scholarly journals Lysosomal Exoglycosidase Profile and Secretory Function in the Salivary Glands of Rats with Streptozotocin-Induced Diabetes

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Mateusz Maciejczyk ◽  
Agnieszka Kossakowska ◽  
Julita Szulimowska ◽  
Anna Klimiuk ◽  
Małgorzata Knaś ◽  
...  
Keyword(s):  
Salivary Glands ◽  
Inverse Correlation ◽  
Salivary Flow ◽  
Diabetic Rats ◽  
Secretory Function ◽  
Submandibular Glands ◽  
Streptozotocin Induced Diabetes ◽  
And Control ◽  
The Relationship

Before this study, there had been no research evaluating the relationship between a lysosomal exoglycosidase profile and secretory function in the salivary glands of rats with streptozotocin- (STZ-) induced type 1 diabetes. In our work, rats were divided into 4 groups of 8 animals each: control groups (C2, C4) and diabetic groups (STZ2, STZ4). The secretory function of salivary glands—nonstimulated and stimulated salivary flow,α-amylase, total protein—and salivary exoglycosidase activities—N-acetyl-β-hexosaminidase (HEX, HEX A, and HEX B),β-glucuronidase,α-fucosidase,β-galactosidase, andα-mannosidase—was estimated both in the parotid and submandibular glands of STZ-diabetic and control rats. The study has demonstrated that the activity of most salivary exoglycosidases is significantly higher in the parotid and submandibular glands of STZ-diabetic rats as compared to the healthy controls and that it increases as the disease progresses. Reduced secretory function of diabetic salivary glands was also observed. A significant inverse correlation between HEX B,α-amylase activity, and stimulated salivary flow in diabetic parotid gland has also been shown. Summarizing, STZ-induced diabetes leads to a change in the lysosomal exoglycosidase profile and reduced function of the salivary glands.

scholarly journals Activity, distribution and regulation of phosphofructokinase in salivary gland of rats with streptozotocin-induced diabetes

2006 ◽  
Vol 20 (2) ◽  
pp. 108-113 ◽  
Author(s):  
José Nicolau ◽  
Douglas Nesadal Souza ◽  
Fernando Neves Nogueira
Keyword(s):  
Parotid Gland ◽  
Salivary Glands ◽  
Specific Activity ◽  
Active Form ◽  
Diabetic Rats ◽  
Phosphate Content ◽  
Soluble Enzyme ◽  
Parotid Glands ◽  
Streptozotocin Induced Diabetes ◽  
And Control

Although the influence of diabetes on salivary glands is well studied, it still presents conflicting results. In this work, the regulation of the phosphofructokinase-1 enzyme (PFK-1) was studied utilizing the salivary glands of rats. Diabetes was induced by a single intraperitoneal injection of streptozotocin (60 mg/Kg of body weight) in rats (180-200 g). The animals were killed 30 days after the induction of diabetes and the submandibular and parotid salivary glands were used. Hyperglycemia was evaluated by blood sugar determination. The distribution of PFK-1 between the soluble and cytoskeleton fractions, the phosphate content of PFK-1, the content of fructose-2,6-bisphosphate and the activity of the PFK-2 enzyme were determined. The calculated relative glandular weight showed a higher value for the parotid gland in comparison with the control, but not for the submandibular gland. The activity of PFK-1 expressed per gland showed no variation between diabetic and control animals. However, considering the specific activity, the soluble enzyme presented a value 50% higher than that of the control and the cytoskeleton bound form increased by 84% compared to the control. For the parotid gland, no difference in the specific activity between diabetic and control animals was observed. On the other hand, the activity per gland of the soluble enzyme increased in the diabetic animals. The phosphate content of PFK-1 increased in the submandibular and parotid glands of diabetic rats. Both the content of fructose-2,6-bisphosphate and the active form of PFK-2 were reduced in the diabetic glands. In conclusion, the increase in the activity of PFK-1 observed in the salivary glands of rats with streptozotocin-induced diabetes does not seem to be due to its modulator fructose-2,6-bisphosphate.

