Effect of bradykinin and insulin on glucose oxidation in adipocytes from normal and streptozotocin diabetic rats

1988 ◽  
Vol 16 (6) ◽  
pp. 1012-1013 ◽  
Author(s):  
P. RUTH SYMINGTON ◽  
ALAN ASHFORD ◽  
GRAHAM S. BAILEY
Keyword(s):  
Glucose Oxidation ◽  
Diabetic Rats ◽  
Streptozotocin Diabetic Rats

Myocardial metabolic effects of in vivo hydralazine treatment of streptozotocin-diabetic rats

1991 ◽  
Vol 260 (2) ◽  
pp. H516-H521
Author(s):  
A. H. Burns ◽  
L. A. Burns ◽  
L. U. Jurenka ◽  
W. R. Summer
Keyword(s):  
Glucose Oxidation ◽  
Mechanical Response ◽  
Treated Group ◽  
Diabetic Rats ◽  
Metabolic Effects ◽  
Mechanical Function ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Streptozotocin Diabetic Rats

We determined myocardial pumping capacity, glucose oxidation, and mechanical response to ischemia in streptozotocin-diabetic rats treated for 4 wk with or without hydralazine (0.5 mg/g of chow). Plasma triglycerides and cholesterol were decreased 73 and 50%, respectively, in the treated animals. Blood glucose levels were greater than 400 mg/100 g in both groups. Hearts were perfused in the working configuration with buffer containing 5 mM [U-14C]glucose. Starling curves were constructed by increasing left atrial filling pressure from 5 to 20 cm of water. Diabetic heart mechanical function was depressed compared with control and hydralazine treatment restored function to normal. Oxidation of [U-14C]glucose was comparably depressed in the treated and untreated diabetics. The provision of 1 mM dichloroacetate in the perfusate increased glucose oxidation in the hearts from hydralazine-treated rats, however. Twenty minutes of global ischemia resulted in 65% decrease in mechanical function in the hearts of hydralazine-treated group vs. 15% for hearts from nontreated diabetics. The data suggest that measures to normalize lipid metabolism may not normalize myocardial glucose oxidation or permit better mechanical recovery after ischemia in the diabetic myocardium.

scholarly journals Adenosine effects on glucose oxidation of adipocytes isolated from streptozotocin-diabetic rats

1985 ◽  
Vol 232 (1) ◽  
pp. 301-304 ◽  
Author(s):  
E H Wong ◽  
J A Smith ◽  
L Jarett
Keyword(s):  
Glucose Oxidation ◽  
Diabetic Rats ◽  
Physiological Concentration ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats

Streptozotocin-induced diabetes did not impair the response of adipocytes to adenosine effects in glucose oxidation. The greatest effect of adenosine in potentiating the action of insulin was in the physiological concentration range of insulin (10-100 mu units/ml). The desensitization of cells by diabetes to the effects of insulin is therefore probably not related to the response of cells to adenosine.

Insulin binding and glucose metabolism in adipocytes of streptozotocin-diabetic rats.

1978 ◽  
Vol 235 (2) ◽  
pp. E175
Author(s):  
M Kasuga ◽  
Y Akanuma ◽  
Y Iwamoto ◽  
K Kosaka
Keyword(s):  
Glucose Metabolism ◽  
Glucose Transport ◽  
Glucose Oxidation ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Diabetic Rats ◽  
Glucose Transport System ◽  
Streptozotocin Diabetic Rats ◽  
Intracellular Glucose ◽  
Insulin Insensitivity

To investigate the mechanism of the cellular insulin insensitivity of diabetic rats, insulin binding, glucose transport, and glucose oxidation were studied in adipocytes from streptozotocin-diabetic rats. Increased insulin binding was found in cells from diabetic rats, and this was due to an increased number of insulin receptors rather than a change in receptor affinity. Basal and insulin-stimulated glucose oxidation was decreased in adipocytes from diabetic rats when the data are expressed in absolute terms or as percent increased above basal. Although the absolute rate of basal and insulin-stimulated glucose transport was decreased in adipocytes from diabetic rats, the percent increase above basal of insulin-stimulated glucose transport was not decreased. In conclusion, although the cellular insulin insensitivity exists in adipocytes from diabetic rats, the number of insulin receptors was increased, coupling between insulin receptors and the glucose transport system is intact in adipocytes from diabetic rats, and a defect in intracellular glucose metabolism rather than glucose transport plays a major role in the insulin insensitivity of adipocytes from diabetic rats.

scholarly journals Decreased activity of the heparan sulfate-modifying enzyme glucosaminyl N-deacetylase in hepatocytes from streptozotocin-diabetic rats

1991 ◽  
Vol 266 (14) ◽  
pp. 8671-8674
Author(s):  
E. Unger ◽  
I. Pettersson ◽  
U.J. Eriksson ◽  
U. Lindahl ◽  
L. Kjellén
Keyword(s):  
Heparan Sulfate ◽  
Diabetic Rats ◽  
Streptozotocin Diabetic Rats
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