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 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.

FUNCTIONAL DISORDERSOF THE SALIVARY GLANDS IN PATIENTS WITH COMPRESSION AND DISLOCATION DYSFUNCTION OF THE TEMPOROMANDIBULAR JOINT AND THEIR CORRECTION

2021 ◽  
Vol 74 (7) ◽  
pp. 1695-1698
Author(s):  
Oleg V. Rybalov ◽  
Pavel I. Yatsenko ◽  
Olga Yu. Andriyanova ◽  
Elena S. Ivanytska ◽  
Maria A. Korostashova
Keyword(s):  
Parotid Gland ◽  
Salivary Glands ◽  
Functional State ◽  
Oral Fluid ◽  
Healthy Individuals ◽  
Parotid Glands ◽  
Posterior Teeth ◽  
Fluid Content ◽  
Lower Jaw ◽  
Before And After

The aim: Is to assess the functional state of parotid glands and general secretion in patients with compression, dislocation dysfunction of TMJ, to correct the revealed disorders. Materials and methods: We examined 46 patients with dysfunction of TMJ. Examination included TMJ zonography and salivary glands sonography. We studied the general and parotid secretion, transparency, viscosity, pH of the oral fluid and the secretions of the parotid glands before and after treatment. The treatment of dysfunction and hyposialosis included the repositioning of the articular heads of the lower jaw in the correct anatomical position, the use of a repositioning plate on the posterior teeth at the compression side of the articular head, bougienage of the duct of the parotid gland, administration of 10% magnesium-mineral solution of bischofite into the gland. Results: In patients with TMJ dysfunction, a significant decrease in the oral fluid content was noted before treatment. The saliva transparency was reduced, the viscosity was increased, the pH was slightly acidic. A study, which was carried out a month after completion of the course of treatment showed that all the studied parameters corresponded to those in healthy individuals. Conclusions: The study confirmed that in compression and dislocation dysfunction of TMJ, there are disorders of the functional state of the salivary glands.

scholarly journals Effects of Diabetes and Insulin on α-amylase Messenger RNA Levels in Rat Parotid Glands

1990 ◽  
Vol 69 (8) ◽  
pp. 1500-1504 ◽  
Author(s):  
S.K. Kim ◽  
L.M. Cuzzort ◽  
R.K. McKean ◽  
E.D. Allen
Keyword(s):  
Parotid Gland ◽  
Beta Cell ◽  
Messenger Rna ◽  
Secretory Protein ◽  
Diabetic Rats ◽  
Mrna Levels ◽  
Mrna Synthesis ◽  
Parotid Glands ◽  
Protein Levels ◽  
Rat Parotid

Previous studies have shown that amylase levels are reduced significantly in the pancreas and parotid gland of diabetic rats and that insulin reverses this effect and increases the secretory protein levels. In the pancreas, these changes in amylase protein levels are accompanied by parallel changes in amylase mRNA levels. In the present study, the effects of diabetes and subsequent insulin treatments on contents ( per cell) of amylase protein and its mRNA in parotid glands were compared in rats rendered diabetic with an injection of a beta-cell toxin, streptozotocin (STZ). Both amylase protein and its mRNA contents were reduced significantly in diabetic rats, compared with control rats, and this reduction was reversed following insulin injections of diabetic rats. In insulin-injected diabetic rats, amylase protein contents increased before a detectable increase in amylase mRNA levels was seen. The mRNA contents of a non-secretory protein, actin, did not change during diabetogenesis or subsequent insulin treatments. The reductions in parotid contents of amylase and its mRNA in diabetic rats and the reversal of these changes by insulin are similar to those changes that occur in the pancreas under the same conditions. However, the magnitude of these changes in parotid glands was much smaller than in the pancreas, and the effect of insulin on amylase mRNA synthesis was not as immediate as in the latter gland.

Bilateral aplasia of parotid glands correlated with accessory parotid tissue

2006 ◽  
Vol 120 (4) ◽  
pp. 327-329 ◽  
Author(s):  
D Z Antoniades ◽  
A K Markopoulos ◽  
E Deligianni ◽  
D Andreadis
Keyword(s):  
Parotid Gland ◽  
Salivary Glands ◽  
Branchial Arch ◽  
Interesting Case ◽  
Rare Entity ◽  
Parotid Glands ◽  
Radiological Findings ◽  
Salivary Gland Tissue ◽  
Developmental Disturbances ◽  
Gland Tissue

Congenital absence of major salivary glands, especially the parotid gland, is a rare entity. It is usually monolateral and is not correlated with accessory salivary gland tissue. Aplasia of parotid gland may occur alone or in association with abnormalities of other salivary glands, first branchial arch developmental disturbances or other congenital anomalies.We report an interesting case of bilateral aplasia of the parotid glands together with bilateral accessory parotid tissue, without other congenital or developmental anomalies, and we describe the clinical and radiological findings.

