4.7 Article

Mechanisms for the acute effect of fructose on postprandial lipemia

Journal

AMERICAN JOURNAL OF CLINICAL NUTRITION
Volume 85, Issue 6, Pages 1511-1520

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/ajcn/85.6.1511

Keywords

fructose; hypertriglyceridemia; de novo lipogenesis; mechanisms; high-carbohydrate diets; stable isotopes; lipoprotein lipase; carbohydrate oxidation

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Background: A high fructose intake can lead to postprandial hypertriacylglycerolemia. The underlying mechanism is unclear. Objective: The objective of the study was to investigate the mechanisms involved in fructose-induced hypertriacylglycerolemia and the contribution of de novo lipogenesis in an acute setting. Design: In a randomized, crossover study, 14 subjects were given a fructose or glucose test meal after an overnight fast. [H-2(2)] Palmitate and [(UC)-C-13]D-fructose or [(UC)-C-13]D-glucose were added to trace the handling of dietary fats and the fate of dietary sugars in the body. Blood samples were taken before and after the meal. Respiratory exchange ratio was measured by using indirect calorimetry, and breath samples were collected. Results: Plasma triacylglycerol and VLDL-triacylglycerol concentrations were significantly higher (P = 0.001 for both), whereas the concentrations of insulin and [H-2(2)]palmitate in nonesterified fatty acids were significantly lower after fructose than after glucose (P = 0.002 and 0.03, respectively). The respiratory exchange ratio was higher after fructose (P = 0.04); significantly (P = 0.003) more carbon from sugars was recovered in breath carbon dioxide over 6 h after fructose (30.5%) than after glucose (24.5%). At 240 min, newly synthesized fatty acids from fructose made up approximate to 0.4% of circulating VLDL-triacylglycerol, whereas newly synthesized triacylglycerolglycerol made up 38%. Newly synthesized fatty acids and triacylglycerol-glycerol from glucose contributed almost none of VLDL-triacylglycerol (P = 0.002 and 0.007 for glucose and fructose, respectively). Conclusions: The lower insulin excursion after fructose may result in less activation of adipose tissue lipoprotein lipase, which led to impaired triacylglycerol clearance. The contribution of de novo lipogenesis to fructose-induced hypertriacylglycerolemia is small, but its effect on altering the partitioning of fatty acids toward esterification may be considerable.

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