Literature DB >> 14985229

Addition of glucose to an oral fat load reduces postprandial free fatty acids and prevents the postprandial increase in complement component 3.

Antonie J van Oostrom1, Hans van Dijk, Caroline Verseyden, Allan D Sniderman, Katherine Cianflone, Ton J Rabelink, Manuel Castro Cabezas.   

Abstract

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.
DESIGN: 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.

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Year:  2004        PMID: 14985229     DOI: 10.1093/ajcn/79.3.510

Source DB:  PubMed          Journal:  Am J Clin Nutr        ISSN: 0002-9165            Impact factor:   7.045


  12 in total

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Review 2.  An immune origin of type 2 diabetes?

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4.  Extended-release niacin acutely suppresses postprandial triglyceridemia.

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5.  Measuring short-term liver metabolism non-invasively: postprandial and post-exercise ¹H and ³¹P MR spectroscopy.

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8.  Model-Based Quantification of the Systemic Interplay between Glucose and Fatty Acids in the Postprandial State.

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Review 9.  Dyslipidemia in obesity: mechanisms and potential targets.

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10.  Effects of sugar-sweetened beverages on plasma acylation stimulating protein, leptin and adiponectin: relationships with metabolic outcomes.

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