Recent findings in the study of postprandial lipemia

Abstract

The study of postprandial metabolism is in the early stages compared with other areas of atherosclerosis research. Recent advances in postprandial research have included improvements in methodology and the investigation of factors that modulate the lipemic response to a meal. Enough studies have now been performed that normal ranges have been identified for blood triacylglycerol (TAG) concentrations that occur after a healthy patient consumes a standardized-mixed meal or a high-fat shake designed to elicit lipemia. Typical postprandial concentrations of other metabolites, such as apolipoproteins B48 and B100 or gastrointestinal hormones (eg, cholecystokinin), have not been studied sufficiently to be able to qualify what represents a standard postprandial response. The method of data analysis is also a key point to consider. Data from children are now becoming available, and the specific effects of ethnicity have just begun to be explored. New areas of study include the effects of different fatty acids (monosaturates or polyunsaturates), the sources of chylomicron lipids (dietary TAG and cholesterol versus that newly synthesized in the body), and the effects of alcoholic beverages consumed with the meal. Variables that can also affect the results of a meal test are under investigation. These include the type of food that is consumed the day before the meal test, the time of day the test is performed, and the palatability of the food. Given solid evidence that delayed postprandial lipemia is an independent risk factor for coronary heart disease, future scientific investigation in the area of postprandial metabolism is likely to yield discoveries that will significantly contribute to advancements in disease treatment.

The postprandial state does not impair endothelial function in women with Type 2 diabetes irrespective of glycaemic control

“…In Type 2 diabetes postprandial hyperglycaemia is an independent risk factor for cardiovascular disease [2] and a stronger predictor of cardiovascular mortality than fasting plasma glucose [3]. There is mounting evidence to suggest that delayed postprandial lipaemia represents an independent cardiovascular risk factor [4]. Endothelial dysfunction precedes [5] and predicts [6] overt cardiovascular disease and is therefore a potential mechanism linking the postprandial state to cardiovascular risk [7].…”

Candesartan effect on inflammation in hypertension

“…The most adequate way to experimentally reproduce the postprandial lipemia condition appears to be the administration of a standardized OFL to fasting patients. 28 This model has been widely applied in relatively small sample of subjects to study the postprandial lipemia effect on inflammatory parameters, 29,30 circulating markers of endothelial dysfunction 31,32 and prothrombotic variables. 33,34 So, we observed that 6-month treatment is associated to a significant improvement of basal level of sICAM-1 (À17.3%), IL-6 (À31.6%) and Hs-CRP (À33.3%) in nondiabetics, whereas in BG (À3.7%), Tg (À11.2%), sICAM-1 (À16.5%), IL-6 (À36.6%) and Hs-CRP (À25.0%) in diabetics.…”

Alcohol, nutrition and health maintenance: selected aspects

“…modulate particle size and/or composition) so that they become less atherogenic. In general, any factor that reduces postprandial lipidaemia may be considered to be cardio-protective (Parks, 2001;Petitt & Cureton, 2003).…”