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.

Effects of acute insulin deficiency on catecholamine and indoleamine content and catecholamine turnover in microdissected hypothalamic nuclei in streptozotocin-diabetic rats

1989 ◽  
Vol 120 (3) ◽  
pp. 343-350 ◽  
Author(s):  
E. H. Oliver ◽  
J. L. Sartin ◽  
G. Dieberg ◽  
C. H. Rahe ◽  
D. N. Marple ◽  
...  
Keyword(s):  
Rapid Onset ◽  
Diabetic Rats ◽  
Female Rats ◽  
Insulin Deficiency ◽  
Turnover Rates ◽  
Catecholamine Turnover ◽  
Hypothalamic Nuclei ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats ◽  
Induced Changes

Abstract. The effects of streptozotocin-induced diabetes on catecholamine and indoleamine concentrations and catecholamine turnover rates in individual microdissected hypothalamic nuclei known, or believed, to be involved in the control of neuroendocrine function, were examined in control, insulin-treated diabetic and acutely insulin-withdrawn diabetic female rats. Streptozotocin-induced diabetes and acute insulin deficiency were demonstrated to result in increased concentrations of epinephrine in the suprachiasmatic nucleus, decreased turnover of epinephrine in the arcuate nucleus and decreased turnover of dopamine in the ventromedial nucleus was found to be increased in the insulin-treated diabetic animals. These data indicate that experimental diabetes and acute insulin deficiency result in the rapid onset of detectable alterations in epinephrine and dopamine activity in specific hypothalamic nuclei. These diabetes-induced changes may cause, or contribute to, the development of secondary neuroendocrine abnormalities known to occur in the diabetic condition.

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.

Progressive defect in biliary GSH secretion in streptozotocin-induced diabetic rats

1997 ◽  
Vol 272 (2) ◽  
pp. G374-G382 ◽  
Author(s):  
S. C. Lu ◽  
J. Kuhlenkamp ◽  
H. Wu ◽  
W. M. Sun ◽  
L. Stone ◽  
...  
Keyword(s):  
Reduced Glutathione ◽  
Diabetic Rats ◽  
High Dose ◽  
Gamma Glutamyl Transpeptidase ◽  
Irreversible Inhibitor ◽  
Kinase C ◽  
Before And After ◽  
Streptozotocin Induced Diabetes ◽  
And Control ◽  
Glutamyl Transpeptidase

This study examined the effect of streptozotocin-induced diabetes on biliary reduced glutathione (GSH) efflux. Biliary GSH efflux was measured before and after acivicin, an irreversible inhibitor of gamma-glutamyl transpeptidase (GGT). One week after streptozotocin treatment, liver GGT activity doubled in diabetic rats but was inhibited by approximately 90% after acivicin to levels comparable to controls. Despite maximal GGT inhibition, biliary GSH efflux in untreated diabetic rats decreased progressively to approximately 10% of control levels by week 4 and was partially restored by insulin. The mechanism for the decrease in biliary GSH efflux was not increased paracellular permeability. GSH transport kinetics, ATP-stimulated taurocholate, and oxidized glutathione (GSSG) transport in canalicular liver plasma membrane prepared from diabetic and control rats were similar. Inhibition of protein kinase C (PKC) with high-dose H-7 increased biliary GSH efflux in diabetic animals to near control basal levels. In conclusion, streptozotocin-induced diabetic rats exhibit a progressive impairment in biliary GSH transport. One of the responsible mechanisms is heightened PKC tone in diabetic animals.

scholarly journals Noninvasive Orthogonal Polarization Spectral Imaging as Applied to Microvascular Studies in Mice

2004 ◽  
Vol 5 (3) ◽  
pp. 211-217 ◽  
Author(s):  
P. Nivoit ◽  
A. M. Chevrier ◽  
M. Lagarde ◽  
C. Renaudin ◽  
N. Wiernsperger
Keyword(s):  
Spectral Imaging ◽  
Diabetic Microangiopathy ◽  
Orthogonal Polarization ◽  
High Contrast ◽  
Hormonal Stimulation ◽  
Orthogonal Polarization Spectral ◽  
Before And After ◽  
Topical Applications

In vivo observations of the mouse microcirculation can hardly be performed due to technical difficulties, limiting the knowledge that could be obtained from gene manipulated mice models. The aim of the present study was to check the applicability of a novel optical system, the orthogonal polarization spectral technology, to study the mouse microcirculation. In anaesthetized mice, the spinotrapezius muscle microcirculation was observed in situ. The diameter of precapillary arterioles was measured before and after a pharmacological or hormonal stimulation. High-contrast images of the muscle microcirculation were obtained and significant vasodilatation of arterioles was observed after topical applications of acetylcholine, sodium nitroprusside, and insulin. As compared to conventional techniques, orthogonal polarization spectral imaging makes it possible to assess and study microvascular beds in mice, which were inaccessible until now, allowing the use of gene manipulated mice to investigate, for example, the mechanisms involved in the development of diabetic microangiopathy.

Role of vasopressin in diabetes mellitus-induced changes in medullary transport proteins involved in urine concentration in Brattleboro rats

2004 ◽  
Vol 286 (4) ◽  
pp. F760-F766 ◽  
Author(s):  
Dongun Kim ◽  
Jeff M. Sands ◽  
Janet D. Klein
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Rats ◽  
Urine Concentration ◽  
Transport Proteins ◽  
Protein Abundance ◽  
Brattleboro Rats ◽  
Urea Transporter ◽  
Streptozotocin Induced Diabetes ◽  
Induced Changes

In rats with streptozotocin-induced diabetes mellitus for 10–20 days, we showed that the abundance of the major medullary transport proteins involved in the urinary concentrating mechanism, urea transporter (UT-A1), aquaporin-2 (AQP2), and the Na+-K+-2Cl- cotransporter (NKCC2/BSC1), is increased, despite the ongoing osmotic diuresis. To test whether vasopressin is necessary for these diabetes mellitus-induced changes in UT-A1, AQP2, or NKCC2/BSC1, we studied Brattleboro rats because they lack vasopressin. Brattleboro rats were given vasopressin (2.4 μg/day via osmotic minipump) for 5 or 12 days. At 5 days, vasopressin increased AQP2 protein abundance but decreased UT-A1 abundance compared with untreated Brattleboro rats. At 12 days, vasopressin increased the abundance of both UT-A1 and AQP2 proteins but did not alter NKCC2/BSC1. Next, untreated Brattleboro rats were made diabetic for 10 days by injecting them with streptozotocin (40 mg/kg). Diabetes mellitus increased the abundance of AQP2 and NKCC2/BSC1 proteins, but UT-A1 protein abundance did not increase. Third, vasopressin-treated Brattleboro rats were made diabetic with streptozotocin for 10 days. In vasopressin-treated Brattleboro rats, diabetes mellitus increased UT-A1, AQP2, and NKCC2/BSC1 protein abundances. Vasopressin significantly increased UT-A1 phosphorylation in vasopressin-treated diabetic Brattleboro rats but not in the other groups of Brattleboro rats. We conclude that 1) administering vasopressin to Brattleboro rats for 12 days, but not for 5 days, increases UT-A1 protein abundance and 2) vasopressin is necessary for the increase in UT-A1 protein in diabetic rats but is not necessary for the increase in AQP2 or NKCC2 proteins.

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.

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