Effect of glucose or fructose feeding on cholesterol synthesis in diabetic animals

1985 ◽  
Vol 249 (5) ◽  
pp. G634-G641 ◽  
Author(s):  
K. R. Feingold ◽  
A. H. Moser
Keyword(s):  
Cholesterol Synthesis ◽  
Reductase Activity ◽  
Active Form ◽  
Diabetic Rats ◽  
Hepatic Cholesterol ◽  
Hmg Coa Reductase ◽  
Hepatic Cholesterol Synthesis ◽  
Streptozotocin Induced Diabetes ◽  
Intestinal Hypertrophy ◽  
Coa Reductase

Previous studies have demonstrated that cholesterol synthesis is increased twofold in the small intestines of rats with streptozotocin-induced diabetes. The purpose of the present study was to determine the effect of adding glucose or fructose to standard rat chow on cholesterol synthesis in control and diabetic rats. In control rats a 25% glucose or fructose diet fed for 21 days markedly inhibited hepatic cholesterol synthesis in the liver. In contrast, in diabetic animals only fructose inhibited hepatic cholesterol synthesis. In both control and diabetic animals the addition of these simple sugars to the diet did not markedly alter extrahepatic cholesterol synthesis. The enhancement of small intestinal cholesterol synthesis observed in diabetic animals was present regardless of the dietary manipulations. Further studies demonstrated that the addition of smaller concentrations of fructose (10%) to standard rat chow decreased hepatic cholesterol synthesis in both control and diabetic rats. Similarly the addition of fructose to the diet of control and diabetics for a period as short as 2 days was also sufficient to inhibit hepatic cholesterol synthesis. In both control and diabetic animals, fructose feeding decreased hepatic 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase activity but did not alter the percentage of HMG-CoA reductase in the active form. Finally, the intestinal hypertrophy and stimulation of intestinal cholesterogenesis that are characteristic of streptozotocin-induced diabetes occurred when either glucose or fructose was the sole caloric source.

scholarly journals IS THERE AN EARLY ULTRASONOGRAPHIC PATTERN IN SALIVARY GLANDS IN BOTH PRIMARY AND SECONDARY SJÖGREN SYNDROME?

2017 ◽  
Vol 26 (1) ◽  
pp. 30-37
Author(s):  
Vasilia Iorgoveanu ◽  
◽  
Violeta Bojinca ◽  
Madalina Gheorghe ◽  
Diana Mazilu ◽  
...  
Keyword(s):  
Parotid Gland ◽  
Salivary Glands ◽  
Early Period ◽  
Sjögren Syndrome ◽  
Biological Data ◽  
Inflammatory Disorder ◽  
Sjogren Syndrome ◽  
Parotid Glands ◽  
Submandibular Glands ◽  
Left And Right

Background. Sjögren syndrome (SS) is a systemic chronic inflammatory disorder characterized by lymphocytic infiltrates in exocrine organs. Ultrasonography (US) demonstrates specificity and sensibility in major salivary glands (SG) evaluation. Recent data confirm US might be used as primary evaluation technique for its ability to show structural alterations of parenchyma (1). Objective. To assess the gray scale (GS) parenchymal inhomogeneity of major SG in patients with established primary and secondary SS and correlate with clinical and biological data. Methods. Consecutive patients with SS were recruited and SG US was performed. Inhomogeneity of glandular parenchyma was quantified binary on each gland. ESSDAI and ESSPRI scores were calculated. Statistics was performed with SPSS. Results. Twenty one (42.85% primary SS, 90.47% female) consecutive patients were included. Mean age was 53.66+/-12.99 years and disease duration 5.33+/-3.74 years. Antibody SSA/SSB presence was found in 85.7% (18/21). ESSDAI mean was 8.67+/-8.9 (0-29), ESSPRI 10.13+/-5.59(0-20). There were no differences regarding ESSDAI and ESSPRI in the two groups (primary and secondary SS). Right parotid gland showed alterations in 71.4% patients (77% with primary SS, 66% with secondary SS). Frequently inhomogeneity was found in all major SG (33%, 22% left and right submandibular, 77%, 44.4% left and right parotid glands) in primary SS. Both submandibular glands were symmetrically involved (p<0.02). Duration of disease was negatively correlated to inhomogeneity of right parotid gland (p<0.02). Conclusion. Inhomogeneity in major SG in GS US was found in the majority of patients with primary and secondary SS. The symmetrical involvement of submandibular glands was significant. The inhomogeneity appears in the early period of diagnosis. No major differences were found between two groups.

