Abstract
Fasting and postprandial hypertriglyceridemia are causal risk factors for atherosclerosis. The prevalence of hypertriglyceridemia is approximately 25–30% and most hypertriglyceridemic patients suffer from mild to moderate hypertriglyceridemia. Data regarding dietary interventions on postprandial triglyceride metabolism of mildly to moderately hypertriglyceridemic patients is, however, sparse. In a randomized controlled trial, eight mildly hypertriglyceridemic patients and five healthy, normolipidemic controls received three separate standardized fat-meals containing either saturated fatty acids (SFA), mono-unsaturated fatty acids (MUFA), or medium-chain fatty acids (MCFA) in a randomized order. Fasting and postprandial lipid parameters were determined over a 10 h period and the (incremental) area under the curve (AUC/iAUC) for plasma triglycerides and other parameters were determined. MCFA do not lead to a significant elevation of postprandial total plasma triglycerides and other triglyceride parameters, while both SFA (patients: p = 0.003, controls: p = 0.03 compared to MCFA) and MUFA (patients: p = 0.001; controls: p = 0.14 compared to MCFA) do lead to such an increase. Patients experienced a significantly more pronounced increase of plasma triglycerides than controls (SFA: patients iAUC = 1006 mg*h/dL, controls iAUC = 247 mg*h/dL, p = 0.02; MUFA: patients iAUC = 962 mg*h/dL, controls iAUC = 248 mg*h/dL, p = 0.05). Replacing SFA with MCFA may be a treatment option for mildly to moderately hypertriglyceridemic patients as it prevents postprandial hypertriglyceridemia.
Highlights
Fasting and postprandial hypertriglyceridemia (HTG) affects approximately 20% of the adult population in industrialized countries [1,2,3] and represents an established risk factor for atherosclerosis and acute pancreatitis [4,5,6,7]
Studies suggest that postprandial hypertriglyceridemia in particular increases the risk of myocardial infarction [15,16]
We evaluated postprandial triglyceride metabolism after an oral fat-meal with either
Summary
Fasting and postprandial hypertriglyceridemia (HTG) affects approximately 20% of the adult population in industrialized countries [1,2,3] and represents an established risk factor for atherosclerosis and acute pancreatitis [4,5,6,7]. Severe HTG (>1000 mg/dL; >11.4 mmol/L) [5] For postprandial triglycerides, such cut-off values are not established, postprandial triglycerides in normolipidemic subjects (unlike in HTG where massive increases can be observed) rarely exceed 400 mg/dL [5]. Considering that postprandial hypertriglyceridemia is a relevant residual risk factor for cardiovascular disease, it seems obvious to evaluate whether lipid modifying interventions affect postprandial lipid metabolism. Such studies have been performed for statins [17,18], fibrates [19], ezetimibe [20], proprotein convertase subtilisin/kexin type. MCFA, saturated fatty acids (SFA) or monounsaturated fatty acids (MUFA) in normolipidemic subjects and patients with mild to moderate HTG
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