scholarly journals Chronic Vascular Inflammation in Patients With Type 2 Diabetes: Endothelial biopsy and RT-PCR analysis

Diabetes Care ◽  
2005 ◽  
Vol 28 (2) ◽  
pp. 379-384 ◽  
Author(s):  
L. Feng ◽  
C. Matsumoto ◽  
A. Schwartz ◽  
A. M. Schmidt ◽  
D. M. Stern ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Vascular Inflammation ◽  
Pcr Analysis ◽  
Rt Pcr

scholarly journals A Network Pharmacology Approach to Investigate the Mechanism of Erjing Prescription in Type 2 Diabetes

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jiexin Wang ◽  
Haiqing Chu ◽  
Hangying Li ◽  
Wenqian Yang ◽  
Yu Zhao ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Song Dynasty ◽  
Signal Pathway ◽  
Network Pharmacology ◽  
Pcr Analysis ◽  
Signal Pathways ◽  
Rt Pcr ◽  
Bioactive Constituents ◽  
Lycium Barbarum

Erjing prescription (EJP) was an ancient formula that was recorded in the General Medical Collection of Royal Benevolence of the Song Dynasty. It has been frequently used to treat type 2 diabetes mellitus (T2DM) in the long history of China. The formula consists of Lycium barbarum L. and Polygonatum sibiricum F. Delaroche with a ratio of 1 : 1. This study aimed to identify the potential effects and mechanisms of EJP treatment T2DM. The target proteins and possible pathways of EJP in T2DM treatment were investigated by the approach of network pharmacology and real-time PCR (RT-PCR). 99 diabetes-related proteins were regulated by 56 bioactive constituents in EJP in 26 signal pathways by Cytoscape determination. According to GO analysis, 606 genes entries have been enriched. The PPI network suggested that AKT1, EGF, EGFR, MAPK1, and GSK3β proteins were core genes. Among the 26 signal pathways, the PI3K-AKT signal pathway was tested by the RT-PCR. The expression level of PI3K p85, AKT1, GSK3β, and Myc mRNA of this pathway was regulated by EJP. The study based on network pharmacology and RT-PCR analysis revealed that the blood sugar level was regulated by EJP via regulating the PI3K-AKT signal pathway. Plenty of new treatment methods for T2DM using EJP were provided by network pharmacology analysis.

scholarly journals Determinants of Increased Serum Calprotectin in Patients with Type 2 Diabetes Mellitus

2020 ◽  
Vol 21 (21) ◽  
pp. 8075
Author(s):  
Milou M. Oosterwijk ◽  
Stephan J.L. Bakker ◽  
Tom Nilsen ◽  
Gerjan Navis ◽  
Gozewijn D. Laverman
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Vascular Inflammation ◽  
Strong Association ◽  
Median Serum ◽  
Potential Biomarker ◽  
Calprotectin Level ◽  
Peripheral Artery Diseases

Circulating calprotectin is a potential biomarker for endovascular inflammation in type 2 diabetes mellitus (T2DM). We investigated the determinants of calprotectin and its relationship with the presence of cardiovascular disease (CVD) in 362 T2DM patients included in the Diabetes and Lifestyle Cohort Twente-1 (DIALECT-1) study. Lifestyle exposures, including nutrition, were determined by validated questionnaires. CVD was defined as coronary artery diseases, strokes, and peripheral artery diseases. Median serum calprotectin levels were 1.04 mg/L [IQR: 0.73–1.46 mg/L] and were higher in women (1.11 mg/L) than men (0.96 mg/L, p = 0.007). Current smoking was a major independent determinant of circulating calprotectin, with a 51% higher calprotectin compared to never smoking (p < 0.001). Albuminuria (p = 0.011), former smoking (p = 0.023), and intake of mono- and disaccharides (p = 0.005) also contributed independently to circulating calprotectin. Each incremental increase in calprotectin level was associated with 1.36-times higher odds for CVD (95% CI 1.04–1.77, p = 0.026). In the current study, calprotectin was the only inflammatory parameter significantly associated with CVD. The strong association of circulating calprotectin with smoking, a well-known direct cause of vascular inflammation, and also with CVD, stresses the urge for further research to define its role as a biomarker in T2DM.

Daidzein, its effects on impaired glucose and lipid metabolism and vascular inflammation associated with type 2 diabetes

BioFactors ◽  
2018 ◽  
Vol 44 (5) ◽  
pp. 407-417 ◽  
Author(s):  
Dibyendu Das ◽  
Sanjib Sarkar ◽  
Jijnasa Bordoloi ◽  
Sawlang Borsingh Wann ◽  
Jatin Kalita ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Lipid Metabolism ◽  
Vascular Inflammation ◽  
Glucose And Lipid Metabolism

RAGE modulates vascular inflammation and atherosclerosis in a murine model of type 2 diabetes

2006 ◽  
Vol 185 (1) ◽  
pp. 70-77 ◽  
Author(s):  
Thoralf Wendt ◽  
Evis Harja ◽  
Loredana Bucciarelli ◽  
Wu Qu ◽  
Yan Lu ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Murine Model ◽  
Vascular Inflammation

Prophylactic role of vitamin K supplementation on vascular inflammation in type 2 diabetes by regulating the NF-κB/Nrf2 pathwayviaactivating Gla proteins

2018 ◽  
Vol 9 (1) ◽  
pp. 450-462 ◽  
Author(s):  
Anjum Dihingia ◽  
Dibyajyoti Ozah ◽  
Pranab Kumar Baruah ◽  
Jatin Kalita ◽  
Prasenjit Manna
Keyword(s):  
Type 2 Diabetes ◽  
Vitamin K ◽  
Vascular Inflammation ◽  
Vitamin K1 ◽  
The Relationship