scholarly journals Electroacupuncture-Induced Cholinergic Nerve Activation Enhances the Hypoglycemic Effect of Exogenous Insulin in a Rat Model of Streptozotocin-Induced Diabetes

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Yu-Chen Lee ◽  
Te-Mao Li ◽  
Chung-Yuh Tzeng ◽  
Yu-Wen Cheng ◽  
Ying-I Chen ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Challenge Test ◽  
Diabetic Rats ◽  
Hypoglycemic Effect ◽  
Control Group ◽  
Exogenous Insulin ◽  
Glucose Lowering ◽  
Cholinergic Nerve ◽  
Streptozotocin Induced Diabetes ◽  
The Relationship

The aim of this study is to explore the mechanisms by which electroacupuncture (EA) enhances the hypoglycemic effect of exogenous insulin in a streptozotocin- (STZ-) diabetic rats. Animals in the EA group were anesthetized and subjected to the insulin challenge test (ICT) and EA for 60 minutes. In the control group, rats were subjected to the same treatment with the exception of EA stimulation. Blood samples were drawn to measure changes in plasma glucose, free fatty acids (FFA), and insulin levels. Western blot was used to assay proteins involved in insulin signaling. Furthermore, atropine, hemicholinium-3 (HC-3), and Eserine were used to explore the relationship between EA and cholinergic nerve activation during ICT. EA augmented the blood glucose-lowering effects of EA by activating the cholinergic nerves in STZ rats that had been exposed to exogenous insulin. This phenomenon may be related to enhancement of insulin signaling rather than to changes in FFA concentration.

scholarly journals Changes in the transcriptional activity of the entero-insular axis genes in streptozotocin-induced diabetes and after the administration of TNF-α non-selective blockers

2020 ◽  
Vol 54 (3) ◽  
pp. 160-171
Author(s):  
Anna S. Degen ◽  
Inna Y. Krynytska ◽  
Aleksandr M. Kamyshnyi
Keyword(s):  
Transcriptional Activity ◽  
Experimental Diabetes ◽  
Quantitative Polymerase Chain Reaction ◽  
Diabetic Rats ◽  
Inflammatory Factors ◽  
Genes Expression ◽  
Tnf Α ◽  
Streptozotocin Induced Diabetes ◽  
Polymerase Chain

AbstractObjective. The aim of the present study was to investigate the transcriptional activity of the GLP-1R, DPP-4, SGLT-1, INSR, and IGF-1R genes in GALT cells of rats with streptozotocin-induced diabetes in both untreated and treated with pentoxifylline, as a non-specific blocker of TNF-α.Methods. The expression of GLP-1R, DPP-4, SGLT-1, INSR, and IGF-1R genes in GALT cells of rats was studied by real time quantitative polymerase chain reaction.Results. It was shown that the development of diabetes was accompanied by the decrease of GLP-1R and an increase of DPP-4 genes expression in rat ileum. The administration of pentoxifyl-line to diabetic animals led to an increase in the transcriptional activity of GLP-1R on the 4th week and decrease in transcriptional activity of DPP-4 on the 2nd and 4th weeks of the experiment. An increase in the normalized expression of SGLT-1 on the 4th week of the experimental diabetes was also noted, while the administration of pentoxifylline to diabetic animals did not lead to significant changes in this index. The transcriptional activity of the INSR and IGF-1R genes was reduced in diabetic rats and the administration of the non-specific TNF-α blocker – pentoxifylline led to a significant increase only for INSR gene in animals on the 4th week of the experimental diabetes.Conclusions. The expression of incretins, glucose transporters, and pro-inflammatory cytokines (e.g. TNF-α) in immune cells may be used as markers of several autoimmune pathologies progression such as type 1 diabetes due to their effect on the balance of pro- and anti-inflammatory factors.

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.