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.

Biophysical and Morphological Properties of Parasympathetic Neurons Controling the Parotid and von Ebner Salivary Glands in Rats

2005 ◽  
Vol 93 (2) ◽  
pp. 678-686 ◽  
Author(s):  
Hideyuki Fukami ◽  
Robert M. Bradley
Keyword(s):  
Parotid Gland ◽  
Salivary Glands ◽  
Membrane Properties ◽  
Morphological Properties ◽  
Similar Response ◽  
Parotid Glands ◽  
Membrane Hyperpolarization ◽  
Parasympathetic Neurons ◽  
Discharge Patterns ◽  
Repetitive Discharge

The inferior salivatory nucleus (ISN) contains parasympathetic neurons controlling the parotid and von Ebner salivary glands. To characterize the neurophysiological and morphological properties of these neurons, intracellular recordings were made from anatomically identified ISN neurons in rat brain slices. Neurons were also filled with Lucifer yellow and morphometrically analyzed. Based on responses to membrane hyperpolarization followed by depolarization, three types of repetitive discharge patterns were defined for neurons innervating the parotid gland. The regular, repetitive discharge response to membrane depolarization was changed by hyperpolarization resulting either in a delay in the occurrence of the first spike or to an increase in the length of the first interspike interval in the action potential train. Membrane hyperpolarization had little effect on the discharge pattern of some neurons. Similar response discharge patterns were found for neurons innervating the von Ebner salivary gland, which also included a further group of neurons that responded with a short burst of action potentials. Neurons innervating the parotid salivary glands differed morphologically from the von Ebner salivary glands having significantly larger soma and more and longer dendrites than von Ebner gland neurons. In addition, the mean membrane input resistance, time constant, and spike half-width of parotid gland neurons was significantly lower than in von Ebner gland neurons. These differences in intrinsic membrane properties and morphology may relate to the functions of the von Ebner and parotid glands. von Ebner glands are involved in taste stimulus delivery and removal from posterior tongue papillae while the parotid glands contribute saliva to the entire mouth.

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 Strain-specific differences in the proline-rich proteins and glycoproteins induced in rat salivary glands by chronic isoprenaline treatment

1985 ◽  
Vol 230 (2) ◽  
pp. 369-378 ◽  
Author(s):  
M G Humphreys-Beher
Keyword(s):  
Amino Acid ◽  
Salivary Glands ◽  
Specific Activity ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Apparent Difference ◽  
Marker Enzyme ◽  
Parotid Glands ◽  
Amino Acid Compositions ◽  
Submandibular Glands

Parotid and submandibular glands were isolated from five strains of rat after chronic injection of the β-adrenergic receptor agonist isoprenaline (isoproterenol). The glands were observed to have undergone a marked increase in wet weight, owing to hypertrophy and hyperplasia. The 100 000 g soluble fraction of gland cell lysates were extracted with 10% (w/v) trichloroacetic acid, and the soluble material subsequently analysed by SDS (sodium dodecyl sulphate)/polyacrylamide-gel electrophoresis. By this procedure, evidence was obtained for the induction, in isoprenaline-treated parotid and submandibular glands, of proline-rich proteins with apparent Mr values ranging from 20 000 to 40 000. Heterogeneity was evident in the proteins produced for a specific gland between the rat strains, although the amino acid compositions were the same. Products from induced mRNAs translated in vitro had similar mobilities in SDS/polyacrylamide gels, despite the apparent difference in mobility of trichloracetic acid-extracted proline-rich proteins from the various strains. Strain-specific differences were noted for the proline-rich glycoproteins from control salivary glands as well as those induced as a consequence of isoprenaline treatment. Although the glycoproteins had similar amino acid compositions, there was considerable heterogeneity in the carbohydrate compositions for these proteins, suggesting that the differences were the result of post-translational modifications during glycosylation. Induction of the increased activity of the Golgi membrane marker enzyme UDP-galactose:2-acetamido-2-deoxy-D-glucosamine 4 β-galactosyltransferase (EC 2.4.1.22) occurred to the same extent in the parotid glands of all strains examined. There was no change in the specific activity of a second enzyme, UDP-galactose:N-acetylgalactosaminyl-protein 3 β-galactosyltransferase (no EC designation).

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