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Louis Monnier; Emilie Mas; Christine Ginet; et al.
JAMA. 2006;295(14):1681-1687 (doi:10.1001/jama.295.14.1681) http://jama.ama-assn.org/cgi/content/full/295/14/1681
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Nutritional and Metabolic Disorders; Nutritional and Metabolic Disorders, Other; Endocrine Diseases; Diabetes Mellitus
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Activation of Oxidative Stress by Acute Glucose Fluctuations Compared With Sustained Chronic Hyperglycemia inPatients With Type 2 Diabetes
Louis Monnier, MD Emilie Mas, PhD Christine Ginet, MD Francoise Michel, MD ¸ Laetitia Villon, MD Jean-Paul Cristol, MD Claude Colette, PhD development of specific microvascular complications and by a high incidence of accelerated atherosclerosis.1-4 Even though a large number of studies have investigated and compared the roles of the different factors that participate indiabetic vascular complications, an accurate assessment of their respective contributions is still difficult.2,5,6 However, as demonstrated by many trials, microvascular and macrovascular complications are mainly7,8 or partly4,8 dependent on hyperglycemia. At least 4 major pathways are involved in hyperglycemia-induced vascular damages: (1) enhanced polyol activity, causing sorbitol and fructoseaccumulation; (2) increased formation of advanced glycation end products; (3) activation of protein kinase C and nuclear factor kB; and (4) increased hexosamine pathway flux.9 There are many reasons to think that hyperglycemic states trigger all of these deleterious metabolic events through a single process:
See also pp 1688 and 1707. Context Glycemic disorders, one of the main risk factors forcardiovascular disease, are associated with activation of oxidative stress. Objective To assess the respective contributions of sustained chronic hyperglycemia and of acute glucose fluctuations to oxidative stress in type 2 diabetes. Design, Setting, and Participants Case-control study of 21 patients with type 2 diabetes (studied 2003-2005) compared with 21 age- and sex-matched controls (studied in2001) in Montpellier, France. Main Outcome Measures Oxidative stress, estimated from 24-hour urinary excretion rates of free 8-iso prostaglandin F2 (8-iso PGF2 ). Assessment of glucose fluctuations was obtained from continuous glucose monitoring system data by calculating the mean amplitude of glycemic excursions (MAGE). Postprandial contribution to glycemic instability was assessed bydetermining the postprandial increment of glucose level above preprandial values (mean postprandial incremental area under the curve [AUCpp]). Long-term exposure to glucose was estimated from hemoglobin A1c, from fasting glucose levels, and from mean glucose concentrations over a 24-hour period. Results Mean (SD) urinary 8-iso PGF2 excretion rates were higher in the 21 patients with diabetes (482 ...