Fasting hepatic de novo lipogenesis is not reliably assessed using circulating fatty acid markers.


Journal

The American journal of clinical nutrition
ISSN: 1938-3207
Titre abrégé: Am J Clin Nutr
Pays: United States
ID NLM: 0376027

Informations de publication

Date de publication:
01 02 2019
Historique:
received: 09 08 2018
accepted: 03 10 2018
pubmed: 6 2 2019
medline: 23 10 2019
entrez: 6 2 2019
Statut: ppublish

Résumé

Observational 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. We investigated associations between fasting hepatic DNL and proposed FA markers of DNL in subjects consuming their habitual diet. Fasting 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. Neither 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. 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.

Sections du résumé

Background
Observational 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.
Objectives
We investigated associations between fasting hepatic DNL and proposed FA markers of DNL in subjects consuming their habitual diet.
Methods
Fasting 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.
Results
Neither 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.
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.

Identifiants

pubmed: 30721918
pii: S0002-9165(22)03118-5
doi: 10.1093/ajcn/nqy304
pmc: PMC6367991
doi:

Substances chimiques

Biomarkers 0
Fatty Acids 0
Lipoproteins, VLDL 0
Palmitates 0
Triglycerides 0
very low density lipoprotein triglyceride 0
Deuterium AR09D82C7G
Deuterium Oxide J65BV539M3

Types de publication

Journal Article Research Support, Non-U.S. Gov't Validation Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

260-268

Subventions

Organisme : Biotechnology and Biological Sciences Research Council
ID : BB/N005600/1
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/09/003
Pays : United Kingdom
Organisme : British Heart Foundation
ID : FS/11/18/28633
Pays : United Kingdom
Organisme : British Heart Foundation
ID : FS/15/56/31645
Pays : United Kingdom
Organisme : Biotechnology and Biological Sciences Research Council
ID : BB/N015665/1
Pays : United Kingdom

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Auteurs

Fredrik Rosqvist (F)

Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, United Kingdom.
Department of Public Health and Caring Sciences, Clinical Nutrition and Metabolism, Uppsala University, Uppsala, Sweden.

Catriona A McNeil (CA)

Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, United Kingdom.

Camilla Pramfalk (C)

Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, United Kingdom.
Division of Clinical Chemistry, Department of Laboratory Medicine, Karolinska Institute at Karolinska University Hospital Huddinge, Stockholm, Sweden.

Sion A Parry (SA)

Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, United Kingdom.

Wee Suan Low (WS)

Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, United Kingdom.

Thomas Cornfield (T)

Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, United Kingdom.

Barbara A Fielding (BA)

Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom.

Leanne Hodson (L)

Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, United Kingdom.
Oxford NIHR Biomedical Research Centre, Churchill Hospital, Oxford, United Kingdom.

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