Use of antioxidant in the attempt recovery of insulin receptors in salivary glands of spontaneously diabetic mice

2012 ◽  
Vol 23 (2) ◽  
pp. 35-39
Author(s):  
Raphael Oliveira Ramos Franco Netto ◽  
Rafael Mancio ◽  
Rodrigo Eduardo Silva ◽  
Eliézer Guimarães Moura ◽  
Marco Antonio Dias ◽  
...  
Keyword(s):  
Salivary Glands ◽  
Insulin Receptors ◽  
Diabetic Mice

scholarly journals CD4/CD8 Antibodies Reduce Histopathological Damage in Salivary Glands of Spontaneously Diabetic Mice

2019 ◽  
Vol 26 (2) ◽  
pp. 149-157
Author(s):  
Raphael Oliveira Ramos Franco Netto ◽  
Eliézer Guimarães Moura ◽  
Luan Oenning Col ◽  
Magda Jaciara Barros ◽  
Juliana de Almeida Rodrigues Franco Netto ◽  
...  
Keyword(s):  
Salivary Glands ◽  
Nod Mice ◽  
Insulin Receptors ◽  
Nonparametric Test ◽  
Diabetic Mice ◽  
Parotid Glands ◽  
Submandibular Glands ◽  
Group Iii ◽  
Group I ◽  
Group Ii

Abstract Background and aims: Diabetes affects the metabolism promoting damage in different tissues, including salivary glands. Current treatments, such as insulin, are ineffective to recovery of these tissues. In this aspect, the immunotherapy has been tested, but it can be inefficient as an agent for the control of damage caused by diabetes. The aim of this study to evaluate the association in anti-CD4 and anti-CD8 monoclonal antibody in the recovery of salivary glands of diabetic NOD mice. Material and methods: Fifteen spontaneously diabetic mice (NOD) were divided into three groups with 5 animals each: group I (Balb/C control mice), group II (untreated NOD mice), group III (NOD mice treated with CD4 and CD8 antibodies). The CD4 and CD8 antibodies (IMUNY, Rheabiotech Ltda, Brazil) were administered by intravenously injections (25 ug/days: 0, 7, 14, and 21). After treatment salivary glands samples were analyzed by immunofluorescence, microscopy, light microscopy and stereology. (ethical approval process: 304/11), Analysis of variance (ANOVA) and Kruskal-Wallis nonparametric test were used. Results: Elevated levels of glucose (mg/dl) were observed in untreated animals (group II) (605.25 ± 31.23, p≤0.05), whereas in treated animals (group III), were noted a decrease in these levels (464.77 ± 39.66, p≤0.05). Tissue restructure, characterized by cell volume recovery, also was observed in group III (nuclear volume of parotid glands: (109.91 ± 02.03, p≤0.05) and submandibular glands: (107.52 ± 02, p≤0.05) (cytoplasmic volume of parotid glands: (356.14 ± 26.34, p≤0.05) and submandibular glands: (331.22 ± 32.11, p≤0.05). Intense signaling (+++) of insulin receptors was observed in animals of group I. On the other hand, in group II was noted a reduction of these receptors (+). In treated animals (group III) were observed a recovery of the insulin receptors (+++). Conclusions: This treatment was effective in the recovery of salivary acinar cells, contributed also to homeostasis of body metabolism. Thus, this immunomodulation promoted a beneficial effect on the recovery of these tissues.

scholarly journals Local Administration of Soluble CD40:Fc to the Salivary Glands of Non-Obese Diabetic Mice Does Not Ameliorate Autoimmune Inflammation

PLoS ONE ◽  
2012 ◽  
Vol 7 (12) ◽  
pp. e51375 ◽  
Author(s):  
Nienke Roescher ◽  
Jelle L. Vosters ◽  
Zhenan Lai ◽  
Toshimitsu Uede ◽  
Paul P. Tak ◽  
...  
Keyword(s):  
Salivary Glands ◽  
Local Administration ◽  
Diabetic Mice ◽  
Autoimmune Inflammation

scholarly journals PEPTIDE VACCINE TO RECOVERY THE SALIVARY GLANDS OF DIABETIC MICE

