Comparative evaluation of atenolol and metoprolol on cardiovascular complications associated with streptozotocin-induced diabetic rats

2007 ◽  
Vol 85 (8) ◽  
pp. 831-836 ◽  
Author(s):  
Shraddha V. Bhadada ◽  
Ramesh K. Goyal
Keyword(s):  
Heart Rate ◽  
Serum Insulin ◽  
Cardiovascular Complications ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Diabetic Patients ◽  
Cardiac Tissues ◽  
Insulin Levels ◽  
Beneficial Effects ◽  
Glucose Levels

Recently, various clinical studies have indicated that lipophilic β-blockers reduce the coronary mortality in diabetic patients; however, systematic studies have not been reported. The objective of the present investigation was to compare the effects of chronic treatment with metoprolol and atenolol on cardiovascular complications in streptozotocin (STZ)-induced diabetic rats. Injection of STZ produced hyperglycemia, hypoinsulinemia, hyperlipidemia, increased blood pressure, cardiac hypertrophy, reduction in heart rate, and structural alterations in cardiac tissues. Metoprolol and atenolol effectively prevented the development of hypertension in diabetic rats. Metoprolol treatment produced a slight but significant reduction in serum glucose levels with elevation in serum insulin levels, while atenolol produced a slight increase in glucose levels but no effect on insulin levels. Moreover, neither metoprolol nor atenolol treatment reduced the elevated cholesterol levels in diabetic rats. Metoprolol treatment significantly prevented STZ-induced increase in triglyceride levels, but atenolol failed to produce this effect. Metoprolol exhibited a minimal improvement in STZ-induced bradycardia, whereas atenolol produced a further reduction in heart rate. Histological examination showed metoprolol treatment also prevented STZ-induced hypertrophy and some of the alterations in cardiomyocytes. In conclusion, our data suggest that metoprolol has some beneficial effects over atenolol with respect to cardiovascular complications associated with diabetes mellitus.

Hepatoprotective effects of selenium during diabetes in rats

2015 ◽  
Vol 35 (2) ◽  
pp. 114-123 ◽  
Author(s):  
C Zou ◽  
Q Qiu ◽  
H Chen ◽  
L Dou ◽  
J Liang
Keyword(s):  
Enzyme Activities ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Total Glutathione ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Selenium Treatment ◽  
Male Wistar Rats

The present study investigated the hepatoprotective role of selenium during alloxan-induced diabetes in rats. Male Wistar rats were divided into four groups, namely, normal control, selenium treated, diabetic, and selenium-treated diabetic. Diabetes was induced in the animals by injecting alloxan intraperitoneally at a dose rate of 150 mg/kg body weight. Selenium in the form of sodium selenite was supplemented to rats at a dose level of 1 ppm in drinking water, ad libitum for two time durations of 2 and 4 weeks. The effects of different treatments were studied on various parameters in rat liver, which included serum glucose levels, serum insulin levels, alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lipid peroxidation (LPO), glutathione reduced (GSH), oxidized glutathione (GSSG), total glutathione (TG), superoxide dismutase (SOD), catalase (CAT), glutathione reductase, glutathione peroxidase, metallothionein (MT), and histoarchitecture. A significant increase in the serum glucose levels, LPO levels, and in enzyme activities of ALP, ALT, and AST was observed in diabetic rats which, however, got decreased significantly upon supplementation with selenium. On the contrary, decreased enzyme activities of GSSG, SOD, and CAT and depressed levels of GSH as well as serum insulin levels were observed in diabetic rats which got improved following selenium supplementation. Interestingly, MT levels were increased both in diabetic and selenium-treated diabetic rats. Further, marked alterations in histoarchitecture were seen in diabetic rats with the prominent features being congestion in sinusoids, lipid accumulation, and centrilobular hepatocyte degeneration. However, selenium treatment to diabetic rats showed overall improvement in the hepatic histoarchitecture.

