scholarly journals Role of some serum biomarkers in the early detection of diabetic cardiomyopathy

2021 ◽  
pp. FSO682
Author(s):  
Amany H Abdelrahman ◽  
Iman I Salama ◽  
Somaia I Salama ◽  
Dalia M Elmosalami ◽  
Mona H Ibrahim ◽  
...  
Keyword(s):  
Early Detection ◽  
Diastolic Dysfunction ◽  
Diabetic Cardiomyopathy ◽  
Systolic Dysfunction ◽  
Area Under The Curve ◽  
Serum Biomarkers ◽  
Control Groups ◽  
Tnf Α

Aim: To assess the role of serum biomarkers in early prediction of diabetic cardiomyopathy. Materials and methods: The participants were three groups of Type 2 diabetes mellitus (DM) patients having diastolic dysfunction (DM-DD), systolic dysfunction (DM-SD) and normal echocardiography (DM-N) with two control groups: non-DM diastolic dysfunction patients (DD) and healthy controls. AGEs, TNF-α, IL-6, IGFBP-7, creatinine and insulin were assessed. Results: TNF-α, AGEs, creatinine and insulin panel had area under the curve (AUC) of 0.913 in distinguishing DM-DD from DM-N (78.7% sensitivity and 100% specificity). IL-6 and AGEs panel had AUC 0.795 for differentiating DM-SD from DM-DD (90.6% sensitivity). IL-6, TNF-α and AGEs panel had AUC 0.924 for differentiating diabetic cardiomyopathy from DM-N (85% sensitivity and specificity). Conclusion: A panel of AGEs, IL-6, TNF-α, insulin and creatinine might be used for early detection of DM-DD among T2DM patients.

scholarly journals Role of Serum Biomarkers in Early Detection of Diabetic Cardiomyopathy in the West Virginian Population

2016 ◽  
Vol 13 (3) ◽  
pp. 161-168 ◽  
Author(s):  
Adam Shaver ◽  
Alexandra Nichols ◽  
Ellen Thompson ◽  
Amrita Mallick ◽  
Kristen Payne ◽  
...  
Keyword(s):  
Early Detection ◽  
Diabetic Cardiomyopathy ◽  
Serum Biomarkers ◽  
The West

Abstract 204: Loss Of Akt Caused Aging-induced Cardiac Systolic Dysfunction But Is Independent From Comorbid Diastolic Dysfunction In Aging.

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Morihiko Aoyama ◽  
Yasuko K Bando ◽  
Akio Monji ◽  
Toko Mitusi ◽  
Haruya Kawase ◽  
...  
Keyword(s):  
Diastolic Dysfunction ◽  
Cardiac Dysfunction ◽  
Systolic Dysfunction ◽  
The Body ◽  
Heart Weight ◽  
Control Groups ◽  
Cardiac Geometry ◽  
Induced Changes ◽  
Sam Mice

PURPOSE: Aging is one of the primary factors causing cardiac dysfunction. Diastolic dysfunction (DD) is primary characteristics for aging-induced heart failure. Clinical evidences demonstrate a sustained exercise (EX) ameliorates DD; however, it remains unclear whether EX may ameliorate the aging-related DD and the underlying molecular mechanism. We thus evaluated whether EX may ameliorate cardiac dysfunction in aging and the role of Akt in the EX-induced effects on aging heart. Methods: Male senescence-accelerated (SAM) mice (P10) and its aging-resistant control (R1) were allocated to exercise [EX; 60-min running on treadmill every single day for 6 months (P10-EX and R1-EX)] and exercise-free control groups (P10-ctl and R1-ctl). Age-matched C57BL6 mice were subjected to the same EX protocol (C57-EX and C57-ctl) to compare any influence of genetic background. To elucidate the role of Akt in aging-induced changes in heart, analysis of aged Akt knockout mice (AktKO) were conducted. Results: At baseline, cardiac geometry of R1 strain revealed normal, whereas P10 strain exhibited reduced LV wall thickness and DD. The s-LVF of both strains was preserved. After EX, the body and heart weight of R1 mice were increased (BW; +6.7% and HW; +3.5% versus R1-ctl); however, EX had no influence on BW and HW of P10. EX promoted LV hypertrophy in R1, which was absent in P10-EX. The d-LVF of R1-EX was impaired but their s-LVF was unchanged. In contrast, s-LVF of P10-EX turned impaired [EF(%) 68.9±1.5 vs 74.3±1.2 for P10-ctl], whereas the underlying DD of P10 was unaffected by EX. In C57-EX, cardiac function exhibited the similar trends observed in R1-EX. Cardiac Akt activity of R1-EX and C57-EX were enhanced compared to controls, which was diminished in P10-EX. Aged AktKO exhibited impaired s-LVF [EF(%)61.3±1.0], nonetheless their DD remained unchanged [E/A=2.5±0.3, Dct (msec)= 35.0±2.4]. Conclusions: Our study demonstrates that #1 Akt is essential for adaptive response of LV hypertrophy to EX, #2 aging impairs Akt signaling in heart, leading to systolic dysfunction, and #3 Akt is independent from modulation of cardiac DD induced by aging. Clinical implications are drawn that the benefit of EX on DD may be irrelevant to the aged population.

