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Updated: Jun 12, 2026

Measurement of Basal and Forskolin-stimulated Lipolysis in Inguinal Adipose Fat Pads
Published on: July 21, 2017
Dynamics of fat absorption and effect of sham feeding on postprandial lipema
Rosa N Chavez-Jauregui1, Richard D Mattes, Elizabeth J Parks
1Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9052, USA.
Background & Aims:
Given the importance of postprandial hyperlipidemia to increase risk for atherosclerosis, in the present study, stable isotope-labeled meals were fed to healthy subjects (7 males and 3 females) to investigate the kinetics chylomicron synthesis and the effect of sensory exposure to lipid on metabolism.
Methods:
Subjects performed two, 24-hour inpatient studies that entailed consumption of a liquid formula evening meal containing 30 g of oil (+ (13)C(2) triolein) on day 1. Breakfast (day 2) consisted of triacylglycerols (TAGs) fed as capsules (30 g oil + (13)C(7) triolein) to avoid activation of mouth taste receptors. Next, modified sham feeding of cream cheese occurred over 2 hours. In the 2 trials, the stimulus was either higher fat (HF) or lower fat (LF) cream cheese. A liquid meal was consumed at lunch. Blood sampling occurred intermittently, and chylomicron particles S(f) >400 TAGs were analyzed by gas chromatography-mass spectrometry.
Results:
(13)C(2)-Label was found in fasting-state lipoproteins, and persons with higher body fat percentages showed greater dilution of meal TAGs from endogenous sources. For both trials, 13% ± 4% of lipoprotein TAGs oleic acid was derived from the previous evening meal. Incremental area under the curve for TAGs during HF was ∼2.5 times higher than after LF exposure (46 ± 15 vs 17 ± 5 μmol/L/h; P = .04). The greater HF morning lipemia occurred with elevated glucose, insulin, and nonesterified fatty acids peak after lunch.
Conclusions:
These data support a connection between enteral lipid metabolism and oral fat exposure, resulting in elevated postprandial lipemia. The results suggest that the intestine may participate in a mechanism coordinating oral fat signaling with control of subsequent macronutrient disposal in the body.
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