scholarly journals Effect of alloxan-induced diabetes on serum and cardiac butyrylcholinesterases in the rat

2002 ◽  
Vol 175 (1) ◽  
pp. 241-250 ◽  
Author(s):  
KR Dave ◽  
SS Katyare
Keyword(s):  
Insulin Treatment ◽  
Elevated Serum ◽  
Diabetic Rats ◽  
Female Rats ◽  
Diabetic Rat ◽  
Slight Reduction ◽  
Bche Activity ◽  
Male And Female Rats ◽  
Membrane Bound ◽  
Substrate Kinetics

Elevated serum butyrylcholinesterase (BChE) activity in the diabetic rat, mouse and human is very evident. The source of the increased level of BChE in the diabetic condition is not known. The effect of diabetes on cardiac BChE has not been studied so far, in spite of high BChE levels in the heart. In the present study, we investigated the effect of alloxan-induced diabetes on serum and on the soluble as well as the membrane-bound form of cardiac BChE activity and their substrate kinetics. We included rats of both sexes in the study. Serum BChE activity increased only in male diabetic rats (2.3-fold), while the activities of the soluble as well as the membrane-bound form of cardiac BChE activity increased 2.2- to 2.8-fold in male diabetic rats. A smaller increase (30%) was observed in the activity of the membrane-bound form of cardiac BChE in female diabetic rats. A slight reduction in BChE activity was observed in male and female rats after insulin treatment. The activity ratio of the soluble to the membrane-bound form of cardiac BChE was higher in diabetic and insulin-treated diabetic rats as compared with controls. The K(m) values of component II of the serum and soluble forms of cardiac BChE were comparable. In conclusion, the diabetes-induced increase in serum and cardiac BChE activity was sex dependent. Insulin was not able to rectify the diabetes-induced abnormalities in serum and cardiac BChE activity. The heart could be one of the possible sources of the increased level of serum BChE.

scholarly journals Sex-specific vascular responses of the rat aorta: effects of moderate term (intermediate stage) streptozotocin-induced diabetes

2016 ◽  
Vol 94 (4) ◽  
pp. 408-415 ◽  
Author(s):  
Xiaoyuan Han ◽  
Sonali Shaligram ◽  
Rui Zhang ◽  
Leigh Anderson ◽  
Roshanak Rahimian
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mrna Expression ◽  
Intermediate Stage ◽  
Diabetic Rats ◽  
Female Rats ◽  
Diabetic Rat ◽  
Male And Female ◽  
Male And Female Rats ◽  
Oxide Synthase

Hyperglycemia affects male and female vascular beds differently. We have previously shown that 1 week after the induction of diabetes with streptozotocin (STZ), male and female rats exhibit differences in aortic endothelial function. To examine this phenomenon further, aortic responses were studied in male and female rats 8 weeks after the induction of diabetes (intermediate stage). Endothelium-dependent vasodilation (EDV) to acetylcholine (ACh) was measured in phenylephrine (PE) pre-contracted rat aortic rings. Concentration response curves to PE were generated before and after L-NAME, a nitric oxide synthase (NOS) inhibitor. Furthermore, mRNA expression of endothelial nitric oxide synthase (eNOS) and NADPH oxidase subunit (Nox1) were determined. At 8 weeks, diabetes impaired EDV to a greater extent in female than male aortae. Furthermore, the responsiveness to PE was significantly enhanced only in female diabetic rats, and basal NO, as indicated by the potentiation of the response to PE after L-NAME, was reduced in female diabetic rat aortae to the same levels as in males. In addition, eNOS mRNA expression was decreased, while the Nox1 expression was significantly enhanced in diabetic female rats. These results suggest that aortic function in female diabetic rats after 8 weeks exhibits a more prominent impairment and that NO may be involved.

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.