There is no previous study that has examined the relationship between circulating vitamin K1 (VK1) and vascular inflammation in type 2 diabetes (T2D).

scholarly journals Diabetes mellitus is a risk factor for prolonged SARS-CoV-2 viral shedding in lower respiratory tract samples of critically ill patients

Endocrine ◽  
2020 ◽  
Vol 70 (3) ◽  
pp. 454-460 ◽  
Author(s):  
Niccolò Buetti ◽  
Pierpaolo Trimboli ◽  
Timothy Mazzuchelli ◽  
Elia Lo Priore ◽  
Carlo Balmelli ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Cox Model ◽  
Viral Rna ◽  
Rt Pcr ◽  
Viral Shedding

Abstract Purpose The length of time a critically ill coronavirus disease 2019 (COVID-19) patient remains infectious and should therefore be isolated remains unknown. This prospective study was undertaken in critically ill patients to evaluate the reliability of single negative real-time polymerase chain reaction (RT-PCR) in lower tracheal aspirates (LTA) in predicting a second negative test and to analyze clinical factors potentially influencing the viral shedding. Methods From April 9, 2020 onwards, intubated COVID-19 patients treated in the intensive care unit were systematically evaluated for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by RT-PCR of nasopharyngeal swabs and LTA. The time to negativity was defined as the time between the onset of symptoms and the viral clearance in LTA. In order to identify risk factors for prolonged viral shedding, we used univariate and multivariate Cox proportional hazards models. Results Forty-eight intubated SARS-CoV-2 patients were enrolled. Overall, we observed that the association of the first negative RT-PCR with a second negative result was 96.7%. Median viral shedding was 25 (IQR: 21.5–28) days since symptoms’ onset. In the univariate Cox model analysis, type 2 diabetes mellitus was associated with a prolonged viral RNA shedding (hazard ratio [HR]: 0.41, 95% CI: 0.06–3.11, p = 0.04). In the multivariate Cox model analysis, type 2 diabetes was associated with a prolonged viral RNA shedding (HR: 0.31, 95% CI: 0.11–0.89, p = 0.029). Conclusion Intubated patients with type 2 diabetes mellitus may have prolonged SARS-CoV-2 shedding. In critically ill COVID-19 patients, one negative LTA should be sufficient to assess and exclude infectivity.

Abstract P632: Nlrp3/inflammasome Activation Contributes To Aldosterone-induced Vascular Dysfunction In Type 2 Diabetes.

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Nathanne S Ferreira ◽  
Thiago Bruder-Nascimento ◽  
Camila A Pereira ◽  
Camila Z Zanotto ◽  
Douglas S Prado ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Endothelial Dysfunction ◽  
Nlrp3 Inflammasome ◽  
Vascular Dysfunction ◽  
Vascular Inflammation ◽  
Diabetic Patients ◽  
Inflammasome Activation ◽  
Caspase 1

Diabetic patients and animal models of type 2 diabetes (DM2) display increased plasma aldosterone (aldo) levels. Aldo induces vascular inflammation and endothelial dysfunction. NOD-like receptors, which are pattern recognition receptors involved in a variety of host innate immune responses, promote vascular inflammation. We hypothesized that aldo via mineralocorticoid receptors (MR) activates the inflammasome platform in the vasculature of DM2 mice. Control (db/+) and diabetic (db/db) mice were treated with vehicle or spironolactone (spiro - MR antagonist, 50 mg/Kg/day). Mesenteric resistance arteries (MA) from db/db mice exhibited reduced acetylcholine (ACh) dilation, which was reversed by spiro [Emax (% of relaxation): db/+: 78.5±4.1; db/db: 40.5±6.4; db/+spiro: 77.0±3.8; db/db+spiro: 62.8±5.9 n=3-6 p<0.05]. Spiro treatment reduced caspase-1 and mature IL-1β content in MA from db/db mice. Spiro also reduced caspase-1 activity in macrophages from peritoneal lavage of db/db mice [% of activity: db/+: 33.9±2.5; db/db: 51.8±7.4; db/+spiro: 31.1±1.9; db/db+spiro: 34.8±3.8 n=4-7, p<0.05]. In vitro, aldo increased mature IL-1β in vascular smooth muscle cells (VSMC) (cont: 0.9±0.01 ; LPS+Nigericine: 6.1±2.1 ; Aldo 4h: 9.7±2.6; LPS+Aldo 4h: 12.8±1.9 n=3-5, p<0.05). To determine whether aldo in vivo directly activates NLRP3/inflammasome in the vasculature and whether NLRP3 activation contributes to aldo-induced vascular injury, aldo was infused (600 ug/Kg/day for 14 days) in wild type (WT) and NLRP3 knockout mice ( NLRP3-/- ) after bone marrow transplantation from WT donor. The groups were constituted: WT->WT, WT->WT+aldo and WT-> NLRP3 -/-+aldo. NLRP3 -/- mice were protected against aldo-induced endothelial dysfunction [Emax: WT: 89.3±2.9; WT+aldo: 39.8±1.8; NLRP3-/- +aldo: 87.7±4.2, p<0.05]. Aldo treatment leaded to endothelial dysfunction in WT ->WT mice, but WT-> NLRP3 -/- mice were protected from aldo-induced endothelial dysfunction [Emax: WT->WT: 95.1±3.1; WT->WT+aldo: 57.1±4.7; WT->NLRP3-/-+aldo: 85.3±3.1 p<0.05]. These results suggest that NLRP3/inflammasome in the vasculature plays a crucial role on aldo/MR-induced vascular damage and on DM2-associated vascular dysfunction. Financial Support: FAPESP, CAPES, CNPq.

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