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 Serum Proinsulin in Bangladeshi Subjects with Impaired Glucose Tolerance

2015 ◽  
Vol 7 (2) ◽  
pp. 41-46
Author(s):  
S Sultana ◽  
Z Zeba ◽  
A Hossain ◽  
A Khaleque ◽  
R Zinnat ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Glucose Load ◽  
Fasting Serum ◽  
Insulin Secretory Capacity ◽  
Proinsulin Level ◽  
Secretory Capacity

Hyperproinsulinemia is commonly present in subjects with impaired glucose tolerance. The present study was undertaken to investigate the proinsulin level in Bangladeshi IGT subjects and to explore its association with insulin resistance. This observational study was conducted under a case-control design with IGT subjects (n=50) and controls (n=44). IGT was diagnosed following the WHO Study Group Criteria. Serum glucose was measured by glucose-oxidase method, serum lipid profile by enzymatic method and serum insulin and serum proinsulin were measured by ELISA method. Insulin secretory capacity (HOMA%B) and insulin sensitivity (HOMA%S) were calculated from fasting serum glucose and fasting serum insulin by homeostasis model assessment. The study subjects were age- and BMI- matched. Mean (±SD) age (yrs) of the control and IGT subjects were 40±6 and 40±5 respectively (p=0.853). Mean (±SD) BMI of the control and IGT subjects were 23±3 and 22±2 respectively (p=0.123). Fasting glucose was not significantly higher in IGT subjects, but serum glucose 2 hours after 75 gm glucose load was significantly higher in IGT subjects. Median (Range) value of fasting serum glucose (mmol/l) of control and IGT subjects were 5.3 (3.8-6) and 5.2 (4-12) respectively; (p=0.297). Median (Range) value of serum glucose (mmol/l) 2 hours after 75 gm glucose load of control and IGT subjects were 6.1 (3-7.8) and 7.9 (5- 21) respectively; (p=0.001). Fasting TG was significantly higher in IGT subjects and LDL-c was significantly lower in IGT subjects. Serum Total cholesterol and HDL-c were not significantly different between the IGT and control subjects. Median (Range) value of fasting serum TG (mg/dl) of control and IGT subjects were 119 (51-474) and 178 (82-540) respectively; (p=0.001). Median (Range) value of fasting serum T chol (mg/dl) of control and IGT subjects were 180 (65-272) and 186 (140-400) respectively; (p=0.191). Median (Range) value of fasting serum HDL-C (mg/dl) of control and IGT subjects were 29 (19-45) and 31 (15-78) respectively; (p=0.914). Median (Range) value of fasting serum LDL-C (mg/dl) of control and IGT subjects were 117(29-201) and 111(41- 320) respectively; (p=0.001). Fasting serum proinsulin was significantly higher in IGT subjects. Median (Range) value of fasting serum proinsulin (pmol/l) of control and IGT subjects were 9.2(1.8-156) and 17(3-51) respectively; (p=0.001). Insulin secretory capacity (HOMA%B) was higher but insulin sensitivity (HOMA%S) was significantly lower in case of IGT subjects. Median (Range) value of HOMA%B of control and IGT subjects were 97(46-498) and 164(17-300) respectively; (p=0.001). Median (Range) value of HOMA%S of control and IGT subjects were 68(19-270) and 39(15-110) respectively (p=0.001). In multiple regression analysis a significant negative association was found between fasting proinsulin and insulin sensitivity (p=0.037). The data led to the following conclusions: a) Insulin resistance is the predominant defect in Bangladeshi IGT subjects. b) Basal proinsulin level is significantly increased in IGT subjects. c) Insulin resistance is negatively associated with serum proinsulin in IGT subjects. DOI: http://dx.doi.org/10.3329/bjmb.v7i2.22411 Bangladesh J Med Biochem 2014; 7(2): 41-46

Bicycling but not Walking Is Independently Associated With Fasting Insulin in Abdominally Obese Women

