scholarly journals Human cytomegalovirus in the pancreas of patients with type 2 diabetes: Is there a relation to clinical features, mRNA and protein expression of insulin, somatostatin, and MHC class II?

1992 ◽  
Vol 421 (5) ◽  
pp. 371-378 ◽  
Author(s):  
M. Löhr ◽  
B. Bergstrome ◽  
R. Maekawa ◽  
M. B. A. Oldstone ◽  
G. Klöppel
Keyword(s):  
Type 2 Diabetes ◽  
Protein Expression ◽  
Mhc Class Ii ◽  
Clinical Features ◽  
Human Cytomegalovirus ◽  
Class Ii ◽  
Mrna And Protein Expression

Type 2 diabetes: increased expression and contribution of IKCa channels to vasodilation in small mesenteric arteries of ZDF rats

2014 ◽  
Vol 307 (8) ◽  
pp. H1093-H1102 ◽  
Author(s):  
Christian Schach ◽  
Markus Resch ◽  
Peter M. Schmid ◽  
Guenter A. Riegger ◽  
Dierk H. Endemann
Keyword(s):  
Type 2 Diabetes ◽  
Protein Expression ◽  
Experimental Models ◽  
Diabetic Rats ◽  
Mesenteric Arteries ◽  
Rt Pcr ◽  
Mrna And Protein Expression ◽  
Zdf Rats ◽  
Endothelium Dependent Relaxation

Impaired endothelial function, which is dysregulated in diabetes, also precedes hypertension. We hypothesized that in Type 2 diabetes, the impaired endothelium-dependent relaxation is due to a loss of endothelium-derived hyperpolarization (EDH) that is regulated by impaired ion channel function. Zucker diabetic fatty (ZDF), Zucker heterozygote, and homozygote lean control rats were used as the experimental models in our study. Third-order mesenteric arteries were dissected and mounted on a pressure myograph; mRNA was quantified by RT-PCR and channel proteins by Western blotting. Under nitric oxide (NO) synthase and cyclooxygenase inhibition, endothelial stimulation with ACh fully relaxes control but not diabetic arteries. In contrast, when small-conductance calcium-activated potassium (KCa) channels and intermediate- and large-conductance KCa (I/BKCa) are inhibited with apamin and charybdotoxin, NO is able to compensate for ACh-induced relaxation in control but not in diabetic vessels. After replacement of charybdotoxin with 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34; IKCa inhibitor), ACh-induced relaxation in diabetic animals is attenuated. Specific inhibition with TRAM-34 or charybdotoxin attenuates ACh relaxation in diabetes. Stimulation with 1-ethyl-2-benzimidazolinone (IKCa activator) shows a reduced relaxation in diabetes. Activation of BKCa with 1,3-dihydro-1-[2-hydroxy-5-(trifluoromethyl)phenyl]-5-(trifluoromethyl)-2H-benzimidazol-2-one NS619 leads to similar relaxations of control and diabetic arteries. RT-PCR and Western blot analysis demonstrate elevated mRNA and protein expression levels of IKCa in diabetes. Our results suggest that the compensatory effect of NO and EDH-associated, endothelium-dependent relaxation is reduced in ZDF rats. Specific blockade of IKCa with TRAM-34 reduces NO and EDH-type relaxation in diabetic rats, indicating an elevated contribution of IKCa in diabetic small mesenteric artery relaxation. This finding correlates with increased IKCa mRNA and protein expression in this vessel.

scholarly journals Molecular Mechanisms of Estrogen Receptors' Suppression of Lipogenesis in Pancreatic β-Cells

Endocrinology ◽  
2012 ◽  
Vol 153 (7) ◽  
pp. 2997-3005 ◽  
Author(s):  
Joseph P. Tiano ◽  
Franck Mauvais-Jarvis
Keyword(s):  
Type 2 Diabetes ◽  
Protein Expression ◽  
Β Cells ◽  
Β Cell ◽  
Element Binding Protein ◽  
Mrna And Protein Expression ◽  
Amp Activated Protein Kinase ◽  
G Protein Coupled

