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Hemostasis, endothelial stress, inflammation, and the metabolic syndrome.
Semin. Immunopathol. 40, 215-224 (2018)
Obesity and the metabolic syndrome (MS) are two of the pressing healthcare problems of our time. The MS is defined as increased abdominal obesity in concert with elevated fasting glucose levels, insulin resistance, elevated blood pressure, and plasma lipids. It is a key risk factor for type 2 diabetes mellitus (T2DM) and for cardiovascular complications and mortality. Here, we review work demonstrating that various aspects of coagulation and hemostasis, as well as vascular reactivity and function, become impaired progressively during chronic ingestion of a western diet, but also acutely after meals. We outline that both T2DM and cardiovascular disease should be viewed as inflammatory diseases and describe that chronic overload of free fatty acids and glucose can trigger inflammatory pathways directly or via increased production of ROS. We propose that since endothelial stress and increases in platelet activity precede inflammation and overt symptoms of the MS, they are likely the first hit. This suggests that endothelial activation and insulin resistance are probably causative in the observed chronic low-level metabolic inflammation, and thus both metabolic and cardiovascular complications linked to consumption of a western diet.
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Publication type
Article: Journal article
Document type
Review
Keywords
Coagulation ; Endothelial Stress ; Hemostasis ; Inflammation ; Metabolic Syndrome ; No ; Nitric Oxide ; Obesity ; Platelets ; Ros ; Reactive Oxygen Species ; Type 2 Diabetes
Language
english
Publication Year
2018
Prepublished in Year
2017
HGF-reported in Year
2017
ISSN (print) / ISBN
1863-2297
Journal
Seminars in Immunopathology
Quellenangaben
Volume: 40,
Issue: 2,
Pages: 215-224
Publisher
Springer
Publishing Place
Berlin ; Heidelberg
Institute(s)
Institute of Diabetes and Obesity (IDO)
POF-Topic(s)
30201 - Metabolic Health
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-502200-007
PubMed ID
29209827
Scopus ID
85037632641
WOS ID
WOS:000424880800007
Erfassungsdatum
2018-02-22