Exogenous substrate utilization by isolated myocytes from chronically diabetic rats

1983 ◽  
Vol 245 (1) ◽  
pp. C46-C51 ◽  
Author(s):  
V. Chen ◽  
G. J. Bagby ◽  
J. J. Spitzer
Keyword(s):  
Inhibitory Effect ◽  
Diabetic Rats ◽  
Lactate Oxidation ◽  
Palmitate Oxidation ◽  
Exogenous Substrate ◽  
Streptozotocin Induced Diabetes ◽  
And Control ◽  
Effect Of Glucose ◽  
Substrate Concentrations

The effect of chronic streptozotocin-induced diabetes on the utilization of exogenous substrates by freshly isolated, Ca2+-tolerant nonbeating myocytes was investigated. The rates of glucose (5 or 25 mM) and lactate (1 mM) oxidation were significantly reduced in myocytes of diabetic rats, whereas palmitate (0.4 or 1 mM) oxidation was similar to the controls. Glucose oxidation in diabetic (but not in control) and palmitate oxidation in control (but not in diabetic) myocytes were increased by raising the respective substrate concentrations in the medium to levels found in vivo in diabetic rats. Inhibition of glucose and lactate oxidation in the presence of competing substrates were generally similar between control and diabetic myocytes. However, the inhibitory effect of glucose on lactate oxidation was greater in control cells. The rate of palmitate oxidation was diminished by glucose in the controls, but this was not observed in the diabetic myocytes. Oxygen consumption by the myocytes of diabetic rats was below that of control cells when lactate or palmitate was present in the medium. ATP and phosphocreatine contents were similar in the myocytes of diabetic and control rats. All the observed changes in myocytes prepared from diabetic rats were reversed by in vivo insulin treatment.

scholarly journals Plasma oxalate and eGFR are correlated in primary hyperoxaluria patients with maintained kidney function—data from three placebo-controlled studies

2021 ◽  
Author(s):  
Dawn S. Milliner ◽  
Pierre Cochat ◽  
Sally-Anne Hulton ◽  
Jerome Harambat ◽  
Ana Banos ◽  
...  
Keyword(s):  
Kidney Function ◽  
Primary Hyperoxaluria ◽  
Correlation Coefficients ◽  
Inverse Correlation ◽  
Individual Study ◽  
Severe Chronic Kidney Disease ◽  
Urinary Oxalate Excretion ◽  
The Relationship ◽  
Spearman’S Correlation

Abstract Background In patients with primary hyperoxaluria (PH), endogenous oxalate overproduction increases urinary oxalate excretion, leading to compromised kidney function and often kidney failure. Highly elevated plasma oxalate (Pox) is associated with systemic oxalate deposition in patients with PH and severe chronic kidney disease (CKD). The relationship between Pox and estimated glomerular filtration rate (eGFR) in patients with preserved kidney function, however, is not well established. Our analysis aimed to investigate a potential correlation between these parameters in PH patients from three randomized, placebo-controlled trials (studies OC3-DB-01, OC3-DB-02, and OC5-DB-01). Methods Baseline data from patients with a PH diagnosis (type 1, 2, or 3) and eGFR > 40 mL/min/1.73 m2 were analyzed for a correlation between eGFR and Pox using Spearman’s rank and Pearson’s correlation coefficients. Data were analyzed by individual study and additionally were pooled for Studies OC3-DB-02 and OC5-DB-01 in which the same Pox assay was used. Results A total of 106 patients were analyzed. A statistically significant inverse Spearman’s correlation between eGFR and Pox was observed across all analyses; correlation coefficients were − 0.44 in study OC3-DB-01, − 0.55 in study OC3-DB-02, − 0.51 in study OC5-DB-01, and − 0.49 in the pooled studies (p < 0.0064). Conclusions Baseline evaluations showed a moderate and statistically significant inverse correlation between eGFR and Pox in patients with PH already at early stages of CKD (stages 1–3b), demonstrating that a correlation is present before substantial loss in kidney function occurs. Graphical abstract

scholarly journals The Synergistic Effects of Ixeris dentata and Lactobacillus gasseri Extracts on a Diabetes-induced Dry Mouth Model by Enhancing Antioxidation

