Background: Prolonged postprandial hypertriglyceridemia is a potential risk factor for cardiovascular diseases. In the context of obesity, this is associated with a chronic imbalance of lipid partitioning oriented toward storage and not toward b-oxidation. Objective: We tested the hypothesis that the physical structure of fat in a meal can modify the absorption, chylomicron transport, and further metabolic handling of dietary fatty acids. Design: Nine normal-weight and 9 obese subjects were fed 40 g milk fat (+[13 C]triacylglycerols), either emulsified or nonemulsified, in breakfasts of identical composition. We measured the postprandial triacylglycerol content and size of the chylomicron-rich fraction, plasma kinetics of [ 13 C]fatty acids, exogenous lipid oxidation with breath-test/indirect calorimetry, and fecal excretion. Results: The emulsified fat resulted in earlier (.1 h) and sharper chylomicron and [13 C]fatty acid peaks in plasma than in spread fat in both groups (P , 0.0001). After 2 h, the emulsified fat resulted in greater apolipoprotein B-48 concentrations (9.7 6 0.7 compared with 7.1 6 0.9 mg/L; P , 0.05) in the normal-weight subjects than did the spread fat. In the obese subjects, emulsified fat resulted in a 3-fold greater chylomicron size (218 6 24 nm) compared with the spread fat (P , 0.05). The emulsified fat induced higher dietary fatty acid spillover in plasma and a sharper 13 CO 2 appearance, which provoked increased exogenous lipid oxidation in each group: from 45% to 52% in normal-weight subjects (P , 0.05) and from 40% to 57% in obese subjects (P , 0.01). Conclusion: This study supports a new concept of "slow vs fast fat," whereby intestinal absorption can be modulated by structuring dietary fat to modulate postprandial lipemia and lipid b-oxidation in humans with different BMIs. This trial was registered at clinicaltrials.gov as NCT01249378.Am J Clin Nutr 2013;97:23-36.
Characteristics of sc adipose tissue appear therefore to contribute to the development of visceral fat depot, supporting the adipose tissue expandability theory and extending it to early stages of weight gain in nonobese subjects.
Unlike SPL, MPL in the high-fat diet did not induce WAT hypertrophy and inflammation but increased colonic goblet cells. This supports further clinical exploration of different sources of dietary emulsifiers in the frame of obesity outbreak.
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