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Abstract: S1-4 FRUCTOSE CONSUMPTION: RECENT RESULTS AND THEIR IMPLICATIONS
- Pre-meeting symposia - Nutrition, Lifestyle, and Atherosclerosis Abstract: S1-4 Citation: Atherosclerosis Supplement 2009, Vol. 10, Issue 2
FRUCTOSE CONSUMPTION: RECENT RESULTS AND THEIR IMPLICATIONS K Stanhope, P Havel Molecular Biosciences: VM, Univerity of California, Davis, Davis, CA We have reported that fructose consumption at 25% of energy requirements results in increased visceral adiposity, lipid dysregulation, and decreased insulin sensitivity in older, overweight/obese adults, whereas glucose consumption does not. We have proposed a model to explain the differential effects of the two sugars. Hepatic glucose metabolism is regulated by phosphofructokinase, which is inhibited by ATP and citrate when energy status is high, thus limiting hepatic uptake of dietary glucose and production of lipogenic substrates. The hepatic metabolism of dietary fructose is independent of energy status, resulting in unregulated hepatic fructose uptake and increased production of lipogenic substrates. The resulting increase in de novo lipogenesis and hepatic lipid supply leads to lipid dysregulation as well as decreased insulin sensitivity. Consumption of glucose-sweetened beverages with meals increases, while consumption of fructose-sweetened beverages lowers, meal-associated plasma glucose and insulin excursions. Insulin increases lipoprotein lipase (LPL) expression and activity, and LPL in subcutaneous adipose tissue (SAT) is more responsive to the effects of insulin than LPL in visceral adipose tissue (VAT). Thus, increases of insulin after consumption of glucosesweetened beverages with meals leads to greater LPL activity in SAT and increased TG uptake by SAT. Conversely, decreased insulin responses to fructose consumption lead to decreased insulin-mediated LPL activity in SAT, allowing for greater TG uptake by VAT. Our study results and model do not support the hypothesis that consumption of high glycemic diets increases the risk of chronic lifestyle-related diseases as a result of increased postprandial glucose and insulin excursions.
FRUCTOSE CONSUMPTION: RECENT RESULTS AND THEIR IMPLICATIONS K Stanhope, P Havel Molecular Biosciences: VM, Univerity of California, Davis, Davis, CA We have reported that fructose consumption at 25% of energy requirements results in increased visceral adiposity, lipid dysregulation, and decreased insulin sensitivity in older, overweight/obese adults, whereas glucose consumption does not. We have proposed a model to explain the differential effects of the two sugars. Hepatic glucose metabolism is regulated by phosphofructokinase, which is inhibited by ATP and citrate when energy status is high, thus limiting hepatic uptake of dietary glucose and production of lipogenic substrates. The hepatic metabolism of dietary fructose is independent of energy status, resulting in unregulated hepatic fructose uptake and increased production of lipogenic substrates. The resulting increase in de novo lipogenesis and hepatic lipid supply leads to lipid dysregulation as well as decreased insulin sensitivity. Consumption of glucose-sweetened beverages with meals increases, while consumption of fructose-sweetened beverages lowers, meal-associated plasma glucose and insulin excursions. Insulin increases lipoprotein lipase (LPL) expression and activity, and LPL in subcutaneous adipose tissue (SAT) is more responsive to the effects of insulin than LPL in visceral adipose tissue (VAT). Thus, increases of insulin after consumption of glucosesweetened beverages with meals leads to greater LPL activity in SAT and increased TG uptake by SAT. Conversely, decreased insulin responses to fructose consumption lead to decreased insulin-mediated LPL activity in SAT, allowing for greater TG uptake by VAT. Our study results and model do not support the hypothesis that consumption of high glycemic diets increases the risk of chronic lifestyle-related diseases as a result of increased postprandial glucose and insulin excursions.