scholarly journals The role of serum and urinary biomarkers in the diagnosis of early diabetic nephropathy in patients with type 2 diabetes

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7079 ◽  
Author(s):  
Deyuan Zhang ◽  
Shandong Ye ◽  
Tianrong Pan
Keyword(s):  
Type 2 Diabetes ◽  
Diabetic Nephropathy ◽  
Early Stage ◽  
Area Under The Curve ◽  
Diagnostic Value ◽  
Urinary Biomarkers ◽  
Necrosis Factor Alpha ◽  
Tnf Α

Background Previous studies have shown that a variety of biomarkers are closely related to the occurrence and development of early-stage diabetic nephropathy (DN) in patients. The aim of this study was to evaluate the role of multiple sera and urinary biomarkers in the diagnosis of early-stage DN in patients with type 2 diabetes. Methods We enrolled 287 patients with type 2 diabetes, who were classified into normoalbuminuria (n = 144), microalbuminuria (n = 94), or macroalbuminuria (n = 49) groups based on their urine albumin to creatinine ratios (UACR), along with 42 healthy controls. We assessed 13 biomarkers, including transferrin (Tf), immunoglobulin G (IgG), podocalyxin, neutrophil gelatinase-associated lipocalin (NGAL), N-acetyl-beta-glucosaminidase, α-1-microglobulin, 8-hydroxy-deoxyguanosine, tumor necrosis factor-alpha (TNF-α), and interleukin-18 in urine samples, along with cystatin C, total bilirubin, and uric acid in sera samples, to evaluate their diagnostic roles. From the measurements, the blood neutrophil to lymphocyte ratio was also calculated. Results Urinary Tf, IgG, NGAL, and TNF-α were significantly related to the UACR. We calculated the area under the receiver operating characteristic curves (area under the curve) and found that urinary IgG (0.894), NGAL (0.875), Tf (0.861), TNF-α (0.763), and the combination of urinary Tf + IgG + TNF-α + NGAL (0.922) showed good diagnostic value for early-stage DN. Conclusions Urinary Tf, IgG, NGAL, TNF-α, and the combination of all four biomarkers demonstrated excellent diagnostic value for early-stage DN in patients with type 2 diabetes.

Investigating ADAMTS7 and ADAMTS12 levels in prediabetic and Type 2 diabetic patients

2021 ◽  
Author(s):  
Mercan Taştemur ◽  
Selvihan Beysel ◽  
Sema Hepşen ◽  
Sanem Öztekin ◽  
Erman Çakal ◽  
...  
Keyword(s):  
Inflammatory Markers ◽  
Diabetic Patients ◽  
Control Groups ◽  
Type 2 Diabetic Patients ◽  
Human Enzyme ◽  
Significant Difference ◽  
And Control ◽  
Type 2 Diabetic

Background: This study aims to investigate the role of ADAMTS7 and ADAMTS12 on atherosclerosis and inflammation in prediabetic and diabetic patients. Patients & methods: Serum ADAMTS7 and ADAMTS12 levels were compared with the atherosclerotic and inflammatory markers in diabetic (n = 65, female 30.9%, mean age = 53 years), prediabetic (n = 55, female 36.6%, mean age = 49 years) and control groups (n = 55, females 32.5%, mean age = 49 years). Serum ADAMTS levels were determined by a human enzyme-liked immunoassay. Results: In terms of ADAMTS7, there was no significant difference between diabetic, prediabetic and control groups (50.93, 44.34, 59.07, respectively; p > 0.05). ADAMTS12 is lower in diabetics (p < 0.05), whereas it is similar in prediabetics and controls (14.53, 20.76, 25.05, respectively; p > 0.05). ADAMTS7 and ADAMTS12 levels did not differ in diabetic nephropathy, retinopathy and neuropathy (p > 0.05). Conclusion: While ADAMTS12 was significantly lower in diabetics and prediabetics, ADAMTS7 and ADAMTS12 were not related to diabetic complications (nephropathy, retinopathy and neuropathy).

