Seven fasting subjects were fitted with nasogastric and nasoduodenal tubes and received intragastrically a coarsely emulsified test meal. Gastric and duodenal aspirates were collected after 1, 2, 3, and 4 h. In the duodenum, most lipids (> 90%) were present as emulsified droplets 1-100 microns in size. Large droplets and unemulsified material present in the test meal (> 100 micron) disappeared, whereas smaller droplets (1-50 microns) were generated after 1 h of digestion. Thus the median lipid droplet diameter significantly decreased (19.6 vs. 56.5 microns in the test meal) and the droplet surface area significantly increased (1.58 vs. 0.70 micron2/g fat). Intermediate droplet diameters were 34.3, 46.3, and 27.6 microns after 2, 3, and 4 h, respectively. In the stomach, a comparable emulsion particle size pattern was observed, with median droplet diameters of 17.2, 37.9, 52.4, and 41.6 microns after 1, 2, 3, and 4 h, respectively. However, the extent of triglyceride hydrolysis was much lower in the stomach (6-16%) than in the duodenum (42-45%), where small droplets were enriched in lipolytic products, cholesterol, and phospholipids. The present findings show for the first time that most dietary lipids are present in the human duodenum as emulsified droplets 1-50 microns in size and that no further marked emulsification of dietary fat occurs in the duodenum compared with the stomach.

Fasting subjects were intragastrically intubated and received a coarsely emulsified test meal. Gastric aspirates were collected after 1, 2, 3, and 4 h. During digestion in the stomach, unemulsified lipids (> or = 100 microns) represented a minor fraction. A significant amount of the large 70- to 100-microns lipid droplets disappeared, and fine 1- to 10-microns droplets were generated. The median lipid droplet diameter significantly decreased (21.9 vs. 52.9 microns) after 1 h and kept intermediate values for longer periods of time. The emulsion surface area was 100-120 m2/l and was basically provided by 1- to 100-microns droplets. Lipolysis catalyzed by gastric lipase primarily occurred within the first hour of digestion (11.9%). Smaller droplets were enriched in triglyceride lipolytic products. The free fatty acid concentrations were in the range of 5.6-8.2 mM over 1-4 h. The present finding demonstrates for the first time that in the human stomach most dietary lipids are present in the form of emulsified droplets, in the range of 20-40 microns, and that gastric lipolysis can help to increase emulsification in the stomach.

Eight normolipidemic males ingested on separate days and in a random order five mixed meals containing 0, 15, 30, 40, or 50 g fat. Fasting and postprandial blood samples were obtained for 7 h and chylomicrons and lipoproteins were isolated. The nonfat and 15-g fat meals did not generate noticeable postprandial variations except for HDL phospholipids (P < 0.05). The serum and chylomicron triacylglycerol responses obtained after the meals correlated positively with the amount of fat ingested and peaked after 2-3 h. Serum free cholesterol and phospholipids increased and esterified cholesterol decreased postprandially in a dose-response manner. At the same time, triacylglycerol-rich-lipoprotein triacylglycerols, esterified cholesterol, LDL free cholesterol, HDL triacylglycerols, phospholipids, and free cholesterol increased whereas LDL and HDL esterified cholesterol decreased when the amount of ingested fat increased. The data showed that increasing the amount of fat in the usual range of ingestion (0-50 g) led to stepwise increases in the postprandial rise of chylomicron and serum triacylglycerols and induced marked changes in serum lipoproteins postprandially. The existence of a no-effect level of dietary fat (15 g) on postprandial lipemia and lipoproteins in healthy adults was shown.