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Eduardo José Caldeira ◽  
Rodrigo Eduardo Silva ◽  
Marco Antônio Dias ◽  
Rafael Dias Mancio ◽  
Raphael Oliveira Netto ◽  
...  
Keyword(s):  
Salivary Glands ◽  
Peptide Vaccine ◽  
Diabetic Mice

scholarly journals Recovery of INS-R and ER-alpha expression in the salivary glands of diabetic mice submitted to hormone replacement therapy

2011 ◽  
Vol 56 (10) ◽  
pp. 1129-1136 ◽  
Author(s):  
Eliana Tiemi Maekawa ◽  
Éber Emanuel Maioral ◽  
Hugo Tadeu Metidieri ◽  
Paty Karoll Picardi ◽  
Eduardo José Caldeira
Keyword(s):  
Hormone Replacement Therapy ◽  
Replacement Therapy ◽  
Salivary Glands ◽  
Hormone Replacement ◽  
Diabetic Mice ◽  
Er Alpha

scholarly journals Blockade of lymphotoxin-beta receptor signaling reduces aspects of Sjögren syndrome in salivary glands of non-obese diabetic mice

2009 ◽  
Vol 11 (1) ◽  
pp. R24 ◽  
Author(s):  
Margaret K Gatumu ◽  
Kathrine Skarstein ◽  
Adrian Papandile ◽  
Jeffrey L Browning ◽  
Roy A Fava ◽  
...  
Keyword(s):  
Salivary Glands ◽  
Sjögren Syndrome ◽  
Sjogren Syndrome ◽  
Receptor Signaling ◽  
Diabetic Mice ◽  
Beta Receptor ◽  
Lymphotoxin Beta Receptor

Regulation of pancreatic acinar cell insulin receptors by insulin

1984 ◽  
Vol 247 (2) ◽  
pp. G155-G160 ◽  
Author(s):  
J. Mossner ◽  
C. D. Logsdon ◽  
I. D. Goldfine ◽  
J. A. Williams
Keyword(s):  
Acinar Cell ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Pancreatic Acinar Cell ◽  
Diabetic Mice ◽  
Pancreatic Acini ◽  
Endogenous Insulin ◽  
High Concentrations ◽  
Triton X

In vivo pancreatic acini from normal mice are exposed to very high concentrations of insulin. To determine whether insulin receptors in these acini are downregulated by this endogenous insulin, insulin receptors on acini from both normal and diabetic mice were studied. Isolated acini from normal mice, which have accompanying islets of Langerhans, were studied under conditions where endogenous insulin was minimized. These acini bound 50% less 125I-insulin than acini from mice made diabetic with streptozotocin. Computer analysis of competition-inhibition curves showed a decrease in the number of insulin receptors in acini from normal mice when compared with acini from diabetic mice; however, the IC50 (a measure of receptor affinity) remained unchanged at approximately 1 nM. To study further the regulation of acinar cell insulin receptors, acini from diabetic mice were placed in suspension culture for 24 h. Addition of 1 microM insulin during the culture period led to a 30% decrease in subsequent 125I-insulin binding; the presence or absence of either epidermal growth factor or carbachol was without effect on insulin binding. The decrease in binding induced by insulin resulted from a change in receptor number without an alteration of the IC50. Measurement of total acinar cell insulin receptors by solubilization of these acini in 1% Triton X-100 showed that this insulin-induced decrease was due to a change in the total number of cellular insulin receptors. The present study suggests, therefore, that insulin can regulate its own receptor on pancreatic acini and that in vivo insulin receptors in normal pancreatic cells are downregulated, presumably due to high ambient insulin concentrations.

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