scholarly journals In vivo quantification of removal of asialo-orosomucoid from the circulation in anaesthetized streptozotocin-diabetic rats

Diabetologia ◽  
1986 ◽  
Vol 29 (6) ◽  
pp. 383-387 ◽  
Author(s):  
M. Appel ◽  
P. Potrat ◽  
J. Feger ◽  
C. Mas-Chamberlin ◽  
G. Durand
Keyword(s):  
Diabetic Rats ◽  
Streptozotocin Diabetic Rats

Parotid Gland Function in Streptozotocin-diabetic Rats

1987 ◽  
Vol 66 (2) ◽  
pp. 425-429 ◽  
Author(s):  
L.C. Anderson
Keyword(s):  
Protein Composition ◽  
Diabetic Rats ◽  
Response Threshold ◽  
Maximal Response ◽  
Parotid Glands ◽  
Threshold Response ◽  
Parotid Acinar Cells ◽  
Streptozotocin Diabetic Rats ◽  
Gland Function

The in vivo response of parotid glands to adrenergic, cholinergic, and peptidergic agonists was studied in control, streptozotocin- (one month's duration), and insulin-treated (three hr) diabetic rats. Neither diabetes nor insulin had an effect on the response to physalaemin. In contrast, physalaemin threshold-dose was lower and maximal response greater in control rats placed on a bulk diet. As previously described, diabetes resulted in nonparallel changes in parotid protein composition, including a reduction in amylase and an increase in peroxidase concentrations (mg/mg protein). In contrast to the results observed with physalaemin, response to methacholine was significantly reduced in diabetic animals, and could be restored to control levels by insulin. Placement of animals on a bulk-diet, however, had no effect on threshold response to methacholine. Finally, response threshold for epinephrine was unaffected by diabetes, insulin, or bulk diet. Thus, insulin appears, directly and specifically, to alter the response of parotid acinar cells to cholinergic stimulation.

scholarly journals The metabolism of l-phenylalanine and l-tyrosine by liver cells isolated from adrenalectomized rats and from streptozotocin-diabetic rats

1985 ◽  
Vol 228 (1) ◽  
pp. 249-255 ◽  
Author(s):  
J C Stanley ◽  
M J Fisher ◽  
C I Pogson
Keyword(s):  
Insulin Treatment ◽  
Maximal Activity ◽  
Liver Cells ◽  
Diabetic Rats ◽  
Steroid Treatment ◽  
Phosphorylation State ◽  
Tyrosine Metabolism ◽  
Streptozotocin Diabetic Rats ◽  
Adrenalectomized Rats

Flux through, and maximal activities of, key enzymes of phenylalanine and tyrosine degradation were measured in liver cells prepared from adrenalectomized rats and from streptozotocin-diabetic rats. Adrenalectomy decreased the phenylalanine hydroxylase flux/activity ratio; this was restored by steroid treatment in vivo. Changes in the phosphorylation state of the hydroxylase may mediate these effects; there was no significant change in the maximal activity of the hydroxylase. Tyrosine metabolism was enhanced by adrenalectomy; this was not related to any change in maximal activity of the aminotransferase. Steroid treatment increased the maximal activity of the aminotransferase. Both acute (3 days) and chronic (10 days) diabetes were associated with increased metabolism of phenylalanine; insulin treatment in vivo did not reverse these changes. Although elevated hydroxylase protein concentration was a major factor, changes in the enzyme phosphorylation state may contribute to differences in phenylalanine degradation in the acute and chronic diabetic states. Tyrosine metabolism, increased by diabetes, was partially restored to normal by insulin treatment in vivo. These changes can, to a large extent, be interpreted in terms of changes in the maximal activity of the aminotransferase.

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.

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