scholarly journals A luminometric assay for peroxisomal β-oxidation. Effects of fasting and streptozotocin-diabetes on peroxisomal β-oxidation

1989 ◽  
Vol 260 (1) ◽  
pp. 215-220 ◽  
Author(s):  
H Osmundsen ◽  
B Brodal ◽  
R Hovik
Keyword(s):  
Oxidase Activity ◽  
Liver Homogenate ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Urate Oxidase ◽  
Glycollate Oxidase ◽  
Streptozotocin Diabetic Rats ◽  
Liver Homogenates ◽  
Acyl Coa Oxidase ◽  
Good Agreement

1. A luminometric assay for acyl-CoA oxidase activity is described. The assay uses the luminol/microperoxidase system to monitor continuously acyl-CoA-dependent generation of H2O2. The assay is rapid, convenient, and lends itself to automation with an LKB 1251 luminometer. The assay is extremely sensitive, requiring at the most 10 micrograms of liver-homogenate protein per assay. 2. The assay can also be used to measure other oxidases, e.g. glycollate oxidase (EC 1.1.3.15), D-aspartate oxidase (EC 1.4.3.1) and urate oxidase (EC 1.7.3.3), the only modification being substitution of substrates to appropriate concentration. 3. With rat liver homogenates, spectrophotometrically measured rates of palmitoyl-CoA-dependent NAD+ reduction and acyl-CoA oxidase activity [Hryb & Hogg (1979) Biochem. Biophys. Res. Commun. 87, 1200-1206] was generally found in good agreement with luminometrically measured acyl-CoA oxidase activity. 4. With liver homogenates from streptozotocin-diabetic rats, however, rates of palmitoyl-CoA-dependent NAD+ reduction were consistently lower than the corresponding acyl-CoA oxidase activity. This difference was most marked with respect to luminometrically assayed acyl-CoA oxidase activity.

Improvement in cardiac function in streptozotocin-diabetic rats by salt loading

1994 ◽  
Vol 72 (11) ◽  
pp. 1288-1293 ◽  
Author(s):  
Soter Dai ◽  
Heather Fraser ◽  
Violet G. Yuen ◽  
John H. McNeill
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Cardiac Function ◽  
Body Weight Gain ◽  
Myocardial Dysfunction ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Salt Loading ◽  
Glucose Levels ◽  
Streptozotocin Diabetic Rats

Effects of salt loading by drinking 0.9% NaCl solution on the myocardial performance in nondiabetic and diabetic Wistar rats were studied using the isolated working heart apparatus. Body weight and fluid and food intakes of these animals were monitored. Blood pressure and plasma levels of glucose, insulin, cholesterol, and triglycerides were also measured. Diabetes was induced by intravenous injection of streptozotocin (60 mg/kg). Diabetic rats were found to develop myocardial dysfunction at 8 weeks after STZ injection, accompanied by significant increases in food and fluid intakes, slowed body weight gain, hyperglycemia, hypoinsulinemia, and hyperlipidemia but without significant changes in blood pressure. Salt loading did not cause significant changes in any of the parameters studied in nondiabetic rats. However, in streptozotocin-diabetic rats given saline to drink, the impaired myocardial function was significantly improved and was associated with a significant reduction in hyperphagia and hyperlipidemia. Plasma glucose levels significantly decreased at weeks 1–3 but increased to the levels of untreated diabetic animals at weeks 4–7. There was an increase in fluid intake, but neither blood pressure nor plasma insulin levels were significantly affected. It is suggested that the improvements in cardiac function and hyperlipidemia in diabetic rats by salt loading may be related to each other; however, the mechanisms for these effects are not clear but are unlikely to be due to changes in glycemic control.Key words: streptozotocin diabetes, salt loading, cardiac dysfunction.

scholarly journals Transport of myo-inositol into endoneurial preparations of sciatic nerve from normal and streptozotocin-diabetic rats

1983 ◽  
Vol 210 (3) ◽  
pp. 775-781 ◽  
Author(s):  
K R W Gillon ◽  
J N Hawthorne
Keyword(s):  
Sciatic Nerve ◽  
Glucose Concentration ◽  
Reductase Inhibitor ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Aldose Reductase Inhibitor ◽  
Similar Extent ◽  
Elevated Glucose ◽  
Streptozotocin Diabetic Rats ◽  
Energy Dependent

myo-Inositol transport by a viable rat sciatic-nerve preparation is described. Such ‘endoneurial’ nerve preparations accumulated myo-inositol by an energy-dependent saturable system. Streptozotocin-diabetes reduced myo-inositol transport into sciatic nerve by approx. 40%. Elevated medium glucose concentration reduced myo-inositol transport into control nerves to a similar extent. Fructose and sorbitol did not inhibit myo-inositol transport. Inclusion of an aldose reductase inhibitor in the medium counteracted the reduced myo-inositol transport caused by elevated glucose concentration. The importance of these results to the problem of diabetic neuropathy is discussed.