scholarly journals Role of TNF-α and FGF-2 in the Fracture Healing Disorder of Type 2 Diabetes Model Induced by High Fat Diet Followed by Streptozotocin

2020 ◽  
Vol Volume 13 ◽  
pp. 2279-2288
Author(s):  
Heqing Huang ◽  
Ling Luo ◽  
Zhitao Liu ◽  
Yan Li ◽  
Zhaochen Tong ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Fracture Healing ◽  
High Fat Diet ◽  
High Fat ◽  
Diabetes Model ◽  
Tnf Α

The Role of TNF-α and its Receptors in the Production of β-1,4-galactosyltransferase I mRNA by Rat Primary Type-2 Astrocytes

2007 ◽  
Vol 28 (2) ◽  
pp. 223-236 ◽  
Author(s):  
Meijuan Yan ◽  
Chunlin Xia ◽  
Shuqiong Niu ◽  
Chun Cheng ◽  
Xiaoyi Shao ◽  
...  
Keyword(s):  
Tnf Α ◽  
Primary Type ◽  
Galactosyltransferase I

scholarly journals Activation of angiotensin II type 2 receptor suppresses TNF-α-induced ICAM-1 via NF-кB: possible role of ACE2

2015 ◽  
Vol 309 (5) ◽  
pp. H827-H834 ◽  
Author(s):  
Liping Zhu ◽  
Oscar A. Carretero ◽  
Jiang Xu ◽  
Pamela Harding ◽  
Nithya Ramadurai ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Ang Ii ◽  
Human Coronary Artery ◽  
Activity Inhibition ◽  
Tnf Α ◽  
System Activation ◽  
Interfering Rna ◽  
Stimulation Of

ANG II type 2 receptor (AT2) and ANG I-converting enzyme 2 (ACE2) are important components of the renin-ANG system. Activation of AT2 and ACE2 reportedly counteracts proinflammatory effects of ANG II. However, the possible interaction between AT2 and ACE2 has never been established. We hypothesized that activation of AT2 increases ACE2 activity, thereby preventing TNF-α-stimulated ICAM-1 expression via inhibition of NF-κB signaling. Human coronary artery endothelial cells were pretreated with AT2 antagonist PD123319 (PD) or ACE2 inhibitor DX600 and then stimulated with TNF-α in the presence or absence of AT2 agonist CGP42112 (CGP). We found that AT2 agonist CGP increased both ACE2 protein expression and activity. This effect was blunted by AT2 antagonist PD. ICAM-1 expression was very low in untreated cells but greatly increased by TNF-α. Activation of AT2 with agonist CGP or with ANG II under concomitant AT1 antagonist reduced TNF-α-induced ICAM-1 expression, which was reversed by AT2 antagonist PD or ACE2 inhibitor DX600 or knockdown of ACE2 with small interfering RNA. AT2 activation also suppressed TNF-α-stimulated phosphorylation of inhibitory κB (p-IκB) and NF-κB activity. Inhibition of ACE2 reversed the inhibitory effect of AT2 on TNF-α-stimulated p-IκB and NF-κB activity. Our findings suggest that stimulation of AT2 reduces TNF-α-stimulated ICAM-1 expression, which is partly through ACE2-mediated inhibition of NF-κB signaling.

scholarly journals Mechanisms and Therapeutic Prospects of Diabetic Cardiomyopathy Through the Inflammatory Response

2021 ◽  
Vol 12 ◽  
Author(s):  
Namrita Kaur ◽  
Yingshu Guan ◽  
Rida Raja ◽  
Andrea Ruiz-Velasco ◽  
Wei Liu
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Systolic Dysfunction ◽  
Clinical Complications ◽  
Cytokines And Chemokines ◽  
Patients With Diabetes ◽  
Potential Benefits ◽  
Artery Disease ◽  
The Impact ◽  
Precise Role

