Postprandial hyperglycemia and hyperlipidemia-generated glycoxidative stress: its contribution to the pathogenesis of diabetes complications.
Postprandial glucose and triglyceride increments after a mixed meal are more prolonged in people with type 1 and 2 diabetes or with impaired glucose tolerance than in normal individuals. Evidence in the literature suggests that these transient increases represent an additional and independent risk for chronic hyperglycemia to induce endothelial dysfunction, an important fact for the development of diabetic vascular complications. This article presents the more relevant mechanisms by which acute postprandial hyperglycemia and hyperlipidemia have been proved to determine the risk of reactive oxygen species overproduction, an increased synthesis of non enzymatic early-glycated and nitrated proteins, and a more atherogenic lipoprotein profile. Recent recommendations suggest that care for this transient glycoxidative stress should be associated with fasting glucose or HbA1c care, to reduce the risk of macro- and microvascular complications in people with diabetes.
Rebolledo
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CENEXA--Center of Experimental and Applied Endocrinology, National University of La Plata--National Research Council, PAHO/WHO Collaborating Center, School of Medical Sciences, La Plata, Argentina.
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D000818:Animals; D003920:Diabetes Mellitus / Q000209:etiology* / Q000378:metabolism; D005609:Free Radicals; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000378:metabolism*; D006949:Hyperlipidemias / Q000150:complications / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D019518:Postprandial Period / Q000502:physiology*
D005609:Free Radicals