Chylomicron-derived fatty acid spillover in adipose tissue: A signature of metabolic health?

Marie Eve Piché, Siôn A. Parry, Fredrik Karpe, Leanne Hodson*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Context and Objectives: Spillover of fatty acids (FAs) into the plasma nonesterified fatty acid (NEFA) pool, because of an inability of adipose tissue (AT) to accommodate sufficient fat uptake, has been suggested to contribute to obesity-related insulin resistance. Using specific labeling techniques, we compared the proportion of spillover-derived NEFA across a range of adiposity. Participants and Methods: Seventy-one healthy men and women were fed a mixed meal (40 g fat) containing [U13C]palmitate to assess the contribution of chylomicron-derived spillover FAs. To investigate subcutaneous abdominal-specific spillover, arteriovenous difference and stable-isotope methodologies were used in substudy (six men, six women). Results: Chylomicron-derived FA spillover was higher in individuals with a BMI ≥25 kg/m2 (n = 18) compared with those with a BMI <25 kg/m2 (n = 53) (22.2 ± 1.6% vs 18.6 ± 0.7%, P = 0.02). Women had higher chylomicron-derived FA spillover than age-and BMI-matched men (21.961.1% vs 15.06 1.6%, P = 0.001). Assessing spillover across subcutaneous abdominal AT showed higher proportions in women than in men (28.5 ± 6.1% vs 9. ± 6 1.3%, P = 0.01). Conclusion: There is a considerable degree of spillover FA into the systemic NEFA pool in the postprandial state; this process is greater and more dynamic in lean individuals and women. Contrary to general perception, spillover of chylomicron-derived FA into systemic circulation is a physiologically normal feature most easily observed in people with a higher capacity for clearance of plasma triglycerides, but does not appear to be a pathway providing excess NEFA in obesity.

Original languageEnglish
Pages (from-to)25-34
Number of pages10
JournalJournal of Clinical Endocrinology and Metabolism
Issue number1
Early online date1 Nov 2017
Publication statusPublished - 1 Jan 2018

Bibliographical note

Funding Information:
Financial Support: This work was supported in part by the British Heart Foundation Fellowships FS/11/18/28633 and FS/15/56/31645 (to L.H.) and Programme Grant RG/17/1/32663 (to F.K.), and the National Institute for Health Research Oxford Biomedical Research Centre (to F.K.). L.H. is a British Heart Foundation Senior Fellow in Basic Science. M.-E.P. is the recipient of a postdoctoral training fellowship grants from the Fonds de Recherche du Québec-Santé and the Heart and Lung Institute Foundation.


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