Abstract
ABSTRACTBackgroundObservational studies often infer hepatic de novo lipogenesis (DNL) by measuring circulating fatty acid (FA) markers; however, it remains to be elucidated whether these markers accurately reflect hepatic DNL.ObjectivesWe investigated associations between fasting hepatic DNL and proposed FA markers of DNL in subjects consuming their habitual diet.MethodsFasting hepatic DNL was assessed using 2H2O (deuterated water) in 149 nondiabetic men and women and measuring the synthesis of very low-density lipoprotein triglyceride (VLDL-TG) palmitate. FA markers of blood lipid fractions were determined by gas chromatography.ResultsNeither the lipogenic index (16:0/18:2n–6) nor the SCD index (16:1n–7/16:0) in VLDL-TG was associated with isotopically assessed DNL (r = 0.13, P = 0.1 and r = −0.08, P = 0.35, respectively). The relative abundances (mol%) of 14:0, 16:0, and 18:0 in VLDL-TG were weakly (r ≤ 0.35) associated with DNL, whereas the abundances of 16:1n–7, 18:1n–7, and 18:1n–9 were not associated. When the cohort was split by median DNL, only the abundances of 14:0 and 18:0 in VLDL-TG could discriminate between subjects having high (11.5%) and low (3.8%) fasting hepatic DNL. Based on a subgroup, FA markers in total plasma TG, plasma cholesteryl esters, plasma phospholipids, and red blood cell phospholipids were generally not associated with DNL.ConclusionsThe usefulness of circulating FAs as markers of hepatic DNL in healthy individuals consuming their habitual diet is limited due to their inability to discriminate clearly between individuals with low and high fasting hepatic DNL.
Highlights
In humans, the process whereby excess nonlipid precursors are synthesized to fat, de novo lipogenesis (DNL), primarily occurs in the cellular cytoplasm of the liver
When compared with DNL in very low-density lipoprotein triglyceride (VLDL-TG), which was 13.7 ± 7.9%, we found it to be significantly lower in all other fractions: 10.2 ± 9.3% in total plasma TG, 1.3 ± 2.1% in plasma cholesteryl esters (CE), 4.2 ± 3.2% in plasma PL, and 2.7 ± 3.2% in red blood cell (RBC) PL, all P ≤ 0.002 compared with very low-density lipoprotein (VLDL)-TG (Figure 4)
Hepatic DNL is measured using stable-isotope methodologies, but, for practical reasons, as proxy markers circulating fatty acid (FA) or FA ratios are often measured. It remains unclear how reflective these markers are of hepatic DNL during habitual dietary conditions, so we investigated the association between fasting hepatic DNL and circulating FA markers that are often used to infer hepatic DNL in healthy individuals consuming their habitual diet
Summary
The process whereby excess nonlipid precursors (e.g., sugars and protein) are synthesized to fat, de novo lipogenesis (DNL), primarily occurs in the cellular cytoplasm of the liver. It requires acetyl-CoA as a precursor and the principal building blocks to produce palmitoyl-CoA, the major quantitative product [1, 2]. Objectives: We investigated associations between fasting hepatic DNL and proposed FA markers of DNL in subjects consuming their habitual diet. Conclusions: The usefulness of circulating FAs as markers of hepatic DNL in healthy individuals consuming their habitual diet is limited due to their inability to discriminate clearly between individuals with low and high fasting hepatic DNL.
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