Acute insulin withdrawal contributes to ischemic heart failure in spontaneously diabetic BB Wistar rats

1990 ◽  
Vol 68 (3) ◽  
pp. 462-466 ◽  
Author(s):  
Gary D. Lopaschuk ◽  
Marguerite A. Spafford
Keyword(s):  
Fatty Acids ◽  
Metabolic Control ◽  
Wistar Rats ◽  
Insulin Treatment ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Metabolic Demand ◽  
Significant Deterioration ◽  
Direct Demonstration

The contribution of poor metabolic control to myocardial ischemic failure was determined in isolated working hearts from insulin-dependent BB Wistar rats. Removal of insulin treatment 24 h prior to study (uncontrolled diabetic rats) resulted in significant increases in serum glucose, serum fatty acids, and myocardial triglyceride, compared with animals in which insulin treatment was not withheld (insulin-treated diabetic rats). Isolated working hearts obtained from these two groups were subjected to a 40% reduction in coronary flow in the presence of a maintained metabolic demand (hearts were paced at 200 beats/min and perfused at an 80 mmHg (1 mmHg = 133.3 Pa) left aortic afterload, 11.5 mmHg left atrial preload). Within 15 min of ischemia, a significant deterioration of mechanical function occurred in the uncontrolled diabetic rats, whereas function was maintained in the insulin-treated diabetic rats. Oxygen consumption by the two groups of hearts was similar prior to the onset of ischemia and decreased during ischemia in parallel with the work performed by the hearts. This suggests that the accelerated failure rate in uncontrolled diabetic rat hearts is unlikely a result of an increased oxygen requirement. These data are a direct demonstration that acute changes in metabolic control of the diabetic can contribute to the severity of myocardial ischemic injury.Key words: diabetes, heart, ischemia, fatty acids.

scholarly journals Anti-diabetic, Antioxidants, Anti-hepatorenaltoxicity Activities of Cyperus rotundus Rhizome Extract in Alloxan-induced Diabetic Rats

2021 ◽  
Author(s):  
Mohammed Al-Awar ◽  
Turki Alqabbani
Keyword(s):  
Elevated Serum ◽  
Density Lipoprotein ◽  
Diabetic Rats ◽  
Cyperus Rotundus ◽  
Lipoprotein Cholesterol ◽  
Male Rats ◽  
Diabetic Rat ◽  
Histological Structure ◽  
Amylase Level ◽  
Liver And Kidney

Objective: The hypoglycemic, hepatorenalprotective, and antioxidant Activities of Cyperus rotundus rhizomes extract in an alloxan-induced diabetic rat model were investigated in this work.Methods: 25 Male rats were divided into 5 groups: normal control, diabetic control, diabetic of C. rotundus (200 mg/kg b.w), diabetic of C. rotundus (400 mg/kg b.w), diabetic of glibenclamide (0.6mg/kg).Treatments were administered orally for 6 weeks.Results: A single injection of alloxan to rats (150mg/kg b.w) caused pathological alterations in all studied parameters and histological structure of the pancreas. On the other hand, results showed that oral administration of C. rotundus rhizomes extract in dose of 200 and 400 mg/kg caused significant reduction in glucose, HbA1C%, α-amylase level and plasma lactate together with significant elevation in serum insulin, serum pyruvate with an improvement in insulin resistance. In line with amelioration of the diabetic state, C. rotundus rhizomes extract improved of the liver and kidney functions, and oxidative marker levels. Moreover, the extract succeeded to reduce the elevated serum total cholesterol, triglyceride (TG) and low-density lipoprotein- cholesterol (LDL-C) levels and to elevate the reduced high-density lipoprotein- cholesterol (HDL-C) level of diabetic rats.Conclusion: The investigation data concluded that C. rotundus rhizomes extract could be used as alternative treatments as antidiabetic, antioxidant and antihyperlipidemic, and agent as well as in liver and kidney protective in alloxan induced-diabetic rats. This may be related to the presence of saponin glycosides, polyphenols, flavonoids, and terpenoids in the ethanolic extract of C. rotundus rhizomes, which was discovered by phytochemical screening in this study to be present in the plant.