Plasma post-heparin diamine oxidase activity in streptozotocin diabetic rats fed with different sterols

1994 ◽  
Vol 109 (1-2) ◽  
pp. 246 ◽  
Author(s):  
H. Kojima ◽  
H. Hidaka ◽  
T. Nakamura ◽  
K. Konaka ◽  
K. Matsumura ◽  
...  
Keyword(s):  
Oxidase Activity ◽  
Diamine Oxidase ◽  
Diabetic Rats ◽  
Diamine Oxidase Activity ◽  
Streptozotocin Diabetic Rats

scholarly journals Nutritional aspects of amino acid metabolism

1972 ◽  
Vol 27 (2) ◽  
pp. 249-259 ◽  
Author(s):  
D. L. Bloxam
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Acid Metabolism ◽  
Normal Animal ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Normal Rat ◽  
Chain Group ◽  
Streptozotocin Diabetic Rats ◽  
Branched Chain

1. Measurements of the concentrations of amino acids in the plasma of blood from the portal vein and hepatic vein in the livers of rats made diabetic with streptozotocin or alloxan and starved for 1 d were compared with similar measurements from normal rats starved for 1 d.2. The concentrations of many of the amino acids in the blood plasma were lower in the streptozotocin diabetic rats than in the normal animal while the liver concentrations tended to be increased. This suggests that there is enhanced concentration of these amino acids by the liver in diabetics, as is also found in starvation, which is probably due to factors other than the direct absence of insulin.3. The direction of flow of the groups of amino acids into and out of the liver was unchanged in the diabetic compared with the normal rat except that the output of tryptophan was abolished, and that of the branched-chain group was abolished in alloxan diabetes though apparently enhanced in streptozotocin diabetes. The rates of movement of amino acids in both directions appeared to be increased in the streptozotocin diabetic animals.4. The changed amino acid pattern in the alloxan diabetic rats was to some extent similar to that of the streptozotocin diabetic rats but the changes were more difficult to interpret, perhaps because of side-effects of alloxan on tissues including liver.

Renal Hypertrophy in Streptozotocin-Diabetic Rats

1976 ◽  
Vol 51 (6) ◽  
pp. 551-555 ◽  
Author(s):  
K. Seyer-Hansen
Keyword(s):  
Weight Gain ◽  
Protein Content ◽  
Dna Content ◽  
Insulin Treatment ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Renal Hypertrophy ◽  
Kidney Weight ◽  
Streptozotocin Diabetic Rats ◽  
Rna And Dna

1. Kidney weight and content of protein, RNA and DNA were measured in rats with streptozotocin diabetes of varying duration. 2. Diabetic rats had larger kidneys than control rats: after 3 days of diabetes the weight increase was 15% and after 42 days of diabetes it was 90%. The protein content rose in parallel to the weight. 3. RNA content was already increased after 36 h of glycosuria, whereas DNA content was unchanged for the first 3 days of diabetes, and increased thereafter. The protein/DNA ratio increased rapidly during the first 3 days but remained constant thereafter. 4. Insulin treatment decreased the renal weight gain by about 67% during the first 8 days of diabetes, but did not prevent the increase in DNA. When insulin was started after 25 days of diabetes there was only a slight regression of kidney growth.

Progressive and concurrent deterioration of vagus-stimulated and hypoglycemia-induced glucagon secretion in streptozotocin-diabetic rats

1992 ◽  
Vol 126 (1) ◽  
pp. 80-84 ◽  
Author(s):  
Zsolt I Hertelendy ◽  
DG Patel ◽  
Kenneth A Skau
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Parasympathetic Nervous System ◽  
Matched Control ◽  
Streptozotocin Diabetes ◽  
Glucagon Secretion ◽  
Diabetic Rats ◽  
Male Rats ◽  
Streptozotocin Diabetic Rats

The effects of left cervical vagus nerve stimulation on glucagon secretion were studied in streptozotocin-diabetic and age-matched control adult male rats. At two-week intervals, after the induction of streptozotocin-diabetes, streptozotocin-diabetic and age-matched control rats were anesthetized with chloral hydrate (350 mg/kg, ip). Left cervical vagus nerves were electrically stimulated via a Grass stimulator with 5-volt monophasic pulses of 3 msec duration at a frequency of 20 Hz for 1, 2, and 4 min. Arginine-induced glucagon secretion was also determined. Vagus nerve-stimulated (2 and 4 min) glucagon secretion deteriorated as the duration of streptozotocin-diabetes increased. Glucagon secretion in response to vagus nerve stimulation was virtually absent by 12 weeks of streptozotocin-diabetes. However, arginine-induced glucagon secretion was unaffected. Subsequent experiments showed that the defect in glucagon secretion from vagal stimulation occurred concurrently with that seen from insulin-induced hypoglycemia. These results indicate that the impaired hypoglycemia-induced glucagon secretion in long-term streptozotocin-diabetic rats may be correlated with the deterioration of the parasympathetic nervous system transmission in streptozotocin-diabetes.

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