Hypothalamic noradrenergic and sympathoadrenal control of glycemia after stress

1989 ◽  
Vol 256 (2) ◽  
pp. E231-E235
Author(s):  
G. A. Smythe ◽  
W. S. Pascoe ◽  
L. H. Storlien
Keyword(s):  
Insulin Release ◽  
Acute Stress ◽  
Serum Insulin ◽  
Elevated Serum ◽  
Serum Glucose ◽  
Neural Pathways ◽  
Swim Stress ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Positive Correlations

Central noradrenergic pathways play a significant role in mediating blood glucose levels after neuroglycopenia. To further investigate hypothalamic noradrenergic neuronal activity (NNA) and sympathoadrenal influences in glucoregulation, we studied the effects of acute stress on glycemia and insulin release in normal and adrenalectomized (ADRX) rats. Within 5 min of exposure of rats to ether or cold-swim stress, significant positive correlations were evident between hypothalamic NNA and serum glucose levels (r = 0.70, P less than 0.001; at 15 min r = 0.78, P less than 0.0001). Five minutes after stress in the intact rat, insulin release was inhibited and serum insulin levels inversely correlated to hypothalamic NNA (r = 0.45, P less than 0.05). This relationship between insulin and NNA was no longer present 15 min after stress, but the levels of insulin remained inappropriately low with respect to the elevated serum glucose levels (approximately 30% above basal). Blockade of sympathetic noradrenergic pathways by treatment of intact rats with guanethidine prevented the rise in glucose after cold-swim stress but did not prevent the inhibition of insulin release. Fifteen minutes after exposure of ADRX rats to cold-swim stress their hypothalamic NNA and serum glucose levels were similar to intact animals. However, in contrast to their intact counterparts, serum insulin levels were significantly elevated (P less than 0.01). These data are consistent with central noradrenergic neural pathways directly mediating hepatic glucose release and indirectly inhibiting pancreatic insulin release via activation of adrenal medullary catecholamines.

scholarly journals Effect of in ovo ghrelin administration on subsequent serum insulin and glucose levels in newly-hatched chicks

2011 ◽  
Vol 56 (No. 8) ◽  
pp. 377-380 ◽  
Author(s):  
A. Lotfi ◽  
H. Aghdam-Shahryar ◽  
J. Ghiasi-Ghalehkandi ◽  
H. Kaiya ◽  
N. Maheri-Sis
Keyword(s):  
Animal Species ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Avian Embryo ◽  
Regulatory Peptide ◽  
In Ovo ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Hatching Time ◽  
Embryonic Life

Ghrelin is a regulatory peptide in glucose homeostasis in animal species. Its effect in the avian embryo is unclear. The aim of this study was to investigate the effects of in ovo ghrelin administration on serum glucose and insulin levels of hatched chicks. A total of 250 fertilized eggs were divided into 5 groups; group T1 as control (without injection), group T2 (in ovo injected with 50 ng/egg ghrelin on day 5), group T3 (in ovo injected with 100 ng/egg ghrelin on day 5), group T4 (in ovo injected with 50 ng/egg ghrelin on day 10) and group T5 (in ovo injected with 100 ng/egg ghrelin on day 10). After hatching, serum insulin and glucose concentrations were determined. Group T4 and T5 showed significantly higher serum insulin levels (0.43 and 0.60 ng/ml, respectively) compared with T1, T2 and T3 (0.09, 0.10, and 0.23 ng/ml, respectively) in hatched chicks. Glucose concentrations have not been affected by in ovo administered ghrelin in all injected groups. It seems that embryonic β-cells were stimulated to secrete a considerable level of insulin in response to in ovo ghrelin in the late embryonic life. The observed stability of glucose rate suggests the incidence of insulin resistance at hatching time or in newly hatched chicks from in ovo ghrelin administered eggs on day 10.

Therapeutic insights of hydromehtanolic leaf extract of Xanthium indi-cum and α-tocopherol in streptozotocin induced diabetic renal oxidative stress

2017 ◽  
Vol 6 (5) ◽  
pp. 158-166
Author(s):  
Anila Devi Meruva ◽  
Ravi Sahukari ◽  
Venkata Subbaiah Ganjikunta ◽  
Shanmugam Bhasha ◽  
Sathyavelu Reddy Kesireddy
Keyword(s):  
Blood Glucose ◽  
Serum Insulin ◽  
Microvascular Complications ◽  
Diabetic Rats ◽  
Albino Rats ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Body Weights ◽  
Mda Content

