[The role of post-prandial lipids in atherogenesis: particularities of diabetes mellitus].
Atherosclerosis is a complex and multifactorial disease, which determines clinical events that cause significant morbidity-mortality, represented by acute myocardial infarction, angina and sudden death. It is associated with lipid disturbances, platelet activation, thrombosis, endothelial dysfunction, inflammation, oxidative stress, altered matrix metabolism, among other disturbances. All these abnormalities are usual and more pronounced in diabetic patients, as well as in the post-prandial state. Among the coronary artery disease risk factors that are not usually employed in clinical practice in the whole population, postprandial hyperlipemia plays a major role, being a possible early marker of metabolic abnormalities and vascular dysfunction not yet seen in the fasting state. Recent results showed that post-oral lipid overload changes are negatively associated with endothelial dysfunction, and vascular reactivity abnormalities are strongly related to atherosclerosis progression and cardiovascular events. These abnormalities could disclose a lipid intolerance state that can be detected in apparently healthy subjects even before fasting abnormalities are seen. This review will deal with the pathophysiology changes involved in post-prandial hyperlipemia and its relationship with atherogenesis, with particular emphasis to diabetes mellitus.
Signori
Luis Ulisses
LU
Instituto de Cardiologia do Rio Grande do Sul, Fundação Universidade de Cardiologia, Porto Alegre, RS, and Unidade de Hipertensão, InCor, Hospital das Clínicas de São Paulo, Brazil.
Plentz
Rodrigo Della Méa
RD
Irigoyen
Maria Cláudia
MC
Schaan
Beatriz D'Agord
BD
D015415:Biomarkers / Q000097:blood; D002784:Cholesterol / Q000097:blood; D003324:Coronary Artery Disease / Q000209:etiology* / Q000503:physiopathology; D048909:Diabetes Complications / Q000097:blood* / Q000503:physiopathology; D004435:Eating / Q000502:physiology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D018149:Glucose Intolerance / Q000503:physiopathology; D006801:Humans; D006943:Hyperglycemia / Q000503:physiopathology; D006946:Hyperinsulinism / Q000503:physiopathology; D050356:Lipid Metabolism / Q000502:physiology; D008055:Lipids / Q000097:blood*; D019518:Postprandial Period / Q000502:physiology; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
D015415:Biomarkers; D008055:Lipids; D014280:Triglycerides; D002784:Cholesterol