2011 ◽  
Vol 8 (6) ◽  
pp. 820-823 ◽  
Author(s):  
Erik Hemmingsson ◽  
Ulf Ekelund ◽  
Joanna Udden
Keyword(s):  
Insulin Resistance ◽  
Body Fat ◽  
Abdominal Obesity ◽  
Serum Insulin ◽  
Whole Body ◽  
Obese Women ◽  
Fasting Serum ◽  
Insulin Levels ◽  
The Impact

Background:The impact of walking and bicycling on insulin resistance (IR) in women with abdominal obesity is unclear.Methods:Pooled analysis of data from a randomized trial on physically active commuting (bicycling + walking vs walking only) in women with abdominal obesity [n = 98; age:47.3 ± 7.6 yrs; waist circumference (WC):103.1 ± 7.8 cm]. Bicycling and walking data were collected during 7 consecutive days by trip meters (Trelock FC-410) and pedometers (Yamax digiwalker SW-200) at baseline, 2, 4, and 6 months. Owing to a skew distribution we analyzed bicycling as a binary dummy variable with a 10 km/week cut-off. Fasting serum insulin and homeostatic model assessment – insulin resistance (HOMA-IR) were assessed at baseline and 6 months, as were body mass index (BMI), WC, and dual x-ray absorptiometry (DXA)-assessed % whole-body fat.Results:Increased bicycling by 10 km/wk was associated with reductions in fasting serum insulin at follow-up independent of age, treatment allocation, baseline phenotype, Δ walking, and Δ % body fat (β = −10.9, P = .042), but not HOMA-IR (β = −2.0, P = .13). Increased walking was not associated with fasting serum insulin (P = .33) or HOMA-IR (P = .44) at follow-up, after adjustment for the same covariates and Δ bicycling.Conclusion:Increased bicycling but not walking was associated with reduced insulin levels at follow-up. Bicycling may be more effective than walking for reducing insulin levels in abdominally obese women.

scholarly journals Fasting serum insulin levels and insulin resistance are associated with colorectal adenoma in Koreans

2013 ◽  
Vol 5 (3) ◽  
pp. 297-304 ◽  
Author(s):  
Eun Hee Kim ◽  
Hong-Kyu Kim ◽  
Sung Jin Bae ◽  
Hye-Sook Chang ◽  
Hye Won Park ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Colorectal Adenoma ◽  
Serum Insulin ◽  
Fasting Serum ◽  
Insulin Levels

scholarly journals Short-term high-fat feeding induces islet macrophage infiltration and β-cell replication independently of insulin resistance in mice

2016 ◽  
Vol 311 (4) ◽  
pp. E763-E771 ◽  
Author(s):  
David C. Woodland ◽  
Wei Liu ◽  
Jacky Leong ◽  
Mallory L. Sears ◽  
Ping Luo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Serum Insulin ◽  
Cell Replication ◽  
Fat Pad ◽  
High Fat ◽  
Fasting Serum ◽  
Β Cell ◽  
Short Term ◽  
Insulin Levels

Short-term high-fat consumption stimulates mouse islet β-cell replication through unknown mechanisms. Resident macrophages (MΦs) are capable of secreting various factors involved in islet development and tissue remodeling. We hypothesized that a short-term high-fat diet (HFD) promotes MΦ infiltration in pancreatic islets and that MΦs serve as a regulator of β-cell replication. To test these hypotheses and dissect mechanisms involved in HFD-induced β-cell replication, adult C57BL/6J mice were fed a HFD for 7 days with or without administration of clodronate-containing liposomes, an MΦ-depleting agent. Mouse body and epididymal fat pad weights, and nonfasting blood glucose and fasting serum insulin levels were measured, and pancreatic islet β-cell replication, oxidative stress, and MΦ infiltration were examined. Short-term HFD promoted an increase in body and epididymal fat pad weight and blood glucose levels, along with an increased fasting serum insulin concentration. β-Cell replication, islet MΦ infiltration, and the percentage of inducible NO synthase positive MΦs in the islets increased significantly in mice fed the HFD. Immunofluorescence staining for 8-oxo-2′-deoxyguanosine or activated caspase-3 revealed no significant induction of DNA damage or apoptosis, respectively. In addition, no change in stromal-derived factor 1-expressing cells was found induced by HFD. Despite continuous elevation of nonfasting blood glucose and fasting serum insulin levels, depletion of MΦs through treatments of clodronate abrogated HFD-induced β-cell replication. These findings demonstrated that HFD-induced MΦ infiltration is responsible for β-cell replication. This study suggests the existence of MΦ-mediated mechanisms in β-cell replication that are independent of insulin resistance.