Diabetic nephropathy (DN) is one of the important microvascular complications of diabetes mellitus. Several phytochemicals have been reported to show beneficial consequences in Xanthium indicum leaves and α-tocopherol is a well known antioxidant, putting a halt to the fatality of renal dysfunc-tions in DN. In the current study, seven groups of male albino rats six in each group, received the following treatment scheduled for 4 weeks: Normal control, Xanthium indicum, α-tocopherol, Diabetes control, Glibenclamaide treated diabetic, α-tocopherol treated diabetic and Xanthium treated diabetic. Evaluations were made for blood glucose levels, body weights, serum insulin levels, MDA content, creatintne in urine as well as in serum and the histopathological changes were monitored kidney tissues in all experimental rats. Blood glucose levels were significantly (***P<0.001) decreased whereas serum insulin levels and body weights were significantly (***P< 0.001) in-creased, MDA content, serum creatinine levels were significantly (***P< 0.01), (***P<0.001), decreased and urine creatinine levels were increased with the treatment of plant extract and α-tocopherol in diabetic rats. Overall, the findings of this study indicated that the hydromethanolic extract of X. indicum leaves and α-tocopherol possesses a potent capacity that attenuates the renal damage to minimize the deleterious effects of free radicals by maintaining renal hemodynamics in diabetic conditions probably through its antioxidative and hypoglycaemic activity.

Comparative effectiveness of carvedilol and propranolol on glycemic control and insulin resistance associated with l-thyroxin-induced hyperthyroidism — an experimental study

2007 ◽  
Vol 85 (5) ◽  
pp. 514-520 ◽  
Author(s):  
Parloop Bhatt ◽  
Dharmesh Makwana ◽  
Devdas Santani ◽  
Ramesh Goyal
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Heart Rate ◽  
Body Mass ◽  
Serum Insulin ◽  
Area Under The Curve ◽  
Serum Glucose ◽  
Fasting Serum ◽  
Insulin Levels ◽  
Propranolol Treatment

The present study was undertaken to investigate the effectiveness of adrenergic antagonists carvedilol and propranolol on l-thyroxin-induced cardiovascular and metabolic disturbances in rats. Treatment with l-thyroxin sodium (75 mg/kg body mass, s.c., every alternate day for 3 weeks), produced a significant increase in food and water intake, body temperature, heart rate, systolic blood pressure, along with an increase in serum T3, T4, and triglyceride levels. Besides a significant reduction in body mass, serum levels of TSH and cholesterol were also reduced following l-thyroxin treatment. Carvedilol (10 mg/kg body mass, orally) and propranolol (10 mg/kg body mass, i.p.) administered daily in the third week to 2 separate groups of l-thyroxin-treated animals reversed thyroxin-induced loss in body mass and rise in body temperature, blood pressure, and heart rate. Propranolol treatment increased TSH levels and decreased T3 and T4 levels in hyperthyroid animals, whereas carvedilol did not produce any effect on thyroid hormones. Carvedilol treatment reversed thyroxin induced hypertriglyceridemia, whereas propranolol treatment had no effect. Both carvedilol and propranolol prevented decrease in cholesterol levels induced by thyroxine. Compared with normal animals, l-thyroxin-treated animals showed a state of hyperglycemia, hyperinsulinaemia, impaired glucose tolerance, and insulin resistance, as inferred from elevated fasting serum glucose and insulin levels, higher area under the curve over 120 min for glucose, and decreased insulin sensitivity index (KITT). Propranolol and carvedilol treatment significantly decreased fasting serum glucose levels. Treatment with propranolol did not alter serum insulin levels, area-under-the-curve glucose, or KITT values. However, treatment with carvedilol significantly reduced area-under-the-curve glucose, decreased fasting serum insulin levels and significantly increased KITT values. In conclusion, carvedilol appears to produce favorable effects on insulin sensitivity and glycemic control and can therefore be considered as more efficacious adjunctive treatment than propranolol in hyperthyroidism.

scholarly journals Exercise Training Attenuates Upregulation of p47phoxand p67phoxin Hearts of Diabetic Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Neeru M. Sharma ◽  
Brandon Rabeler ◽  
Hong Zheng ◽  
Eugenia Raichlin ◽  
Kaushik P. Patel
Keyword(s):  
Exercise Training ◽  
Nadph Oxidase ◽  
Cardiac Function ◽  
Diabetic Cardiomyopathy ◽  
Underlying Mechanism ◽  
Diabetic Rats ◽  
Diabetic Patients ◽  
Cardiac Tissues ◽  
Beneficial Effects ◽  
Collagen Iii

