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Fructose intake and circulating triglycerides: an examination of the roles of APOC 3 and FOXO1
Author(s) -
Campbell Eric S,
Castonguay Thomas W
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1074.8
Subject(s) - fructose , postprandial , high fructose corn syrup , hypertriglyceridemia , medicine , endocrinology , foxo1 , fructolysis , sucrose , corn syrup , chemistry , biology , biochemistry , insulin , triglyceride , cholesterol , transcription factor , gene
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.