Associations of the Dietary Inflammatory Index with total adiposity and ectopic fat through the gut microbiota, LPS, and C-reactive protein in the Multiethnic Cohort–Adiposity Phenotype Study

Author:

Lozano Chloe P1ORCID,Wilkens Lynne R1,Shvetsov Yurii B1ORCID,Maskarinec Gertraud1ORCID,Park Song-Yi1,Shepherd John A1,Boushey Carol J1,Hebert James R2ORCID,Wirth Michael D2,Ernst Thomas3,Randolph Timothy4,Lim Unhee1ORCID,Lampe Johanna W4ORCID,Le Marchand Loïc1ORCID,Hullar Meredith A J4

Affiliation:

1. University of Hawaii Cancer Center, Honolulu, HI, USA

2. University of South Carolina, Cancer Prevention and Control Program, Department of Epidemiology and Biostatistics, Arnold School of Public Health, Columbia, SC, USA

3. University of Maryland, Department of Diagnostic Radiology and Nuclear Medicine, Baltimore, MD, USA

4. Fred Hutchinson Cancer Research Center, Public Health Sciences Division, Seattle, WA, USA

Abstract

ABSTRACT Background Mechanisms linking a proinflammatory diet to obesity remain under investigation. The ability of diet to influence the gut microbiome (GM) in creating chronic low-grade systemic inflammation provides a plausible connection to adiposity. Objectives Assess whether any associations seen between the Energy-Adjusted Dietary Inflammatory Index (E-DII score), total fat mass, visceral adipose tissue (VAT), or liver fat (percentage volume) operated through the GM or microbial related inflammatory factors, in a multiethnic cross-sectional study. Methods In the Multiethnic Cohort–Adiposity Phenotype Study (812 men, 843 women, aged 60–77 y) we tested whether associations between the E-DII and total adiposity, VAT, and liver fat function through the GM, LPS, and high-sensitivity C-reactive protein (hs-CRP). DXA-derived total fat mass, MRI-measured VAT, and MRI-based liver fat were measured. Participants provided stool and fasting blood samples and completed an FFQ. Stool bacterial DNA was amplified and the 16S rRNA gene was sequenced at the V1–V3 region. E-DII score was computed from FFQ data, with a higher E-DII representing a more proinflammatory diet. The associations between E-DII score, GM (10 phyla, 28 genera, α diversity), and adiposity phenotypes were examined using linear regression and mediation analyses, adjusting for confounders. Results There were positive total effects (c) between E-DII and total fat mass (c = 0.68; 95% CI: 0.47, 0.90), VAT (c = 4.61; 95% CI: 2.95, 6.27), and liver fat (c = 0.40; 95% CI: 0.27, 0.53). The association between E-DII score and total fat mass was mediated by LPS, Flavonifractor, [Ruminococcus] gnavus group, and Tyzzerella. The association between E-DII score and ectopic fat occurred indirectly through Fusobacteria, Christensenellaceae R-7 group, Coprococcus 2, Escherichia-Shigella, [Eubacterium] xylanophilum group, Flavonifractor, Lachnoclostridium, [Ruminococcus] gnavus group, Tyzzerella, [Ruminococcus] gnavus group (VAT only), and α diversity (liver fat only). There was no significant association between E-DII score and adiposity phenotype through hs-CRP. Conclusions Associations found between E-DII and adiposity phenotypes occurred through the GM and LPS.

Funder

National Institutes of Health

Publisher

Oxford University Press (OUP)

Subject

Nutrition and Dietetics,Medicine (miscellaneous)

Reference69 articles.

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