Exercise training (ExT) is currently being used as a nonpharmacological strategy to improve cardiac function in diabetic patients. However, the molecular mechanism(s) underlying its beneficial effects remains poorly understood. Oxidative stress is known to play a key role in the pathogenesis of diabetic cardiomyopathy and one of the enzyme systems that produce reactive oxygen species is NADH/NADPH oxidase. The goal of this study was to investigate the effect of streptozotocin- (STZ-) induced diabetes on expression ofp47phoxandp67phox, key regulatory subunits of NADPH oxidase, in cardiac tissues and determine whether ExT can attenuate these changes. Four weeks after STZ treatment, expression ofp47phoxandp67phoxincreased 2.3-fold and 1.6-fold, respectively, in left ventricles of diabetic rats and these increases were attenuated with three weeks of ExT, initiated 1 week after onset of diabetes. In atrial tissues, there was increased expression ofp47phox(74%), which was decreased by ExT in diabetic rats. Furthermore, increased collagen III levels in diabetic hearts (52%) were significantly reduced by ExT. Taken together, ExT attenuates the increased expression ofp47phoxandp67phoxin the hearts of diabetic rats which could be an underlying mechanism for improving intracardiac matrix and thus cardiac function and prevent cardiac remodeling in diabetic cardiomyopathy.

Preventive effects of cyclohexenonic long-chain fatty alcohol on diabetic cystopathy in the rat

2006 ◽  
Vol 84 (2) ◽  
pp. 195-201 ◽  
Author(s):  
Hiroto Suzuki ◽  
Motoaki Saito ◽  
Yukako Kinoshita ◽  
Itaru Satoh ◽  
Tomoharu Kono ◽  
...  
Keyword(s):  
Serum Insulin ◽  
Urine Volume ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Dependent Manner ◽  
Diabetic Cystopathy ◽  
Insulin Levels ◽  
Functional Studies ◽  
Diabetic Status ◽  
Dose Dependent

In this study, we investigated the preventive effect of n-hexacosanol on diabetes-induced bladder dysfunction in the rat. Diabetes was induced in 8-week-old male Sprague–Dawley rats by administering an injection of streptozotocin (50 mg/kg, i.p.). The rats were randomly divided into 4 groups (age-matched control rats, diabetic rats without treatment with n-hexacosanol, and diabetic rats treated with n-hexacosanol (2 and 8 mg/kg, i.p. every day)) and maintained for 4 weeks. The serum glucose and serum insulin levels were determined, and the functions of bladder were estimated by voiding behavior, cystometric, and functional studies to carbachol and KCl. Furthermore, we examined possible diabetic induced histological changes in these rats. Treatment with n-hexacosanol did not alter diabetic status including body mass, bladder mass, and serum glucose and serum insulin levels, but significantly improved the maximum contraction pressure of the detrusor and residual urine volume in cystometric studies and Emax values to carbachol in functional studies in a dose-dependent manner. Diabetes induced bladder smooth muscle hypertrophy, which tended to be ameliorated by treatment with n-hexacosanol in a dose-dependent manner. Treatment with n-hexacosanol did not alter the diabetic status, but significantly improved diabetic cystopathy in a dose-dependent manner.

Insulin-sparing effect of hydroxychloroquine in diabetic rats is concentration dependent

1999 ◽  
Vol 77 (2) ◽  
pp. 118-123 ◽  
Author(s):  
Jaber Emami ◽  
Hertzel C Gerstein ◽  
Franco M Pasutto ◽  
Fakhreddin Jamali
Keyword(s):  
Therapeutic Potential ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Type I ◽  
Time Curve ◽  
Insulin Metabolism ◽  
Glucose Levels ◽  
Percent Change ◽  
Glucose Challenge

To study the effect of hydroxychloroquine (HCQ) on glucose and insulin homeostasis, healthy rats were dosed with160 mg·kg-1·day-1 of HCQ orally, and streptozocin-induced diabetic rats received 80, 120, and 160 mg·kg-1·day-1 of HCQ, while controls received normal saline. Ten days after treatment with HCQ, healthy animals were challenged intravenously with insulin or glucose, while diabetic rats were given only an i.v. injection of insulin. In healthy rats, the areas within and under the glucose concentration - time curve following insulin and glucose challenge were estimated. In diabetic animals, the areas under the curve for both the percent change in serum glucose from baseline (AUG) and the percent change in serum insulin from baseline (AUI) were used as pharmacodynamic end points. In healthy rats, HCQ did not influence fasting serum glucose concentrations or glycemic profiles following i.v. administration of glucose or insulin. In diabetic rats, AUG and AUI were increased dependent on blood HCQ concentrations. The normal homeostatic mechanisms responsible for insulin-glucose regulation may compensate for possible HCQ-induced reduction of insulin metabolism in healthy rats. The HCQ dose- or concentration-effect relationships for glucose and insulin were linear over the range of HCQ concentrations tested. It is concluded that HCQ significantly elevated insulin blood concentration resulting in reduced glucose levels in a concentration-dependent fashion in diabetic rats. HCQ may have therapeutic potential in the treatment of type I and type II diabetes.Key words: hydroxychloroquine, enantiomers, insulin, glucose, diabetes, pharmacokinetics.

