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.

scholarly journals Inhibitory effects of some long-chain unsaturated fatty acids on mitochondrial β-oxidation. Effects of streptozotocin-induced diabetes on mitochondrial β-oxidation of polyunsaturated fatty acids

1985 ◽  
Vol 230 (2) ◽  
pp. 329-337 ◽  
Author(s):  
H Osmundsen ◽  
K Bjørnstad
Keyword(s):  
Fatty Acids ◽  
Unsaturated Fatty Acids ◽  
Reductase Activity ◽  
Liver Mitochondria ◽  
Inhibitory Effect ◽  
Diabetic Rats ◽  
Inhibitory Property ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats ◽  
Coa Reductase

Evidence showing that some unsaturated fatty acids, and in particular docosahexaenoic acid, can be powerful inhibitors of mitochondrial β-oxidation is presented. This inhibitory property is, however, also observed with the cis- and trans-isomers of the C18:1(16) acid. Hence it is probably the position of the double bond(s), and not the degree of unsaturation, which confers the inhibitory property. It is suggested that the inhibitory effect is caused by accumulation of 2,4-di- or 2,4,7-tri-enoyl-CoA esters in the mitochondrial matrix. This has previously been shown to occur with these fatty acids, in particular when the supply of NADPH was limiting 2,4-dienoyl-CoA reductase (EC 1.3.1.-) activity [Hiltunen, Osmundsen & Bremer (1983) Biochim. Biophys. Acta 752, 223-232]. Liver mitochondria from streptozotocin-diabetic rats showed an increased ability to β-oxidize 2,4-dienoyl-CoA-requiring acylcarnitines. Docosahexaenoylcarnitine was also found to be less inhibitory at lower concentrations with incubation under coupled conditions. With uncoupling conditions there was little difference between mitochondria from normal and diabetic rats in these respects. This correlates with a 5-fold stimulation of 2,4-dienoyl-CoA reductase activity found in mitochondria from streptozotocin-diabetic rats.

scholarly journals Glutamine and ketone-body metabolism in the gut of streptozotocin-diabetic rats

1988 ◽  
Vol 249 (2) ◽  
pp. 565-572 ◽  
Author(s):  
M S M Ardawi
Keyword(s):  
Small Intestine ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Diabetic Rats ◽  
Glutamine Metabolism ◽  
Gut Mucosa ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats ◽  
Short And Long Term

1. In short- and long-term diabetic rats there is a marked increase in size of both the small intestine and colon, which was accompanied by marked decreases (P less than 0.001) and increases (P less than 0.001) in the arterial concentrations of glutamine and ketone bodies respectively. 2. Portal-drained viscera blood flow increased by approx. 14-37% when expressed as ml/100 g body wt., but was approximately unchanged when expressed as ml/g of small intestine of diabetic rats. 3. Arteriovenous-difference measurements for ketone bodies across the gut were markedly increased in diabetic rats, and the gut extracted ketone bodies at approx. 7 and 60 nmol/min per g of small intestine in control and 42-day-diabetic rats respectively. 4. Glutamine was extracted by the gut of control rats at a rate of 49 nmol/min per g of small intestine, which was diminished by 45, 76 and 86% in 7-, 21- and 42-day-diabetic rats respectively. 5. Colonocytes isolated from 7- or 42-day-diabetic rats showed increased and decreased rates of ketone-body and glutamine metabolism respectively, whereas enterocytes of the same animals showed no apparent differences in the rates of acetoacetate utilization as compared with control animals. 6. Prolonged diabetes had no effects on the maximal activities of either glutaminase or ketone-body-utilizing enzymes of colonic tissue preparations. 7. It is concluded that, although the epithelial cells of the small intestine and the colon during streptozotocin-induced diabetes exhibit decreased rates of metabolism of glutamine, such decreases were partially compensated for by enhanced ketone-body utilization by the gut mucosa of 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 Alterations in Nitric Oxide Activity and Sensitivity in Early Streptozotocin-Induced Diabetes Depend on Arteriolar Size

2000 ◽  
Vol 1 (3) ◽  
pp. 221-232 ◽  
Author(s):  
Bastiaan vanDam ◽  
Cihan Demirci ◽  
Hans J. Reitsma ◽  
Anton A. van Lambalgen ◽  
Gerard C. van den Bos ◽  
...  
Keyword(s):  
Diabetic Rats ◽  
Diabetic Microangiopathy ◽  
Basal Diameter ◽  
Early Increase ◽  
Before And After ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats ◽  
Induced Changes ◽  
Cholinergic Vasodilatation

