Stereology and ultrastructure of the salivary glands of diabetic Nod mice submitted to long-term insulin treatment

Author(s):  
Eduardo José Caldeira ◽  
José Angelo Camilli ◽  
Valéria Helena Alves Cagnon
Author(s):  
J H Parr

Serum concentration of free T3 and, in female patients, FT4, were found to be lower in 20 asymptomatic, moderately-poor or well controlled, diabetics treated with insulin than in a group of non-diabetic subjects. Over a mean 3-month period of the study a significant fall occurred in HbA1 concentration in both groups of diabetics without change in free thyroid hormone levels. The mean capillary blood glucose, fasting free insulin and fasting lipid concentrations, other than high density lipoprotein (HDL) cholesterol, did not change. No correlations were found between the changes in HbA1 and free thyroid hormone concentrations. Improvement in long term metabolic control did not influence free thyroid hormone levels in well controlled and moderately-poor controlled diabetics, taking insulin.


1996 ◽  
Vol 116 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Süleyman Aydin ◽  
Yusuf Öztürk ◽  
V.Melih Altan ◽  
Nuray Yildizoğlu-Ari ◽  
A.Tanju Özçelikay

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Sundararajan Jayaraman ◽  
Arathi Jayaraman

Induction of autoimmune diseases is predisposed by background genetics and influenced by environmental factors including diet and infections. Since consumption of acidified drinking water leads to eradication of gastrointestinal pathogens in animals, we tested whether it may also influence the development of autoimmune diseases. The frequency of spontaneously occurring type 1 diabetes in female NOD mice that were maintained on acidified drinking water by the vendor did not alter after switching to neutral water in our facility. In addition, experimentally induced autoimmune encephalomyelitis was also unaffected by the pH of the drinking water. Interestingly, administration of complete Freund’s adjuvant alone or emulsified with a neuronal peptide to induce neurodegenerative disease during the prediabetic stage completely prevented the onset of diabetes regardless of the pH of the drinking water. However, exposure to microbial products later in life had only a partial blocking effect on diabetes induction, which was also not influenced by the ionic content of the drinking water. Taken together, these data indicate that the onset of autoimmune diseases is not influenced by the gastrointestinal pathogen-depleting treatment, acidified drinking water. Thus, administration of acidic drinking water does not appear to be an option for treating autoimmune diseases.


Micron ◽  
2020 ◽  
Vol 137 ◽  
pp. 102915
Author(s):  
Magdalena Rost-Roszkowska ◽  
Izabela Poprawa ◽  
Łukasz Chajec ◽  
Alina Chachulska-Żymełka ◽  
Małgorzata Leśniewska ◽  
...  

2019 ◽  
Vol 104 (6) ◽  
pp. 2153-2162 ◽  
Author(s):  
Hui Wang ◽  
Jian Kuang ◽  
Mingtong Xu ◽  
Zhengnan Gao ◽  
Qifu Li ◽  
...  

1994 ◽  
Vol 266 (3) ◽  
pp. G433-G443
Author(s):  
Y. Hu ◽  
K. R. Purushotham ◽  
P. Wang ◽  
R. Dawson ◽  
M. G. Humphreys-Beher

The nonobese diabetic (NOD) mouse is subject to autoimmune disease-associated lymphocytic attack on the salivary glands with a corresponding loss of exocrine function. Downregulation of stimulus response to the beta-adrenoceptor agonist, isoproterenol, appears to be related to a decline in beta-adrenergic receptor density, changes in the level of intracellular second messenger signaling component adenosine 3',5'-cyclic monophosphate, and protein kinase A activity. An autoantibody to the beta 1-adrenergic receptor present in the sera of diabetic NOD mice may be involved in the reduced agonist response by virtue of its ability to retard dihydroalprenolol radioligand binding to receptors in the membranes of salivary glands from control mice and recognition of purified beta 1-adrenergic receptor by immunoblotting techniques.


2017 ◽  
Vol 123 ◽  
pp. 9-17 ◽  
Author(s):  
Ippei Kanazawa ◽  
Ken-ichiro Tanaka ◽  
Masakazu Notsu ◽  
Sayuri Tanaka ◽  
Nobuaki Kiyohara ◽  
...  

2007 ◽  
Vol 16 (8) ◽  
pp. 787-798 ◽  
Author(s):  
Hossein Arefanian ◽  
Eric B. Tredget ◽  
Ray V. Rajotte ◽  
Gregory S. Korbutt ◽  
Ron G. Gill ◽  
...  

Type 1 diabetes mellitus (T1DM) is caused by the autoimmune destruction of pancreatic islet β-cells, which are required for the production of insulin. Islet transplantation has been shown to be an effective treatment option for T1DM; however, the current shortage of human islet donors limits the application of this treatment to patients with brittle T1DM. Xenotransplantation of pig islets is a potential solution to the shortage of human donor islets provided xenograft rejection is prevented. We demonstrated that a short-term administration of a combination of anti-LFA-1 and anti-CD154 monoclonal antibodies (mAbs) was highly effective in preventing rejection of neonatal porcine islet (NPI) xenografts in non-autoimmune-prone B6 mice. However, the efficacy of this therapy in preventing rejection of NPI xenografts in autoimmune-prone nonobese diabetic (NOD) mice is not known. Given that the current application of islet transplantation is for the treatment of T1DM, we set out to determine whether a combination of anti-LFA-1 and anti-CD154 mAbs could promote long-term survival of NPI xenografts in NOD mice. Short-term administration of a combination of anti-LFA-1 and anti-CD154 mAbs, which we found highly effective in preventing rejection of NPI xenografts in B6 mice, failed to promote long-term survival of NPI xenografts in NOD mice. However, addition of anti-CD4 mAb to short-term treatment of a combination of anti-LFA-1 and anti-CD154 mAbs resulted in xenograft function in 9/12 animals and long-term graft (>100 days) survival in 2/12 mice. Immunohistochemical analysis of islet grafts from these mice identified numerous insulin-producing β-cells. Moreover, the anti-porcine antibody as well as autoreactive antibody responses in these mice was reduced similar to those observed in naive nontransplanted mice. These data demonstrate that simultaneous targeting of LFA-1, CD154, and CD4 molecules can be effective in inducing long-term islet xenograft survival and function in autoimmune-prone NOD mice.


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