scholarly journals Neuroendocrine control of the pituitary gonadotropic function in experimental diabetes

2019 ◽  
Vol 43 (3) ◽  
pp. 43-47
Author(s):  
V. N. Babichev ◽  
E. I. Adamskaya ◽  
T. A. Kuznetsova ◽  
I. V. Shishkina
Keyword(s):  
Nuclear Receptors ◽  
Experimental Diabetes ◽  
Diabetic Rats ◽  
Female Rats ◽  
Maximal Response ◽  
Basal Secretion ◽  
Male And Female Rats ◽  
Lh Rh ◽  
Lh Secretion

The hypothalamo-pituitary-gonadal system was examined in male and female rats with experimental diabetes in­duced by streptozotocin (STZ). Injection of STZ caused a decrease of testosterone (T) concentration and of T nuclear receptors in the pituitary. The levels of luteinizing and follicle stimulating hor­mones (LH and FSH) in the blood of diabetic rats did not differ from those in intact animals. In vitro experiments showed that the development of diabetes did not change the basal secretion of LH by the pituitary in males. Maximal response to LH-RH was record­ed in control males after 3-hour incubation, whereas the rate of LH secretion in experimental rats did not differ from basal values. In­jection of STZ to cycling females disordered the estrous cycle and involved decreases of the basal and cyclic secretion of LH, FSH, and sex hormones. The concentrations of estradiol nuclear receptors in the preoptic anterohypothalamic region and pituitary decreased, whereas the number of T-binding sites decreased only in the pitui­tary. Sex hormone-stimulated gonadotropin wave in oophorect- omized females was decreased in diabetes, which was due to changed activity of the LH-RH producing system. The authors hy­pothesize that changes in the mechanism of regulation of the hy­pothalamo-pituitary-gonadal system in experimental diabetes are re­lated to pituitary disorders in males, whereas changed basal and cy­clic secretion of LH and FSH in females is caused by disordered activity of the LH-RH production and receptor binding at the level of the hypothalamo-pituitary complex.

Insulin reversal of biochemical changes in hearts from diabetic rats

1986 ◽  
Vol 251 (3) ◽  
pp. H670-H675
Author(s):  
S. Bhimji ◽  
D. V. Godin ◽  
J. H. McNeill
Keyword(s):  
Insulin Treatment ◽  
Serum Insulin ◽  
Complete Recovery ◽  
Magnesium Content ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Biochemical Changes ◽  
Diabetic Rat ◽  
Lysosomal Hydrolase ◽  
Rat Hearts

Reversal of myocardial biochemical changes with insulin treatment (4 and 8 wk) was studied in 8 and 12 wk streptozotocin (STZ)-diabetic rats. STZ-induced diabetes was characterized by elevations in blood glucose, serum cholesterol, and triglycerides and depressed serum insulin levels. Insulin treatment for 4 and 8 wk completely restored the serum alterations to control values. The polyuria, polydipsia, and polyphagia were also markedly diminished by the insulin treatment. Diabetic rats had pronounced decreases in body, heart, and left ventricular weights, all of which were completely reversed by the insulin treatment. Hydroxyproline accumulation in diabetic rat hearts was only reversed by the 8-wk and not by the 4-wk insulin treatment. STZ produced a significant depletion of left ventricular magnesium content as well as depression of K+-stimulated sarcoplasmic reticulum and myofibrillar ATPase activities. Both the 4- and 8-wk insulin treatment produced a complete recovery of the myocardial magnesium content. No significant changes in sarcolemmal Na+-K+-ATPase and K+-stimulated p-nitrophenyl phosphatase activities were observed in diabetic animals compared with control. The decreased latency of the lysosomal hydrolase, N-acetyl-beta-glucosaminidase, and the increased collagen deposition observed in the diabetic hearts were only partially reversed by the 4-wk insulin treatment, but completely reversed by the 8-wk treatment period.

