|Brousseau, Magaret -|
|Millar, John -|
|Diffenderfer, Margaret -|
|Nartsupha, Chorthip -|
|Asztalos, Bela -|
|Wolfe, Megan -|
|Mancuso, James -|
|Digenio, Andres -|
|Rader, Daniel -|
|Schaefer, Ernst -|
Submitted to: Journal of Lipid Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 28, 2009
Publication Date: July 20, 2009
Citation: Brousseau, M.E., Millar, J.S., Diffenderfer, M.R., Nartsupha, C., Asztalos, B.F., Wolfe, M.L., Mancuso, J.P., Digenio, A.G., Rader, D.J., Schaefer, E.J. 2009. Effects of cholesteryl ester transfer protein inhibition on apolipoprotein A-II-containing HDL subspecies and apoA-II metabolism. Journal of Lipid Research. 50(7):1456-1462. Interpretive Summary: The average American consumes approximately 50% of calories in the form of carbohydrates. Dietary carbohydrates are eaten mainly as starch (glucose polymer), glucose, and fructose. Both table sugar (or sucrose) and high fructose corn syrup contain approximately equal amount of glucose and fructose. The purpose of this study was to directly compare dietary glucose and fructose at 25% of calories in overweight or obese subjects over a 10 week period. In subjects receiving glucose the levels of the major fat on the bloodstream, trilglycerides, increased by 10%, in contrast to no change for fructose. However, subjects receiving fructose had significant increases in the major cholesterol carrying lipoprotein in plasma, low density lipoprotein or LDL, especially in the high risk small dense LDL cholesterol fraction. Moreover subjects receiving fructose increased their insulin levels in contrast to those receiving glucose. These data indicate that dietary fructose at 25% of calories may be more deleterious that dietary glucose in having an adverse effect on small dense LDL and on increasing resistance to insulin, a marker of substantial risk for developing diabetes. The data indicate that dietary fructose intake should be minimized.
Technical Abstract: Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle–triglyceride and –cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.