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ARS Home » Pacific West Area » Davis, California » Western Human Nutrition Research Center » Obesity and Metabolism Research » Research » Publications at this Location » Publication #266261
Title: Circulating concentrations of monocyte chemoattranctant protein-1, plasminogen activator inhibitor-1, & soluble leukocyte adhesion molecule-1 in overweight/obese men/women consuming fructose-or glucose-sweetened beverages

Author
item COX, CHAD - University Of California
item STANHOPE, KIMBER - University Of California
item MARC SCHWARZ, JEAN - University Of California
item GRAHAM, JAMES - University Of California
item GRIFFEN, STEVEN - University Of California
item BREMER, ANDREW - University Of California
item BERGLUND, LARS - University Of California
item MCGAHAN, JOHN - University Of California
item BEYSEN, CARINE - Kinemed
item Keim, Nancy
item HAVEL, PETER - University Of California

Submitted to: Journal of Clinical Endocrinology and Metabolism
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/9/2011
Publication Date: 9/28/2011
Citation: Cox, C.L., Stanhope, K.L., Marc Schwarz, J., Graham, J.L., Griffen, S.C., Bremer, A.A., Berglund, L., Mcgahan, J.P., Beysen, C., Keim, N.L., Havel, P.J. 2011. Circulating concentrations of monocyte chemoattranctant protein-1, plasminogen activator inhibitor-1, & soluble leukocyte adhesion molecule-1 in overweight/obese men/women consuming fructose-or glucose-sweetened beverages. Journal of Clinical Endocrinology and Metabolism. 96(12):E2034-E2038.

Interpretive Summary: Consumption of sweeteners containing fructose has increased dramatically in the American diet over the past 3 decades, in parallel with the increasing incidence of obesity. This study examined the effect of consuming large quantities of beverages (about 25% of total calorie intake) sweetened with fructose over a 10 week period in overweight men and women to determine if measures of inflammation and blood clotting factors were affected by this sugar. The effects with fructose consumption were compared to those produced by an equivalent amount of beverages sweetened with pure glucose. The ingestion of fructose sweetened beverages, but not glucose sweetened beverages, led to increases in certain markers of inflammation and clotting factors that circulate in blood. Chronic inflammation is thought to be a feature commonly associated with the metabolic syndrome. Our results suggest that consumption of large amounts of fructose on a daily basis increases the risk of developing of metabolic syndrome by increasing factors that amplify inflammation and blood clotting.

Technical Abstract: Results from animal studies suggest that consumption of large amounts of fructose can promote inflammation and impair fibrinolysis. Data describing the effects of fructose consumption on levels of pro-inflammatory and pro-thrombotic markers in humans are unavailable. The objective of this study was to determine the effects of 10 wks of dietary fructose or glucose consumption on plasma concentrations of MCP-1, PAI-1, E-Selectin, ICAM, CRP, and IL-6. The study design was a parallel arm study with two inpatient phases (2 wks baseline, final 2 wks intervention), conducted in a clinical research facility, and an outpatient phase (8 wks) during which subjects resided at home. Participants were older, overweight/obese men (n = 16) and women (n = 16). Participants consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Blood samples were collected at baseline and during the 10th week of intervention. Fasting concentrations of MCP-1 (P = 0.0003), PAI-1 (P = 0.002), and E-selectin (P = 0.034) increased in subjects consuming fructose, but not in those consuming glucose. Postprandial concentrations of PAI-1 increased in both groups (Frc: P < 0.0001; Glc: P = 0.032), however responses were greater in subjects consuming fructose (P = 0.024). Fasting levels of CRP, IL-6, and ICAM were not changed in either group. Consumption of fructose for 10 weeks leads to increases of MCP-1, PAI-1 and E-selectin. These findings suggest that fructose may contribute to the development of the metabolic syndrome via effects on pro-inflammatory and pro-thrombotic mediators.