Reduced activity of mtTFA decreases the transcription in mitochondria isolated from diabetic rat heart

2002 ◽  
Vol 282 (4) ◽  
pp. E778-E785 ◽  
Author(s):  
Akio Kanazawa ◽  
Yoshihiko Nishio ◽  
Atsunori Kashiwagi ◽  
Hidetoshi Inagaki ◽  
Ryuichi Kikkawa ◽  
...  
Keyword(s):  
Insulin Treatment ◽  
Mitochondrial Protein ◽  
Mitochondrial Respiratory Chain ◽  
Binding Activity ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Mitochondrial Transcription Factor ◽  
Loop Region ◽  
Rat Hearts ◽  
D Loop

To evaluate abnormalities in the mitochondrial transcription factor A (mtTFA) function as a cause of mitochondrial dysfunction in diabetes, we measured the mRNA contents of the proteins consisting of the mitochondrial respiratory chain as well as transcriptional and translational activities in the mitochondria isolated from controls and streptozotocin-induced diabetic rat hearts. Using Northern blot analysis, we found 40% reduced mRNA contents of mitochondrial-encoded cytochrome b and ATP synthase subunit 6 in diabetic rat hearts compared with control rats ( P< 0.05). These abnormalities were completely recovered by insulin treatment. Furthermore, the mitochondrial activities of transcription and translation were decreased significantly in mitochondria isolated from diabetic rats by 60% ( P < 0.01) and 71% ( P < 0.01), respectively, compared with control rats. The insulin treatment also completely normalized these abnormalities in diabetic rats. Consistently, gel retardation assay showed a reduced binding of mtTFA to the D-loop of mitochondrial DNA in diabetic rats, although there was no difference in the mtTFA mRNA and protein content between the two groups. On the basis of these findings, a reduced binding activity of mtTFA to the D-loop region in the hearts of diabetic rats may contribute to the decreased mitochondrial protein synthesis.

Paper Electrophoresis of Serum Proteins in Control and Diabetic Rats

1958 ◽  
Vol 193 (1) ◽  
pp. 79-82 ◽  
Author(s):  
Ruth D. Peterson ◽  
Clarissa H. Beatty
Keyword(s):  
Serum Protein ◽  
Serum Proteins ◽  
Diabetic Rats ◽  
Female Rats ◽  
Male Rats ◽  
Protein Patterns ◽  
Control Male ◽  
Partial Pancreatectomy ◽  
Male And Female Rats ◽  
Γ Globulins

A comparison of serum protein fractions (electrophoretic separation) between fed female control and alloxan diabetic rats indicates a decrease in percentage albumin and an increase in percentage α2-, ß- and γ-globulins. Total protein also decreased and so did the grams percentage albumin and α1-globulin, while the grams percentage ß-globulin rose. In the depancreatized series there was a decrease in both percentage and grams percentage albumin and α1-globulin and an increase in the percentage and grams percentage ß- and γ-globulins. With the exception of a rise in γ-globulin, sham operated rats showed no change in any category. Control male rats have higher α1 and lower γ-globulin values than female rats, but both male and female rats show the same changes following the production of diabetes by either alloxan administration or partial pancreatectomy. Fasting control or diabetic rats 24 hours produces no change in the serum protein patterns despite the disappearance of observable lipemia during the fast.