scholarly journals Study of Serum Insulin Level in Hypertensive Patients

1970 ◽  
Vol 4 (1) ◽  
pp. 13-16
Author(s):  
MN Uddin ◽  
MZ Ali ◽  
NWB Jahan ◽  
MA Rashid ◽  
MK Sultan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Serum Insulin ◽  
Study Groups ◽  
Serum Glucose ◽  
Ionized Calcium ◽  
Hypertensive Patients ◽  
Significant Difference ◽  
Serum Ionized Calcium ◽  
The Relationship

Background and aims: Hypertension is a frequent and almost ubiquitous health disorder, prevalent both in developed and developing countries. Hyperinsulinemia and insulin resistance have been suggested to be closely associated with the pathogenesis of essential hypertension. However there is considerable controversy in this regards. The present study was designed to explore the relationship between serum insulin and serum ionized calcium in non diabetic and diabetic hypertensive subjects. Subjects and Methods: A total of 57 hypertensive and diabetic hypertensive patients attending out patients department of the BIRDEM and NICVD were included in the study. Fasting serum glucose was measured by glucose oxidase method, lipid profile was measured by enzymatic method. Serum insulin was measured by Enzyme Linked Immunosorbent assay (ELISA) method and serum ionized calcium by the Ion Sensitive Electrode (ISE) technique. Results: Glucose-insulin ratios were calculated as the index for insulin. Serum insulin (pmol/ml), Mean ± SD, 147 ± 48 in DC and 170 ± 80 in DH groups vs 118 ± 21 in NC and 120 ± 41 in EH groups, p= 0.023 and p= 0.031 respectively. Although, from the serum insulin results, the diabetic groups seemed to have insulin resistance, the glucose-insulin ratios in the two groups were significantly lower compared to nondiabetic groups (Glucose-insulin ratio, mmol/pmol, 0.066 ± 0.025 in DC, 0.074 ± 0.025 in DH vs 0.044 ± 0.11 in NC, 0.043 ± 0.012 in EH, p= 0.005 - 0.0001). The serum ionized calcium in the healthy subject, first time reported in the country by an up to date method (1.17 ± 0.05 M ± SD), were within the range found in healthy subjects of the other populations. No significant difference in the serum Ca2+ could be found between any of the study groups. Also, serum Ca2+ did not correlate with blood pressure, glucose or insulin in any of the study groups or with all the patients as a whole. Serum total cholesterol, triglyceride, HDLc and LDLc levels in the DC, EH and DH group did not show any significant difference compared to NC group and among the groups. The lipid abnormality as reflected by the mean LDL-HDL cholesterol ratios was the highest in the DH group but the differences were not statistically significant compared to the NC, DC and EH group. Conclusions: The data suggest the following conclusions: a) Serum ionized calcium level in our population is similar to that reported for other population. b) Serum glucose and insulin by themselves do not have any direct influence on serum ionized calcium. c) Non obese diabetes mellitus subjects in our population do not show insulin resistance as the primary defect. Rather, there is significant decompensation of the insulin secretory capacity in the subjects. d) Insulin resistance should be measured directly in relation to blood pressure and Ca2+ in appropriate groups of subjects to explore the relationship between insulin resistance, hyperinsulinemia and serum ionized calcium. Keywords: Serum Insulin; Hypertension DOI: http://dx.doi.org/10.3329/cardio.v4i1.9384 Cardiovasc. J. 2011; 4(1): 13-16

Insulin resistance and blood pressure in Dahl rats and in one-kidney, one-clip hypertensive rats

1991 ◽  
Vol 261 (6) ◽  
pp. E692-E697 ◽  
Author(s):  
T. A. Kotchen ◽  
H. Y. Zhang ◽  
M. Covelli ◽  
N. Blehschmidt
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Genetic Model ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Oral Glucose ◽  
Hypertensive Rats ◽  
Insulin Resistant ◽  
Sucrose Feeding ◽  
The One