Changes in NO activity may play an important role in the early increase in microvascular flow that has been implicated in the pathogenesis of diabetic microangiopathy. We assessed, in thein situspinotrapezius muscle preparation of 6 weeks' streptozotocin-diabetic rats (n= 6) and of agematched controls (n= 8), basal inside diameters of A2–A4 arterioles and the reactivity to topically applied acetylcholine and nitroprusside, before and afterNG-nitro-L-arginine. In diabetic rats, cholinergic vasodilatation in A2–A4 arterioles was intact. Basal diameter in A3 and A4 arterioles was significantly higher in streptozotocin-diabetic rats. The increased basal diameter in A3 arterioles was partially due to an increased contribution of NO to basal diameter. The response to nitroprusside was impaired in streptozotocin-diabetic rats in A2, but not in A3 and A4 arterioles. Thus, this study shows that NO activity and sensitivity are altered after 6 weeks of streptozotocin-induced diabetes. These streptozotocin-induced changes are anatomically specific and, for arterioles, depend on their position within the vascular tree.

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.

Enhanced arterial contractility to noradrenaline in diabetic rats is associated with increased phosphoinositide metabolism

1991 ◽  
Vol 69 (3) ◽  
pp. 355-361 ◽  
Author(s):  
Worku Abebe ◽  
Kathleen M. MacLeod
Keyword(s):  
Phosphatidic Acid ◽  
Contractile Response ◽  
Inositol Phosphates ◽  
Diabetic Rats ◽  
Male Rats ◽  
Phosphoinositide Metabolism ◽  
Adrenoceptor Antagonist ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats ◽  
Stimulation Of

The purpose of this study was to investigate whether the increased contractile responsiveness of aortae from male rats with 12 – 14 week streptozotocin-induced diabetes to noradrenaline is associated with alterations in phosphoinositide metabolism. The contractile response to noradrenaline (10 μM) in both the presence and absence of extracellular calcium was significantly enhanced in aortae from diabetic rats. No significant differences were found between control and diabetic arteries in the basal incorporation of 32P and [3H]myo-inositol into phosphoinositides, or in the basal accumulation of [32P]phosphatidic acid and [3H]inositol phosphates. However, noradrenaline (10 μM) caused significantly greater breakdown of [32P]phosphatidylinositol 4,5-bisphosphate and formation of [32P]phosphatidic acid and [3H]inositol phosphates in diabetic aortae than in control preparations. The production of [3H]inositol phosphates induced by noradrenaline was selectively reduced by the α1-adrenoceptor antagonist, prazosin, in both control and diabetic tissues. These results indicate that phosphoinositide metabolism in response to noradrenaline via stimulation of α1-adrenoceptors is enhanced in aortae from chronic streptozotocin-diabetic rats. The increase in inositol 1,4,5-trisphosphate and 1,2-diacylglycerol production that presumably results could be responsible, at least in part, for the enhanced contractile response of aortae from diabetic rats to noradrenaline.Key words: diabetes, aortae, phosphoinositide metabolism, noradrenaline, contractile responses.

Secretion and metabolic clearance rates of thyroxine and triiodothyronine in streptozotocin-diabetic rats

1985 ◽  
Vol 110 (3) ◽  
pp. 395-400 ◽  
Author(s):  
Trinidad Jolin ◽  
Javier Ortiz-Caro ◽  
Margarita González
Keyword(s):  
Diabetic Rats ◽  
Control Group ◽  
Metabolic Clearance ◽  
Production Rates ◽  
Metabolic Clearance Rate ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats ◽  
Ethanol Extracts ◽  
Layer Chromatography ◽  
Dramatic Fall

