evidence that oxidative stress in diabetic rats may be attenuated by curcumin by inhibiting polyol pathway associated with down-regulated expression of PKC and PARP, as evidenced by both an increase the antioxidant enzymes levels and glycogen biosynthesis enzymes activities.

scholarly journals Effects of Phenolic Compounds of Fermented Thai Indigenous Plants on Oxidative Stress in Streptozotocin-Induced Diabetic Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Chaiyavat Chaiyasut ◽  
Winthana Kusirisin ◽  
Narissara Lailerd ◽  
Peerasak Lerttrakarnnon ◽  
Maitree Suttajit ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Thiobarbituric Acid ◽  
Diabetic Control ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Indigenous Plants ◽  
Glucose Levels ◽  
Abnormal Glucose Metabolism

We investigated the effects of antioxidant activity of fermentation product (FP) of five Thai indigenous products on oxidative stress in Wistar rats with streptozotocin (STZ)-induced diabetes type II. The rats were fed with placebo and with the FP (2 and 6 mL/kg body weight/day) for 6 weeks. Rutin, pyrogallol and gallic acid were main compounds found in the FP. Plasma glucose levels in diabetic rats receiving the higher dose of the FP increased less when compared to the diabetic control group as well as the group receiving the lower FP dose (13.1%, 29%, and 21.1%), respectively. A significant dose-dependent decrease in plasma levels of thiobarbituric acid reactive substance (P<.05) was observed. In addition, the doses of 2 and 6 mL FP/kg/day decreased the levels of erythrocyte ROS in diabetic rats during the experiment, but no difference was observed when compared to the untreated diabetic rat group. Results imply that FP decreased the diabetes-associated oxidative stress to a large extent through the inhibition of lipid peroxidation. The FP also improved the abnormal glucose metabolism slightly but the difference was not statistically significant. Thus, FP may be a potential therapeutic agent by reducing injury caused by oxidative stress associated with diabetes.

scholarly journals Polyploidy Analysis and Attenuation of Oxidative Stress in Hepatic Tissue of STZ-Induced Diabetic Rats Treated with an Aqueous Extract ofVochysia rufa

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Izabela Barbosa Moraes ◽  
Camilla Manzan-Martins ◽  
Neire Moura de Gouveia ◽  
Luciana Karen Calábria ◽  
Karen Renata Nakamura Hiraki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aqueous Extract ◽  
Morphological Changes ◽  
Liver Homogenate ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Hepatic Tissue ◽  
Polyploid Cell ◽  
Sod Activity ◽  
Rat Livers

Diabetes mellitus (DM) is characterized by hyperglycemia and alterations in the metabolism of lipids, carbohydrates, and proteins. Due to its hypoglycemic effectVochysia rufais frequently used in Uberlandia, Brazil, to treat DM. Despite its popularity, there is little information about its effect on hepatic tissue. Therefore, we evaluated the histoarchitecture, oxidative stress parameters, and polyploidy of liver tissue from streptozotocin- (STZ-) induced diabetic rats treated with aqueous extract ofVochysia rufa(AEV). Histology was determined by fixing the livers, processing, and staining with HE. Oxidative stress was determined by evaluating CAT, GPx, and SOD activity in liver homogenates and hepatic mitochondria fraction and by measuring GST, GSH levels and lipid peroxidation (MDA). Polyploidy was determined by subjecting isolated hepatocyte nuclei to flow cytometry. In the diabetic group, GST activity and GSH rates decreased whereas liver homogenate analysis showed that GPx, SOD activity and MDA increased. AEV treatment restored all parameters to normal levels. The oxidative stress analysis of hepatic mitochondria fraction showed similar results. Lower polyploid cell populations were found in the diabetic rat livers, even after glibenclamide treatment. Thus, AEV treatment efficiently reduced hepatic oxidative stress caused by STZ-induced diabetes and produced no morphological changes in the histological analysis.

Effects of empagliflozin on oxidative stress and endothelial dysfunction in STZ-induced Type 1 diabetic rat

2014 ◽  
Vol 9 (S 01) ◽  
Author(s):  
M Oelze ◽  
S Kröller-Schön ◽  
M Mader ◽  
E Zinßius ◽  
P Stamm ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Diabetic Rat

scholarly journals Oxidative Stress in Rats After 60 Days of Hypergalactosemia or Hyperglycemia

2003 ◽  
Vol 22 (6) ◽  
pp. 423-427 ◽  
Author(s):  
Mary Otsyula ◽  
Matthew S. King ◽  
Tonya G. Ketcham ◽  
Ruth A. Sanders ◽  
John B. Watkins
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Glutathione Disulfide ◽  
Hepatic Lipid Peroxidation ◽  
Streptozotocin Diabetic Rats

Two of the models used in current diabetes research include the hypergalactosemic rat and the hyperglucosemic, streptozotocin-induced diabetic rat. Few studies, however, have examined the concurrence of these two models regarding the effects of elevated hexoses on biomarkers of oxidative stress. This study compared the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase and the concentrations of glutathione, glutathione disulfide, and thiobarbituric acid reactants (as a measure of lipid peroxidation) in liver, kidney, and heart of Sprague-Dawley rats after 60 days of either a 50% galactose diet or insulin deficiency caused by streptozotocin injection. Most rats from both models developed bilateral cataracts. Blood glucose and glycosy-lated hemoglobin A1c concentrations were elevated in streptozotocin diabetic rats. Streptozotocin diabetic rats exhibited elevated activities of renal superoxide dismutase, cardiac catalase, and renal and cardiac glutathione peroxidase, as well as elevated hepatic lipid peroxidation. Insulin treatment of streptozotocin-induced diabetic rats normalized altered markers. In galactosemic rats, hepatic lipid peroxidation was increased whereas glutathione reductase activity was diminished. Glutathione levels in liver were decreased in diabetic rats but elevated in the galactosemic rats, whereas hepatic glutathione disulfide concentrations were decreased much more in diabetes than in galactosemia. Insulin treatment reversed/prevented all changes caused by streptozotocin-induced diabetes. Lack of concomitance in these data indicate that the 60-day galactose-fed rat is not experiencing the same oxidative stress as the streptozotocin diabetic rat, and that investigators must be cautious drawing conclusions regarding the concurrence of the effects of the two animal models on oxidative stress biomarkers.

