Meal ingestion provokes entry of lipoproteins containing fat from the previous meal: possible metabolic implications.
BACKGROUND
Prolonged and exaggerated postprandial plasma triacylglycerol (TAG) concentrations are considered as an independent risk factor for coronary artery disease. Western populations eat many meals at regular intervals, and can be in a postprandial state for at least 17 h of a 24 h period. After consuming 2 meals an early plasma TAG peak has been observed after the second meal, the origin of which is unclear.


OBJECTIVE
To test the hypothesis that the early TAG peak observed following sequential meals was of intestinal origin and represented fat derived from the previous meal.


METHODS
Postprandial plasma lipaemic responses of 17 healthy postmenopausal women were studied by giving a test breakfast followed by a lunch. Watermiscible retinyl palmitate (RP) was added to the breakfast, but not the lunch test meal. Plasma TAG, retinyl esters (RE) and apo B-48 were determined for a 10 h period following breakfast.


RESULTS
In response to the test meals, RE, apo B-48 and TAG showed multiple peaks. Despite omission of RP from the lunch, RE showed an early peak response after ingestion of lunch in 15 of 17 subjects. The peak response after lunch of all three markers appeared significantly earlier compared with their respective peak responses after the breakfast (P < 0.0001). The area of RE response after lunch was significantly correlated with the RE lipaemic response to the breakfast (r = 0.67; P < 0.004) and to the fasting TAG concentration (r = 0.48; P < 0.05).


CONCLUSIONS
Since the lunch did not contain RP, the distinctive second influx of RE after lunch was believed to have originated from the breakfast. This, together with the fact that all three markers showed an earlier response to the lunch than the breakfast, supports the view that ingestion of a second meal provokes entry of fat from the previous meal, from an as yet unidentified site (gut, enterocytes, lymph). The results indicate that the degree of TAG "storage" from previous meals might be a function of TAG tolerance and provide a possible site of regulation of the entry of fat into the systemic circulation.
Silva
K D Renuka R
KD
Hugh Sinclair Unit of Human Nutrition, School of Food Biosciences, University of Reading, 226, Whiteknights Reading (Berks.) RG6 6AP, UK.
Wright
John W
JW
Williams
Christine M
CM
Lovegrove
Julie A
JA
D000368:Aged; D053283:Apolipoprotein B-48; D001055:Apolipoproteins B / Q000097:blood*; D019540:Area Under Curve; D002914:Chylomicrons / Q000378:metabolism; D003327:Coronary Disease / Q000097:blood / Q000453:epidemiology / Q000209:etiology; D004041:Dietary Fats / Q000378:metabolism*; D004063:Digestion; D004224:Diterpenes; D005260:Female; D006801:Humans; D008875:Middle Aged; D017698:Postmenopause; D019518:Postprandial Period; D000084562:Retinyl Esters; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood*; D014801:Vitamin A / Q000031:analogs & derivatives
D053283:Apolipoprotein B-48; D001055:Apolipoproteins B; D002914:Chylomicrons; D004041:Dietary Fats; D004224:Diterpenes; D000084562:Retinyl Esters; D014280:Triglycerides; D014801:Vitamin A; C014794:retinol palmitate