2020 ◽  
Author(s):  
Hwa Young Lee ◽  
Mingkun Gu ◽  
Jinhua Cheng ◽  
Joo Won Suh ◽  
Han-Jung Chae
Keyword(s):  
Synergistic Effects ◽  
Salivary Flow ◽  
Diabetic Rats ◽  
Dry Mouth ◽  
Oxidative Enzymes ◽  
Diabetic Patients ◽  
Aquaporin 5 ◽  
Diabetes Model ◽  
Streptozotocin Induced Diabetes ◽  
Ixeris Dentata

Dry mouth, hyposalivation, or xerostomia is a significant problem in diabetic patients; however, there was no way to relieve these symptoms. This study was aimed to evaluate the effects of Ixeris dentata (IXD) in combination with lactobacillus extract on the salivation rate in diabetes-induced dry mouth, and its mechanism was also investigated. In the streptozotocin-induced diabetes model, dry mouth condition was established as a model. Both control and diabetic rats were treated with a sublingual spray of either water or IXD and subsequently treated with or without a spray of lactobacillus extract. In diabetes condition, the salivary flow rate, amylase activity, and aquaporin-5 and Na+/H+ exchanger (NHE-1) expressions were markedly decreased, whereas they were more significantly recovered in the sequential treatment of IXD-lactobacillus extract than each single treatment. Furthermore, oxidative stress and its related ER stress response were especially regulated in the IXD/lactobacillus extract condition, where the following anti-oxidative enzymes; GSH:GSSG ratio, superoxide dismutase (SOD), and glutathione peroxidase (GPx) were involved. This study suggests that the combination of IXD and lactobacillus would be a potential alternative medicine against diabetes-induced hyposalivation and xerostomia.

Exaggerated coronary reactivity to endothelin-1 in diabetes: reversal with bosentan

2002 ◽  
Vol 80 (10) ◽  
pp. 980-986 ◽  
Author(s):  
Subodh Verma ◽  
Emi Arikawa ◽  
Sammy Lee ◽  
Aaron S Dumont ◽  
Linfu Yao ◽  
...  
Keyword(s):  
Heart Function ◽  
Coronary Perfusion Pressure ◽  
Diabetic Rats ◽  
Diabetic Heart ◽  
Coronary Perfusion ◽  
Receptor Blockade ◽  
Endothelin Receptor ◽  
Endothelin 1 ◽  
Streptozotocin Induced Diabetes ◽  
And Control

We previously demonstrated that chronic endothelin receptor blockade (with bosentan) improved functional cardiac performance in streptozotocin-diabetic rats, suggesting a novel role of endothelin-1 (ET-1) in modulating diabetic heart dysfunction. To gain insight into the mechanism(s) underlying this effect, we examined the coronary vascular responses to ET-1 in hearts from diabetic and control rats treated with or without bosentan. Rats were divided into control, control-treated, diabetic, and diabetic-treated groups. The control-treated and diabetic-treated groups received bosentan (100 mg·kg–1·d–1) for 8 weeks. Following treatment, hearts were isolated and perfused, and coronary reactivity to ET-1 was assessed by measuring the changes in coronary perfusion pressure in response to ET-1 (50 and 100 pM). Additionally, maximal coronary blood flow (assessed with 10–5 M adenosine) was measured in isolated perfused hearts. The key observation is that coronary reactivity to ET-1 was significantly higher in the diabetic than the control rats. This effect was normalized in diabetic rats chronically receiving bosentan. Maximal coronary vasodilation did not differ between the four groups. In conclusion, the reactivity of ET-1 is altered in the isolated perfused coronary vascular bed from diabetic rats, and chronic ET receptor blockade restores this reactivity to control values. These observations provide a possible mechanism for the improvement in diabetic heart function observed after chronic bosentan treatment.Key words: endothelin-1, streptozotocin-induced diabetes, bosentan, endothelin receptor antagonist, coronary artery.