scholarly journals Beneficial Effect of Aqueous Garlic Extract on Inflammation and Oxidative Stress Status in the Kidneys of Type 1 Diabetic Rats

2016 ◽  
Vol 32 (3) ◽  
pp. 329-336 ◽  
Author(s):  
Abolfazl Nasiri ◽  
Nasrin Ziamajidi ◽  
Roghayeh Abbasalipourkabir ◽  
Mohammad Taghi Goodarzi ◽  
Massoud Saidijam ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Beneficial Effect ◽  
Diabetic Rats ◽  
Garlic Extract ◽  
Oxidative Stress Status ◽  
And Oxidative Stress

scholarly journals Ellagic Acid ameliorates Streptozotocin-Induced Diabetic Hyperalgesia in Rat: Involvement of Oxidative Stress

2021 ◽  
Author(s):  
Siamak Shahidi ◽  
◽  
Alireza Komaki ◽  
Safoura Raoufi ◽  
Iraj Salehi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ellagic Acid ◽  
Therapeutic Potential ◽  
Biological Activities ◽  
Antinociceptive Effect ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Tail Flick ◽  
Stress Markers ◽  
Total Antioxidant

Background/Aim: Hyperalgesia is one of the current complications of diabetes mellitus that Oxidative stress and inflammation have principal role in its development. Ellagic Acid (EA) as a herbal component, has some biological activities, including antioxidant and anti-inflammatory effects. This study was designed to evaluate the possible beneficial effect of EA on hyperalgesia in streptozotocin (STZ)-induced diabetic rat. Materials and Methods: Rats were divided into control(vehicle received), diabetic, EA (25, 50 mg/kg)-treated control and EA(25, 50 mg/kg)-treated diabetic groups. Diabetes was induced by a single intraperitoneal (IP) injection of streptozotocin (STZ) (60 mg/Kg). EA was administered daily by oral gavage for 4 weeks. Hyperalgesia was assessed using tail flick (TF) and hot plate (HP) tests. Also, oxidative stress markers including malondialdehyde (MDA), total oxidant status (TOS) and total antioxidant capacity (TAC) in the serum were evaluated. Results: Diabetic animals showed marked reductions in TF and HP latencies, elevation of serum MDA level and TOS and diminution of serum TAC compared to controls significantly. Treatment of Diabetic rats with EA ameliorated reduction of TF latency at the dose of 25 mg/kg and HP latency at the dose of 50 mg/kg. Furthermore EA significantly increased TAC and decreased MDA level at dose of 50 mg/kg and reduced TOS at both doses in the serum of diabetic animals. In EA treated normal rats we could see no significant alterations in the parameters studied. Conclusion: These results displayed potent antinociceptive effect of EA in diabetic rats via attenuating oxidative stress. This proposes therapeutic potential of EA for damping diabetic hyperalgesia.

scholarly journals Liraglutide protects cardiac function in diabetic rats through the PPARα pathway

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Qian Zhang ◽  
Xinhua Xiao ◽  
Jia Zheng ◽  
Ming Li ◽  
Miao Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Cardiac Dysfunction ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Serum Adiponectin ◽  
Diabetic Rat ◽  
Lv Function ◽  
High Dose ◽  
And Oxidative Stress

Increasing evidence shows that diabetes causes cardiac dysfunction. We hypothesized that a glucagon-like peptide-1 (GLP-1) analog, liraglutide, would attenuate cardiac dysfunction in diabetic rats. A total of 24 Sprague–Dawley (SD) rats were divided into two groups fed either a normal diet (normal, n=6) or a high-fat diet (HFD, n=18) for 4 weeks. Then, the HFD rats were injected with streptozotocin (STZ) to create a diabetic rat model. Diabetic rats were divided into three subgroups receiving vehicle (diabetic, n=6), a low dose of liraglutide (Llirag, 0.2 mg/kg/day, n=6), or a high dose of liraglutide (Hlirag, 0.4 mg/kg/day, n=6). Metabolic parameters, systolic blood pressure (SBP), heart rate (HR), left ventricular (LV) function, and whole genome expression of the heart were determined. Diabetic rats developed insulin resistance, increased blood lipid levels and oxidative stress, and impaired LV function, serum adiponectin, nitric oxide (NO). Liraglutide improved insulin resistance, serum adiponectin, NO, HR, and LV function and reduced blood triglyceride (TG), total cholesterol (TC) levels, and oxidative stress. Moreover, liraglutide increased heart nuclear receptor subfamily 1, group H, member 3 (Nr1h3), peroxisome proliferator activated receptor (Ppar) α (Pparα), and Srebp expression and reduced diacylglycerol O-acyltransferase 1 (Dgat) and angiopoietin-like 3 (Angptl3) expression. Liraglutide prevented cardiac dysfunction by activating the PPARα pathway to inhibit Dgat expression and oxidative stress in diabetic rats.

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