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Serum Triglyceride Composition is Affected Qualitatively and Quantitatively by Interactions of Dietary Fat and Carbohydrate
Author(s) -
Kristal Bruce,
Stavrovskaya Irina,
Bird Susan,
Marur Vasant,
Porter Caryn
Publication year - 2015
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.29.1_supplement.389.3
Subject(s) - fructose , triglyceride , context (archaeology) , insulin resistance , carbohydrate , lipidomics , food science , medicine , metabolic syndrome , sucrose , polyunsaturated fatty acid , endocrinology , polyunsaturated fat , chemistry , saturated fat , biochemistry , diabetes mellitus , cholesterol , biology , fatty acid , paleontology
Elevated circulating triglyceride (cTG) levels are an established risk factor for metabolic and cardiovascular disease. cTG populations respond to diet and reflect physiological status, but specific linkages with many clinically‐relevant dietary factors remain unclear and/or controversial. We examined –and partially resolved ‐ several controversial links between dietary fats/carbohydrates and cTGs using a healthy, non‐obese rat model to eliminate influence of disease. Rats were fed one of 20 isocaloric, low‐fat diets containing primarily saturated [SFA], monounsaturated [MUFA], trans [TFA], or polyunsaturated (34:1 or 6:1 ω3/ω6) fat, each combined with starch/sucrose in four glucose:fructose ratios. Mass spectrometry‐based lipidomics profiling method enabled identification of 115 distinct cTGs. TFA‐based diets increased cTG levels; MUFA‐based diets were associated with low cTG levels in a low‐fructose context, but high cTG levels in a high‐fructose context, showing unexpected carbohydrate/fat interaction. Diets containing SFAs and/or fructose at levels comparable to the top third of US intake were directly associated with specific elevations in the shorter chain, more saturated cTGs associated with insulin resistance and metabolic syndrome. These data help unify apparently inconsistent mechanistic, preclinical, and clinical data in the literature (e.g., fructose, MUFA effects), extend understanding of the distinct influence of detrimental fats (SFAs/TFAs) on cTGs, and suggest that the clinically relevant consequence of dietary SFAs and fructose may be as evident in the quality of cTGs as in their quantity (NIH/NIEHS/NIDDK/BWH).