Addition of glucose to an oral fat load reduces postprandial free fatty acids and prevents the postprandial increase in complement component 3.
BACKGROUND
Elevated fasting plasma concentrations of complement component 3 (C3) are associated with elevated fasting and postprandial triacylglycerol concentrations, insulin resistance, obesity, and coronary artery disease. C3 is the central component of the complement system and the precursor of acylation-stimulating protein (ASP). Insulin and ASP are principal determinants of free fatty acid (FFA) trapping by adipose tissue.


OBJECTIVE
Because controversy exists concerning postprandial changes in C3 and because meal composition may influence complement activation, we studied postprandial lipemia in relation to changes in plasma C3.


METHODS
After an overnight fast, 6 healthy men ( +/- SD age: 23 +/- 2 y) underwent 4 oral liquid challenges: fat (50 g/m(2) body surface), glucose (37.5 g/m(2)), fat and glucose (mixed test), and water (as a control test) in a random, crossover design.


RESULTS
Plasma ASP concentrations did not change postprandially in any test. Changes in C3 concentration were observed only after the fat challenge: elevated concentrations occurred between 1 and 3 h, and a maximum increase of 11% occurred at 2 h (P = 0.05). Postprandial triacylglycerolemia did not differ significantly between the fat and mixed tests. The FFA response after the fat challenge was the highest of all the tests (P < 0.05 for all comparisons) and was accompanied by an increase in ketone bodies (maximum at 6 h); this increase did not occur after the mixed test, which suggests less hepatic FFA delivery.


CONCLUSIONS
When glucose is added to an oral fat load, the postprandial FFA response is reduced, and the fat-specific increase in C3 is prevented. After ingestion of fat without glucose, the lack of insulin response may lead to C3-mediated peripheral FFA trapping, which probably serves as a backup system in case of insufficient or inefficient insulin-dependent FFA trapping.
Department of Vascular Medicine, University Medical Center Utrecht, Utrecht, Netherlands.
Antonie J
AJ
van Oostrom
Hans
H
van Dijk
Caroline
C
Verseyden
Allan D
AD
Sniderman
Katherine
K
Cianflone
Ton J
TJ
Rabelink
Manuel
M
Castro Cabezas
D000328:Adult; D019540:Area Under Curve; D001798:Blood Proteins / Q000378:metabolism; D003167:Complement Activation; D003176:Complement C3 / Q000378:metabolism*; D015926:Complement C3a / Q000031:analogs & derivatives*; D018592:Cross-Over Studies; D004041:Dietary Fats / Q000008:administration & dosage* / Q000378:metabolism; D005215:Fasting; D005232:Fatty Acids, Volatile / Q000378:metabolism*; D005947:Glucose / Q000008:administration & dosage* / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D007657:Ketone Bodies / Q000378:metabolism; D008297:Male; D009765:Obesity / Q000097:blood; D019518:Postprandial Period / Q000502:physiology*; D014280:Triglycerides / Q000097:blood
D001798:Blood Proteins; D003176:Complement C3; D004041:Dietary Fats; D005232:Fatty Acids, Volatile; D007328:Insulin; D007657:Ketone Bodies; D014280:Triglycerides; C044541:complement C3a, des-Arg-(77)-; D015926:Complement C3a; D005947:Glucose