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Dietary monounsaturated fat activates metabolic pathways for triglyceride-rich lipoproteins that involve apolipoproteins E and C-III^1,2,3

¹ From the Department of Nutrition, Harvard School of Public Health, Boston, MA (CZ, CK, JF, and FMS), and the Division of Cardiology, Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan (KI)

Background:Dietary monounsaturated fat (MUFA) and complex carbohydrates have different effects on triglyceride-rich lipoprotein (TRL) metabolism.

Objective:We hypothesized that apolipoprotein (apo) E and apo C-III might be involved in these dietary effects because of their crucial role in TRL metabolism.

Design:Twelve adults consumed, for 3 wk each, 2 isocaloric diets: first a carbohydrate-rich diet (48% complex carbohydrate, 8% MUFAs) and then a MUFA-rich diet (31% complex carbohydrate, 24% MUFAs) 12 mo later. The dietary composition of other macronutrients in the 2 diets was similar. Body weight was kept constant. Postprandial apo B kinetic studies using stable-isotope tracers were performed after each dietary intervention. Multiple VLDL, intermediate-density lipoprotein (IDL), and LDL fractions were prepared on the basis of apo E and apo C-III contents.

Results:The MUFA diet increased by 4–6-fold, the secretion of VLDLs and IDLs containing both apo E and apo C-III (E+CIII+) (P < 0.05). These are TRLs that mostly cleared from the circulation and are minor precursors of LDL. The MUFA diet also decreased by 60% (P < 0.05) the secretion of the TRLs without apo E or apo C-III (major precursors of LDL in plasma) and decreased their flux to LDLs. Total LDL flux did not change because the MUFA diet increased the flux to LDL from E–CIII+ TRLs, a process that requires the removal of apo C-III. In addition, the MUFA diet significantly increased the TRL fractional catabolic rate by 50% and doubled the percentage of TRLs that were cleared rather than being converted to LDLs.

Conclusion:MUFA intake activates synthetic and rapid catabolic pathways for TRL metabolism that involve apo E and apo C-III and suppresses the metabolism of more slowly metabolized VLDLs and IDLs, which do not contain these apolipoproteins.