Cardiometabolic Syndrome

2020 ◽  
pp. 801-822
Author(s):  
Anup K. Kanodia ◽  
Diana Noland
Keyword(s):  
Cardiometabolic Syndrome

scholarly journals Retinal Redox Stress and Remodeling in Cardiometabolic Syndrome and Diabetes

2010 ◽  
Vol 3 (6) ◽  
pp. 392-403 ◽  
Author(s):  
Ying Yang ◽  
Melvin R. Hayden ◽  
Susan Sowers ◽  
Sarika V. Bagree ◽  
James R. Sowers
Keyword(s):  
Metabolic Pathways ◽  
Tissue Injury ◽  
Disease Process ◽  
Polyol Pathway ◽  
The United States ◽  
Redox Stress ◽  
Blood Retinal Barrier ◽  
Cardiometabolic Syndrome ◽  
Hexosamine Pathway ◽  
Pathway Flux

Diabetic retinopathy (DR) is a significant cause of global blindness; a major cause of blindness in the United States in people aged between 20–74. There is emerging evidence that retinopathy is initiated and propagated by multiple metabolic toxicities associated with excess production of reactive oxygen species (ROS). The four traditional metabolic pathways involved in the development of DR include: increased polyol pathway flux, advanced glycation end-product formation, activation of protein kinase Cisoforms and hexosamine pathway flux. These pathways individually and synergisticallycontribute to redox stress with excess ROS resulting in retinal tissue injury resulting in significant microvascular blood retinal barrier remodeling. The toxicity of hyperinsulinemia, hyperglycemia, hypertension, dyslipidemia, increased cytokines and growth factors, in conjunction with redox stress, contribute to the development and progression of DR. Redox stress contributes to the development and progression of abnormalities of endothelial cells and pericytes in DR. This review focuses on the ultrastructural observations of the blood retinal barrier including the relationship between the endothelial cell and pericyte remodeling in young nine week old Zucker obese (fa/ fa) rat model of obesity; cardiometabolic syndrome, and the 20 week old alloxan induced diabetic porcine model. Preventing or delaying the blindness associated with these intersecting abnormal metabolic pathways may be approached through strategies targeted to reduction of tissue inflammation and oxidative—redox stress. Understanding these abnormal metabolic pathways and the accompanying redox stress and remodeling mayprovide both the clinician and researcher a new concept of approaching this complicated disease process

scholarly journals Magnesium and the Cardiometabolic Syndrome

2012 ◽  
Vol 1 (2) ◽  
pp. 100-108 ◽  
Author(s):  
Mario Barbagallo ◽  
Ligia J. Dominguez
Keyword(s):  
Cardiometabolic Syndrome

scholarly journals D-ribose-L-cysteine prevents oxidative stress and cardiometabolic syndrome in high fructose high fat diet fed rats

2021 ◽  
Vol 142 ◽  
pp. 112017
Author(s):  
Abodunrin Adebayo Ojetola ◽  
Wale Johnson Adeyemi ◽  
Ubong Edem David ◽  
Temitayo Olabisi Ajibade ◽  
Olumuyiwa Abiola Adejumobi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
High Fat ◽  
Cardiometabolic Syndrome ◽  
High Fructose

scholarly journals Epicardial Adiposity in Relation to Metabolic Abnormality, Circulating Adipocyte FABP, and Preserved Ejection Fraction Heart Failure

Diagnostics ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 397
Author(s):  
Jiun-Lu Lin ◽  
Kuo-Tzu Sung ◽  
Yau-Huei Lai ◽  
Chih-Hsuan Yen ◽  
Chun-Ho Yun ◽  
...  
Keyword(s):  
Heart Failure ◽  
High Risk ◽  
Ejection Fraction ◽  
Renal Insufficiency ◽  
Strain Rates ◽  
Preserved Ejection Fraction ◽  
Fatty Acid Binding ◽  
Cardiometabolic Syndrome ◽  
The Metabolic Syndrome ◽  
New Onset

Epicardial adipose tissue (EAT) as a source of pro-inflammatory cytokines tightly linked to metabolic abnormalities. Data regarding the associations of EAT with adipocyte fatty acid-binding protein (A-FABP), a cytokine implicated in the cardiometabolic syndrome, might play an important part in mediating the association between EAT and cardiac structure/function in preserved ejection fraction heart failure (HFpEF). We conducted a prospective cohort study comprising 252 prospectively enrolled study participants classified as healthy (n = 40), high-risk (n = 161), or HFpEF (n = 51). EAT was assessed using echocardiography and compared between the three groups and related to A-FABP, cardiac structural/functional assessment utilizing myocardial deformations (strain/strain rates) and HF outcomes. EAT thickness was highest in participants with HFpEF (9.7 ± 1.7 mm) and those at high-risk (8.2 ± 1.5 mm) and lowest in healthy controls (6.4 ± 1.9 mm, p < 0.001). Higher EAT correlated with the presence of cardiometabolic syndrome, diabetes and renal insufficiency independent of BMI and waist circumference (pinteraction for all > 0.1), and was associated with reduced LV global longitudinal strain (GLS) and LV mass-independent systolic/diastolic strain rates (SRs/SRe) (all p < 0.05). Higher A-FABP levels were associated with greater EAT thickness (pinteraction > 0.1). Importantly, in the combined control cohort, A-FABP levels mediated the association between EAT and new onset HF. Excessive EAT is independently associated with the metabolic syndrome, renal insufficiency, and higher A-FABP levels. The association between EAT and new onset HF is mediated by A-FABP, suggesting a metabolic link between EAT and HF.

scholarly journals Interplay between Oxidative Stress and Inflammation in Cardiometabolic Syndrome

2016 ◽  
Vol 2016 ◽  
pp. 1-3 ◽  
Author(s):  
Aaron L. Sverdlov ◽  
Gemma A. Figtree ◽  
John D. Horowitz ◽  
Doan T. M. Ngo
Keyword(s):  
Oxidative Stress ◽  
Cardiometabolic Syndrome
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