Details

Autor(en) / Beteiligte

• van Oostrom, Antonie J
• van Dijk, Hans
• Verseyden, Caroline
• Sniderman, Allan D
• Cianflone, Katherine
• Rabelink, Ton J
• Castro Cabezas, Manuel

Titel

Addition of glucose to an oral fat load reduces postprandial free fatty acids and prevents the postprandial increase in complement component 3123

Ist Teil von

• The American journal of clinical nutrition, 2004-03, Vol.79 (3), p.510-515

Ort / Verlag

Elsevier Inc

Erscheinungsjahr

2004

Quelle

Oxford Journals 2020 Medicine

Beschreibungen/Notizen

• 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. 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. After an overnight fast, 6 healthy men (x̄ ± SD age: 23 ± 2 y) underwent 4 oral liquid challenges: fat (50 g/m2 body surface), glucose (37.5 g/m2), fat and glucose (mixed test), and water (as a control test) in a random, crossover design. 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. 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.