The incidence of heart failure (HF) continues to increase rapidly in patients with diabetes. It is marked by myocardial remodeling, including fibrosis, hypertrophy, and cell death, leading to diastolic dysfunction with or without systolic dysfunction. Diabetic cardiomyopathy (DCM) is a distinct myocardial disease in the absence of coronary artery disease. DCM is partially induced by chronic systemic inflammation, underpinned by a hostile environment due to hyperglycemia, hyperlipidemia, hyperinsulinemia, and insulin resistance. The detrimental role of leukocytes, cytokines, and chemokines is evident in the diabetic heart, yet the precise role of inflammation as a cause or consequence of DCM remains incompletely understood. Here, we provide a concise review of the inflammatory signaling mechanisms contributing to the clinical complications of diabetes-associated HF. Overall, the impact of inflammation on the onset and development of DCM suggests the potential benefits of targeting inflammatory cascades to prevent DCM. This review is tailored to outline the known effects of the current anti-diabetic drugs, anti-inflammatory therapies, and natural compounds on inflammation, which mitigate HF progression in diabetic populations.

A key role for IL-13 signaling via the type 2 IL-4 receptor in experimental atopic dermatitis

2020 ◽  
Vol 5 (44) ◽  
pp. eaaw2938 ◽  
Author(s):  
Almog Bitton ◽  
Shmuel Avlas ◽  
Hadar Reichman ◽  
Michal Itan ◽  
Danielle Karo-Atar ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Allergic Diseases ◽  
Proof Of Concept ◽  
Potential Therapeutic Target ◽  
Tnf Α ◽  
Allergic Skin ◽  
Insight Into

IL-13 and IL-4 are potent mediators of type 2–associated inflammation such as those found in atopic dermatitis (AD). IL-4 shares overlapping biological functions with IL-13, a finding that is mainly explained by their ability to signal via the type 2 IL-4 receptor (R), which is composed of IL-4Rα in association with IL-13Rα1. Nonetheless, the role of the type 2 IL-4R in AD remains to be clearly defined. Induction of two distinct models of experimental AD in Il13ra1−/− mice, which lack the type 2 IL-4R, revealed that dermatitis, including ear and epidermal thickening, was dependent on type 2 IL-4R signaling. Expression of TNF-α was dependent on the type 2 IL-4R, whereas induction of IL-4, IgE, CCL24, and skin eosinophilia was dependent on the type 1 IL-4R. Neutralization of IL-4, IL-13, and TNF-α as well as studies in bone marrow–chimeric mice revealed that dermatitis, TNF-α, CXCL1, and CCL11 expression were exclusively mediated by IL-13 signaling via the type 2 IL-4R expressed by nonhematopoietic cells. Conversely, induction of IL-4, CCL24, and eosinophilia was dependent on IL-4 signaling via the type 1 IL-4R expressed by hematopoietic cells. Last, we pharmacologically targeted IL-13Rα1 and established a proof of concept for therapeutic targeting of this pathway in AD. Our data provide mechanistic insight into the differential roles of IL-4, IL-13, and their receptor components in allergic skin and highlight type 2 IL-4R as a potential therapeutic target in AD and other allergic diseases such as asthma and eosinophilic esophagitis.

scholarly journals Right ventricular dysfunction and remodeling in diabetic cardiomyopathy

2019 ◽  
Vol 316 (1) ◽  
pp. H113-H122 ◽  
Author(s):  
Yin Kang ◽  
Sheng Wang ◽  
Jiapeng Huang ◽  
Lu Cai ◽  
Bradley B. Keller
Keyword(s):  
Early Detection ◽  
Right Ventricular ◽  
Diabetic Cardiomyopathy ◽  
Clinical Symptoms ◽  
Systolic Dysfunction ◽  
Right Ventricular Dysfunction ◽  
Biomechanical Properties ◽  
Left Ventricular ◽  
Structure And Function ◽  
And Function

The increasing prevalence of diabetic cardiomyopathy (DCM) is an important threat to health worldwide. While left ventricular (LV) dysfunction in DCM is well recognized, the accurate detection, diagnosis, and treatment of changes in right ventricular (RV) structure and function have not been well characterized. The pathophysiology of RV dysfunction in DCM may share features with LV diastolic and systolic dysfunction, including pathways related to insulin resistance and oxidant injury, although the RV has a unique cellular origin and composition and unique biomechanical properties and is coupled to the lower-impedance pulmonary vascular bed. In this review, we discuss potential mechanisms responsible for RV dysfunction in DCM and review the imaging approaches useful for early detection, protection, and intervention strategies. Additional data are required from animal models and clinical trials to better identify the onset and features of altered RV and pulmonary vascular structure and function during the onset and progression of DCM and to determine the efficacy of early detection and treatment of RV dysfunction on clinical symptoms and outcomes.

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