Effects of β-glucan from Aureobasidium pullulans in a Streptozotocininduced Rat Diabetes Model

2020 ◽  
Vol 16 (7) ◽  
pp. 1052-1063
Author(s):  
Jae-Hak Sohn ◽  
Joo Wan Kim ◽  
Jong-Min Lim ◽  
Go-Woon Jung ◽  
Sae Kwang Ku ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Blood Glucose ◽  
Diabetic Complications ◽  
Aureobasidium Pullulans ◽  
Diabetic Rats ◽  
Female Rats ◽  
Diabetic Rat ◽  
Glucose Levels ◽  
Diabetes Model ◽  
Serum Aspartate Aminotransferase

Background: The alleviating effects of diabetic nephropathy and hepatopathy of β-glucan were evaluated in this study. Objective: The anti-diabetic effects of β -glucan from Aureobasidium pullulans were assessed in a streptozotocin (STZ)-induced rat diabetes model at 62.5 and 125 mg/kg doses. In addition, the possibility of changes in the effects of β-glucan according to the severity of diabetes was also assessed at one dosage (62.5 mg/kg): severe, >360 mg/dL; slight, 130-200 mg/dL. Methods: Test articles were administered orally to STZ-induced diabetic rats from 21 days after STZ dosing for 4 weeks. Each of five or six female rats per group was selected using blood glucose levels at 21 days after STZ dosing. Changes in body weight were recorded during the study, along with blood glucose, blood urea nitrogen, creatinine, and serum aspartate aminotransferase and alanine aminotransferase levels. On the day of sacrifice, livers and kidneys were weighed and observed microscopically for changes in the percentage of degenerative regions and numbers of degenerative tubules in the kidney. Results: β-glucan showed no hypoglycemic effects in the STZ-induced diabetic rat model. However, it had favorable effects on decreasing diabetic complications related to diabetic nephropathy and hepatopathy. Conclusion: Based on the results of this study, it was concluded that β-glucan showed favorable effects in decreasing diabetic complications in STZ-induced rat diabetes model.

Gender differences in ANG II levels and action on multiple K+ current modulation pathways in diabetic rats

2004 ◽  
Vol 287 (1) ◽  
pp. H311-H319 ◽  
Author(s):  
Yakhin Shimoni ◽  
Xiu-Fang Liu
Keyword(s):  
Gender Differences ◽  
Protein Kinase ◽  
Tyrosine Kinases ◽  
Enzyme Inhibitor ◽  
Diabetic Rats ◽  
Female Rats ◽  
Ang Ii ◽  
Control Male ◽  
Male And Female Rats ◽  
In Cells

Gender differences were studied in ventricular myocytes from insulin-deficient (Type 1) diabetic rats. Cells were obtained by enzymatic dispersion of hearts from control male and female rats and from rats made diabetic with streptozotocin (100 mg/kg) 7–14 days before experiments. ANG II content, measured by ELISA, was augmented in diabetic males but unaltered in diabetic females. In diabetic ovariectomized females, ANG II levels were augmented as in males. ANG II affects multiple cellular pathways including activation of protein kinase C (PKC) and several tyrosine kinases as well as inhibition of protein kinase A (PKA). The involvement of these pathways in modulating outward K+ currents was studied. Transient and sustained outward K+ currents were measured using the whole cell voltage-clamp method. In males, these currents are attenuated under diabetic conditions but are augmented by the ANG II-converting enzyme inhibitor quinapril. Activation of PKA by 8-bromo-cAMP enhanced both K+ currents in cells from diabetic males. The augmentation of these currents by quinapril was blocked when PKA inhibition was maintained with the Rp isomer of 3′,5′-cyclic monophosphorothioate. Inhibition of tyrosine kinases by genistein also augmented K+ currents in cells from diabetic males. Action potentials were abbreviated by 8-bromo-cAMP and genistein. However, both genistein and 8-bromo-cAMP had no effect on K+ currents in cells from diabetic females. In cells from ovariectomized diabetic females, 8-bromo-cAMP and genistein enhanced these K+ currents as in males. Inhibition of PKC augmented the transient and sustained K+ currents in cells from diabetic males and females. A contribution of non-ANG II-dependent activation of PKC is suggested. These results describe some of the mechanisms that may underlie gender-specific differences in the development of cardiac disease and arrhythmias.

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