scholarly journals Insulin treatment and myocardial function in isolated, perfused heart from diabetic rat.

1984 ◽  
Vol 48 (3) ◽  
pp. 255-265 ◽  
Author(s):  
SEIBU MOCHIZUKI ◽  
SHIN-ICHIRO ISHIKAWA ◽  
MASAKAZU ABE
1983 ◽  
Vol 61 (5) ◽  
pp. 516-523 ◽  
Author(s):  
Arun G. Tahiliani ◽  
Rao V. S. V. Vadlamudi ◽  
John H. McNeill

Isolated perfused hearts from diabetic rats exhibit a decreased responsiveness to increasing work loads. However, the precise time point at which functional alterations occur is not clearly established. Previous observations in our laboratory have suggested that the alterations in myocardial function are not apparent at 30 days whereas they are clearly seen 100 days after streptozotocin-induced diabetes. We studied the cardiac function of 6-week diabetic rats using the isolated perfused heart preparation. The 6-week time period was found to be sufficient to cause depression of myocardial function in these animals. We also studied the effect of insulin treatment on myocardial performance of diabetic rats. Insulin treatment was initiated 3 days and 6 weeks after injection of streptozotocin (STZ). The treatment was continued for 6 and 4 weeks in the respective groups. Hearts from 6-week diabetic animals exhibited a depressed left ventricular developed pressure (LVDP) and positive and negative dP/dt at higher filling pressures when compared with 6-week control animals. However, the depression was not seen in the 6-week insulin-treated diabetic animals. Ten-week diabetic rat hearts also showed a depression of LVDP and positive and negative dP/dt when compared with 10-week controls. The group of animals that had been diabetic for 6 weeks and then treated for 4 weeks with insulin exhibited a reversal of the depressed myocardial function. These results demonstrate that depression of myocardial performance, which is evident 6 weeks after diabetes is induced, can be prevented if insulin treatment is initiated as the disease is induced. Further, insulin treatment is capable of reversing the abnormalities after they have occurred.


1998 ◽  
Vol 89 (Supplement) ◽  
pp. 136A
Author(s):  
R. Murtaza ◽  
A. Mahmood ◽  
R. Igic ◽  
A. P. Winnie

1987 ◽  
Vol 252 (5) ◽  
pp. E673-E678 ◽  
Author(s):  
C. D. Wolleben ◽  
S. R. Jaspers ◽  
T. B. Miller

The use of adult rat cardiomyocytes to model cardiac glycogen metabolism was investigated by monitoring the response of glycogen phosphorylase and glycogen synthase to epinephrine and insulin treatment. Cardiomyocytes derived from normal rats respond to epinephrine in the range of 1 X 10(-7) to 5.5 X 10(-6) M epinephrine with an increase in the percent of phosphorylase in the AMP-independent form from 11.5 to 24.8%. In the same cells, insulin in the range of 10(-9) to 10(-7) M increased the glucose 6-phosphate independent form of glycogen synthase from 30.5 to 40.5%. Cells derived from alloxan-diabetic hearts exhibit a hypersensitive phosphorylase activation and a refractile synthase inactivation in response to epinephrine treatment. This pattern is similar to that recorded using perfused heart preparations. The data presented suggests that adult rat cardiomyocytes represent a valid model of glycogen metabolism in both the normal and alloxan-diabetic rat.


1985 ◽  
Vol 12 (6) ◽  
pp. 573-576 ◽  
Author(s):  
B. V. Venkataraman ◽  
P. S. Shetty ◽  
Thangam Joseph ◽  
H. Mohamed Arifullah ◽  
P. M. Stephen

2003 ◽  
Vol 22 (6) ◽  
pp. 423-427 ◽  
Author(s):  
Mary Otsyula ◽  
Matthew S. King ◽  
Tonya G. Ketcham ◽  
Ruth A. Sanders ◽  
John B. Watkins

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.


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