scholarly journals Impact of Acute Pancreatic Injury on Sphingolipid Metabolism in the Salivary Glands

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Małgorzata Żendzian-Piotrowska ◽  
Dominika M. Ziembicka ◽  
Bartłomiej Łukaszuk ◽  
Krzysztof Kurek
Keyword(s):  
Diabetes Mellitus ◽  
Acute Pancreatitis ◽  
Type 1 Diabetes ◽  
Salivary Glands ◽  
Pancreatic Injury ◽  
Biologically Active ◽  
Sphingolipid Metabolism ◽  
Submandibular Salivary Glands ◽  
The Relationship

Acute pancreatic injury can be related to both parenchymal (responsible for exocrine functions) and islet (mainly β-cells, responsible for endocrine functions) damage. During embryonic development, both the salivary glands and the pancreas originate from the foregut, which explains many of the observed histological and functional similarities between these two organs. The relationship between several diseases of the pancreas and salivary glands, resulting from morphological and functional similarities, is well established. Sphingolipids constitute a class of biologically active molecules involved in numerous physiological and pathological processes, including acute pancreatitis (AP) and diabetes mellitus. However, the effect of AP on sphingolipid metabolism in the salivary glands remains uncertain. In the presented study, we examined the effect of AP and type 1 diabetes mellitus on sphingolipid metabolism in the salivary glands of rats. We demonstrated that acute pancreatic injury, related to both exocrine and endocrine functions, affects the metabolism of sphingolipids in the parotid, but not submandibular, salivary glands.

Deficient renal 20-HETE release in the diabetic rat is not the result of oxidative stress

2008 ◽  
Vol 294 (5) ◽  
pp. H2305-H2312 ◽  
Author(s):  
Yu-Jung Chen ◽  
Jing Li ◽  
John Quilley
Keyword(s):  
Oxidative Stress ◽  
Aldose Reductase ◽  
Reductase Activity ◽  
Rat Kidney ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Glucose Levels ◽  
Nitric Oxide Formation ◽  
Streptozotocin Induced Diabetes ◽  
And Control

We confirmed that release of 20-hydroxyeicosatetraenoic acid (20-HETE) from the isolated perfused kidney of diabetic rats is greatly reduced compared with age-matched control rats. The present studies were undertaken to examine potential mechanisms for the deficit in renal 20-HETE in rats with streptozotocin-induced diabetes of 3–4 wk duration. A role for oxidative stress was excluded, inasmuch as treatment of diabetic rats with tempol, an SOD mimetic, for 4 wk did not affect the renal release of 20-HETE. Similarly, chronic inhibition of nitric oxide formation with nitro-l-arginine methyl ester or aldose reductase with zopolrestat failed to alter the release of 20-HETE from the diabetic rat kidney. Inasmuch as 20-HETE may be metabolized by cyclooxygenase (COX), the expression/activity of which is increased in diabetes, we included indomethacin in the perfusate of the isolated kidney to inhibit COX but found no effect on 20-HETE release. Diabetic rats were treated for 3 wk with fenofibrate to increase expression of cytochrome P-450 (CYP4A) in an attempt to find an intervention that would restore release of 20-HETE from the diabetic rat kidney. However, fenofibrate reduced 20-HETE release in diabetic and control rat kidneys but increased expression of CYP4A. Only insulin treatment of diabetic rats for 2 wk to reverse the hyperglycemia and maintain blood glucose levels at <200 mg/dl reversed the renal deficit in 20-HETE. We conclude that oxidative stress, increased aldose reductase activity, or increased COX activity does not contribute to the renal deficit of 20-HETE in diabetes, which may be directly related to insulin deficiency.

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