Fructose intake and circulating triglycerides: an examination of the roles of APOC 3 and FOXO1

Abstract

Fructose consumption can promote hypertriglyceridemia (HTG) in both humans and laboratory animals. We have recently reported that giving rats overnight access to a 16% fructose solution results in HTG. Several investigators have suggested that hepatic FOXO1 and/or APOC 3 may be implicated in promoting fructose‐induced HTG. We have found that neither FOXO1 nor APOC 3 expression in the livers of rats fed fructose differed from controls that were fed lab chow only. Similarly, neither FOXO1 nor APOC 3 expression in rats fed glucose, sucrose or high fructose corn syrup solutions were significantly different from controls. These results suggest that the changes in FOXO1 and APOC 3 following fructose consumption are secondary to the changes necessary to cause fructose‐induced HTG. Alternatively, hepatic FOXO1 and/or APOC 3 expression may have been returned to pre‐fructose levels prior to sampling. In future experiments we intend to monitor postprandial hepatic expression of FOX01 and APOC 3 in hourly intervals to better characterize the onset of HTG. Supported in part by a grant from the Maryland Agricultural Experiment Station.

Unanticipated Enhancement of Intestinal TG Output by Apoc3 ASO Inhibition

“…319765 Several factors have been identified as promoters or inhibitors of apoC3 expression and plasma concentration. Of these, glucose 6 and high-fructose corn syrup 7 and sucrose 7 have been shown to increase the hepatic expression of apoC3, thus resulting in increased plasma apoC3 concentrations in response to carbohydrates. [8][9][10][11] Similarly, saturated fatty acids 12,13 have been shown to increase plasma apoC3 concentrations by stimulating TRL apoC3 production rates.…”