In normal rats, sucrose feeding results in insulin resistance and an elevation of arterial pressure. The purpose of this study was twofold: 1) to evaluate the effect of sucrose feeding on blood pressure in a genetic model and in an acquired model of hypertension and 2) to determine whether these models of hypertension are associated with insulin resistance. In Dahl salt-resistant (Dahl-R) rats on both a 0.45 and a 3% NaCl intake, systolic blood pressures were higher (P less than 0.01) in sucrose-drinking than in water-drinking animals. In contrast, blood pressure was not affected by dietary sucrose in Dahl salt-sensitive (Dahl-S) rats. Blood pressure was also not affected by sucrose in the one-kidney, one-clip (1K,1C) hypertensive rat. In response to an oral glucose load, serum glucose was similar in Dahl-R and Dahl-S rats, although serum insulin was higher (P less than 0.05) in Dahl-S rats, suggesting that Dahl-S rats are insulin resistant. In contrast, glucose and insulin responses were similar in hypertensive 1K,1C animals and normotensive controls. In conclusion, sucrose feeding increased blood pressure in Dahl-R but not in Dahl-S or 1K,1C hypertensive rats. Additionally, Dahl-S rats, but not hypertensive 1K,1C rats, are insulin resistant.

scholarly journals Fasting serum insulin levels and insulin resistance are associated with blood rheology in Japanese young adults without diabetes

2016 ◽  
Vol 44 (3) ◽  
pp. 496-507 ◽  
Author(s):  
Kensuke Yoshida ◽  
Takao Kimura ◽  
Tomoyuki Aoki ◽  
Katsuhiko Tsunekawa ◽  
Osamu Araki ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Young Adults ◽  
Serum Insulin ◽  
Blood Rheology ◽  
Fasting Serum ◽  
Insulin Levels

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.

scholarly journals The effects of metformin plus sulfonylurea therapy on clinical features of the metabolic syndrome

2010 ◽  
Vol 63 (9-10) ◽  
pp. 611-615 ◽  
Author(s):  
Branka Koprivica ◽  
Teodora Beljic-Zivkovic ◽  
Tatjana Ille
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Body Mass Index ◽  
Waist Circumference ◽  
Glycemic Control ◽  
Body Mass ◽  
Combined Therapy

Introduction. Insulin resistance is a well-known leading factor in the development of metabolic syndrome. The aim of this study was to evaluate metabolic effects of metformin added to sulfonylurea in unsuccessfully treated type 2 diabetic patients with metabolic syndrome. Material and methods. A group of thirty subjects, with type 2 diabetes, secondary sulfonylurea failure and metabolic syndrome were administered the combined therapy of sulfonylurea plus metformin for six months. Metformin 2000 mg/d was added to previously used sulfonylurea agent in maximum daily dose. Antihypertensive and hypolipemic therapy was not changed. The following parameters were assessed at the beginning and after six months of therapy: glycemic control, body mass index, waist circumference, blood pressure, triglycerides, total cholesterol and its fractions, homeostatic models for evaluation of insulin resistance and secretion (HOMA R, HOMA B) and C- peptide. Results. Glycemic control was significantly improved after six months of the combined therapy: (fasting 7.89 vs. 10.61 mmol/l. p<0.01; postprandial 11.12 vs. 12.61 mmol/l. p<0.01, p<0.01; glycosylated hemoglobin 6.81 vs. 8.83%. p<0.01). the body mass index and waist circumference were significantly lower (26.7 vs. 27.8 kg/m2, p<0.01 and 99.7 vs. 101.4 cm for men, p<0.01; 87.2 vs. 88.5 for women, p<0.01). Fasting plasma triglycerides decreased from 3.37 to 2.45 mmol/l (p<0.001) and HOMA R from 7.04 to 5.23 (p<0.001). No treatment effects were observed on blood pressure, cholesterol, and residual insulin secretion. Conclusion. Administration of metformin in type 2 diabetes with metabolic syndrome decreased cardiovascular risk factors by reducing glycemia, triglycerides, BMI, central obesity and insulin resistance.

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