Abstract. This study was undertaken to evaluate the effects of streptozotocin-induced diabetes on T4 and T3 production rate (PR) and metabolism in rats. [125I]T4 and [125I]T3 were injected iv and sequential blood samples were obtained. Plasma ethanol extracts were analyzed for [125I]T4 and [125I]T3 by thin layer chromatography. T4 and T3 production rates and kinetic parameters of T4 and T3 metabolism in control, diabetic and insulintreated diabetic rats were assessed by applying kinetic analyses to measurements of disappearance of injected T4 and T3 radiotracer from plasma. The metabolic clearance rate (MCR) and the fractional disappearance rate (K) of T4 in diabetic rats (0.72 ± sd, 0.02 ml/h · 100 g, and 0.034 ± 0.006 h−1, respectively) were significantly lower (P 0.001) than in the control group (1.01 ± 0.04 ml/h · 100 g and 0.056 ± 0.004 h−1). Similarly, the MCR and K values of T3 were also significantly reduced (P < 0.001) in the diabetic animals: 16.2 ± 0.7 ml/h · 100 g and 0.088 ± 0.007 h−1 in controls vs 13.0 ± 1.2 ml/h · 100 g and 0.058 ± 0.009 h−1 in diabetics, respectively. Insulin therapy significantly reversed these alterations. There was also a significant reduction (P < 0.001) in plasma T4 (18 ± 6 ng/ml) and T3 (0.20 ± 0.05 ng/ml) concentrations in the diabetic rats compared to control values, whose T4 and T3 levels averaged 65 ± 10 and 0.68 ± 0.09 ng/ml, respectively. In addition, the T4 and T3 production rates in diabetic rats (12.9 ± 5.6 and 2.6 ± 0.2 ng/ml · 100 g, respectively) were significantly different (P < 0.001) from control values (65.6 ± 10 and 11.0 ± 0.7 ng/ml · 100 g). In conclusion, the dramatic fall in plasma T4 and T3 concentrations associated with diabetes appear to be the result of the reduction in the PRs rather than to changes in MCRs.

scholarly journals Temporal Adaptive Changes in Contractility and Fatigability of Diaphragm Muscles from Streptozotocin-Diabetic Rats

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Marco Brotto ◽  
Leticia Brotto ◽  
J.-P. Jin ◽  
Thomas M. Nosek ◽  
Andrea Romani
Keyword(s):  
Insulin Treatment ◽  
Contractile Function ◽  
Fiber Type ◽  
Calcium Sensitivity ◽  
Diabetic Rats ◽  
Time Interval ◽  
Gradual Improvement ◽  
Tetanic Force ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats

Diabetes is characterized by ventilatory depression due to decreased diaphragm (DPH) function. This study investigated the changes in contractile properties of rat DPH muscles over a time interval encompassing from 4 days to 14 weeks after the onset of streptozotocin-induced diabetes, with and without insulin treatment for 2 weeks. Maximum tetanic force in intact DPH muscle strips and recovery from fatiguing stimulation were measured. An early (4-day) depression in contractile function in diabetic DPH was followed by gradual improvement in muscle function and fatigue recovery (8 weeks). DPH contractile function deteriorated again at 14 weeks, a process that was completely reversed by insulin treatment. Maximal contractile force and calcium sensitivity assessed in Triton-skinned DPH fibers showed a similar bimodal pattern and the same beneficial effect of insulin treatment. While an extensive analysis of the isoforms of the contractile and regulatory proteins was not conducted, Western blot analysis of tropomyosin suggests that the changes in diabetic DPH response depended, at least in part, on a switch in fiber type.

Effects of chronic streptozotocin-induced diabetes on the cardiac responses to milrinone

1985 ◽  
Vol 63 (12) ◽  
pp. 1620-1623 ◽  
Author(s):  
Ramesh K. Goyal ◽  
John H. McNeill
Keyword(s):  
Left Atrium ◽  
Right Atrium ◽  
Diabetic Rats ◽  
Chronotropic Response ◽  
Cardiac Responses ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats ◽  
Dose Dependent ◽  
Right Atria ◽  
Positive Chronotropic Effect

We have studied the effects of milrinone on various cardiac preparations obtained from 6-week streptozotocin diabetic rats. The basal rate of spontaneously beating right atrium from diabetics was significantly lower as compared with controls. Milrinone (5 × 10−5 to 8 × 10−4 M) produced a dose-dependent positive inotropic and positive chronotropic effect in left atrium and right atrium, respectively. The positive chronotropic response to milrinone was slightly increased in right atria from diabetic animals. In papillary muscle neither the maximum response nor the pD2 value of milrinone was altered significantly in diabetic animals. The pD2 values of milrinone in right atrium and left atrium were found to be significantly higher in diabetic preparations compared with controls. The data indicate that the responses to milrinone are either unchanged or enhanced in hearts from diabetic animals.

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