The gonadal steroid, 17β-estradiol (E2), suppresses pancreatic islet fatty acid and glycerolipid synthesis and prevents β-cell failure in rodent models of type 2 diabetes. β-Cell estrogen receptors (ER) mediate these actions by suppressing the expression and enzymatic activity of fatty acid synthase (FAS). Here, we explored the mechanism of FAS suppression. We show that E2, and pharmacological agonists for ERα, ERβ, and the G protein-coupled ER, suppress mRNA and protein expression of the transcriptional regulators of FAS, namely, sterol regulatory element-binding protein 1c (SREBP1c) and carbohydrate response element binding protein (ChREBP) in insulin-secreting INS-1 cells. ER suppress SREBP1c and ChREBP mRNA and protein expression via an extranuclear localization. Using two mouse lines with pancreas-specific null deletion of either ERα or the signal transducer and activator of transcription 3 (STAT3), we show that ERα activation in vivo reduces SREBP1c and ChREBP mRNA expression via a direct islet action involving STAT3 activation. The master regulators of lipogenesis, liver X receptor (LXR) α and β, transcriptionally up-regulate SREBP1c and ChREBP. We find that activation of ERα, ERβ, and G protein-coupled ER suppresses LXR's mRNA expression in INS-1 cells. We also observe that activation of ERα in mouse islets in vivo suppresses LXR mRNA in a STAT3-dependent manner. Finally, we show that E2 also activates and uses AMP-activated protein kinase in INS-1 cells to suppress SREBP1c protein expression. This study identifies extranuclear ER pathways involving STAT3 and AMP-activated protein kinase in the genetic control of lipogenesis with therapeutic implications to protect β-cells in type 2 diabetes.

scholarly journals Downregulation in GATA4 and Downstream Structural and Contractile Genes in the db/db Mouse Heart

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Tom L. Broderick ◽  
Marek Jankowski ◽  
Donghao Wang ◽  
Bogdan A. Danalache ◽  
Cassandra R. Parrott ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Atrial Natriuretic Peptide ◽  
Protein Expression ◽  
Natriuretic Peptide ◽  
Transcriptional Factor ◽  
Mouse Heart ◽  
Structural Protein ◽  
Structural Genes ◽  
Mrna And Protein Expression

Reduced expression of GATA4, a transcriptional factor for structural and cardioprotective genes, has been proposed as a factor contributing to the development of cardiomyopathy. We investigated whether the reduction of cardiac GATA4 expression reported in diabetes alters the expression of downstream genes, namely, atrial natriuretic peptide (ANP), B-type natriuretic, peptide (BNP), and α- and β-myosin heavy chain (MHC). db/db mice, a model of type 2 diabetes, with lean littermates serving as controls, were studied. db/db mice exhibited obesity, hyperglycemia, and reduced protein expression of cardiac GLUT4 and IRAP (insulin-regulated aminopeptidase), the structural protein cosecreted with GLUT4. Hearts from db/db mice had reduced protein expression of GATA4 (~35%) with accompanying reductions in mRNA expression of ANP (~40%), BNP (~85%), and α-MHC mRNA (~50%) whereas expression of β-MHC mRNA was increased by ~60%. Low GATA4 was not explained by an increased ligase or atrogin1 expression. CHIP protein content was modestly downregulated (27%) in db/db mice whereas mRNA and protein expression of the CHIP cochaperone HSP70 was significantly decreased in db/db hearts. Our results indicate that low GATA4 in db/db mouse heart is accompanied by reduced expression of GATA4-regulated cardioprotective and structural genes, which may explain the development of cardiomyopathy in diabetes.

scholarly journals P-82 Impact of type 2 diabetes mellitus in overall survival and clinical features of Latin patients with colorectal cancer: A 15-year follow-up

2021 ◽  
Vol 32 ◽  
pp. S125-S126
Author(s):  
G. Calderillo-Ruiz ◽  
C. Diaz ◽  
H. Lopez Basave ◽  
E. Ruiz-Garcia ◽  
A. Apodaca ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Colorectal Cancer ◽  
Type 2 Diabetes ◽  
Overall Survival ◽  
Type 2 Diabetes Mellitus ◽  
Clinical Features

Time-course changes in clinical features of early-onset Japanese type 1 and type 2 diabetes: TWMU hospital-based study

2008 ◽  
Vol 82 (1) ◽  
pp. 80-86 ◽  
Author(s):  
Yasuko Uchigata ◽  
Toshika Otani ◽  
Hiroko Takaike ◽  
Junnosuke Miura ◽  
Mari Osawa ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Clinical Features ◽  
Early Onset ◽  
Time Course ◽  
Course Changes
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