scholarly journals Effects of Apocynin on Heart Muscle Oxidative Stress of Rats with Experimental Diabetes: Implications for Mitochondria

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 335
Author(s):  
Estefanía Bravo-Sánchez ◽  
Donovan Peña-Montes ◽  
Sarai Sánchez-Duarte ◽  
Alfredo Saavedra-Molina ◽  
Elizabeth Sánchez-Duarte ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Sensitivity ◽  
Cardiac Tissue ◽  
Diabetic Rats ◽  
Oxidase Inhibitor ◽  
Beneficial Effects ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Transport Chain ◽  
Male Wistar Rats

Diabetes mellitus (DM) constitutes one of the public health problems today. It is characterized by hyperglycemia through a defect in the β-cells function and/or decreased insulin sensitivity. Apocynin has been tasted acting directly as an NADPH oxidase inhibitor and reactive oxygen species (ROS) scavenger, exhibiting beneficial effects against diabetic complications. Hence, the present study’s goal was to dissect the possible mechanisms by which apocynin could mediate its cardioprotective effect against DM-induced oxidative stress. Male Wistar rats were assigned into 4 groups: Control (C), control + apocynin (C+A), diabetes (D), diabetes + apocynin (D+A). DM was induced with streptozotocin. Apocynin treatment (3 mg/kg/day) was applied for 5 weeks. Treatment significantly decreased blood glucose levels and insulin resistance in diabetic rats. In cardiac tissue, ROS levels were higher, and catalase enzyme activity was reduced in the D group compared to the C group; the apocynin treatment significantly attenuated these responses. In heart mitochondria, Complexes I and II of the electron transport chain (ETC) were significantly enhanced in the D+A group. Total glutathione, the level of reduced glutathione (GSH) and the GSH/ oxidized glutathione (GSSG) ratio were increased in the D+A group. Superoxide dismutase (SOD) and the glutathione peroxidase (GSH-Px) activities were without change. Apocynin enhances glucose uptake and insulin sensitivity, preserving the antioxidant defense and mitochondrial function.

Effects of cortisol and progesterone on insulin binding and lipogenesis in adipocytes from normal and diabetic rats

1985 ◽  
Vol 106 (2) ◽  
pp. 225-231 ◽  
Author(s):  
A.-M. Mendes ◽  
R. J. Madon ◽  
D. J. Flint
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Insulin Receptor ◽  
Body Weight Gain ◽  
Serum Insulin ◽  
Insulin Binding ◽  
Serum Glucose ◽  
Diabetic Rats ◽  
Receptor Concentration

ABSTRACT Cortisol implants in normal and diabetic rats reduced body weight, adiposity, insulin receptor concentration and both basal and insulin-stimulated rates of lipogenesis in isolated adipocytes, whilst insulin sensitivity was unchanged. In normal but not diabetic rats these changes were accompanied by increased serum glucose and insulin concentrations. In contrast, progesterone implants in normal and diabetic rats increased body weight gain, adiposity, insulin receptor concentration and both basal and insulin-stimulated rates of lipogenesis in adipose tissue, again without affecting insulin sensitivity. Progesterone did not affect serum insulin concentrations in normal or diabetic rats but accelerated the decline in serum glucose concentrations which occurred during an overnight fast in diabetic rats. The results suggest that (1) cortisol inhibits lipogenesis in adipose tissue without affecting insulin sensitivity, (2) cortisol reduces insulin binding in adipose tissue without a requirement for hyperinsulinaemia, which might itself indirectly lead to down-regulation of the insulin receptor, and (3) in diabetic rats progesterone stimulates lipogenesis in adipose tissue without any increase in food intake or serum insulin concentrations suggesting that progesterone may have a direct anabolic role in adipose tissue. J. Endocr. (1985) 106, 225–231

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