# A Western-Style Breakfast Induces a More Pro-Inflammatory Postprandial Response and Promotes Greater Macrophage Lipid Accumulation Compared to a Mediterranean-Style Breakfast in Obese and Normal-Weight Individuals

**Authors:** Alejandro Matamoros-Domínguez, Laura Sinausia, Gisela Pérez-Muñoz, Juan Manuel Espinosa-Cabello, Aída García-González, Ana Rodríguez-Rodríguez, José María Castellano, Elena María Yubero-Serrano, Emilio Montero, Javier S. Perona

PMC · DOI: 10.3390/nu18040672 · Nutrients · 2026-02-18

## TL;DR

A Western-style breakfast increases inflammation and fat buildup in immune cells more than a Mediterranean-style breakfast, especially in obese individuals.

## Contribution

This study shows that the type of dietary fat affects post-meal inflammation and macrophage lipid accumulation differently in obese and normal-weight individuals.

## Key findings

- Western-style breakfasts increase pro-inflammatory markers and saturated fatty acids in triglyceride-rich lipoproteins.
- TRL from Western-style breakfasts cause greater lipid accumulation in macrophages, especially in obese individuals.
- Gene expression of lipoprotein uptake receptors is upregulated after consuming a Western-style breakfast.

## Abstract

Background and objectives: Since postprandial lipid metabolism has emerged as a risk factor for cardiovascular disease, the quality of dietary fat may have a crucial role in atherogenesis and metabolic inflammation. In this study, we propose that the quality of dietary fats and the metabolic status of individuals modulate postprandial triglyceride-rich lipoprotein (TRL) composition and the response of macrophages to TRL. Methods: Randomized controlled crossover trial in the postprandial phase in 12 normal-weight adults and 12 adults with obesity. Each participant consumed both a Western-style (WB) and a Mediterranean-style (MB) breakfast in separate sessions, containing butter or olive oil as the fat source, respectively. Blood samples were collected at baseline (0 h), 2 h, and 4 h postprandially, and TRL were isolated and used to treat THP-1 macrophages. Results: The intake of the WB led to higher concentrations of inflammatory-related markers, particularly in individuals with obesity, and resulted in a higher content of saturated fatty acids and lower of monounsaturated fatty acids in TRL compared to the MB. Staining TRL-treated macrophages with Oil Red O revealed substantial lipid accumulation, which was more pronounced in cells cultured with 4 h TRL from individuals with obesity. This was also evidenced by upregulation of gene expression of lipoprotein uptake receptors following the consumption of the WB. Conclusions: Consumption of a WB led to a more pro-inflammatory postprandial profile and promoted greater lipid accumulation in macrophages, particularly in individuals with obesity, compared to a MB. These findings highlight the importance of fat quality in meals for cardiovascular risk management, especially in populations with obesity.

## Linked entities

- **Diseases:** obesity (MONDO:0011122), cardiovascular disease (MONDO:0004995)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, MTTP (microsomal triglyceride transfer protein) [NCBI Gene 4547] {aka ABL, MTP}, APOE (apolipoprotein E) [NCBI Gene 348] {aka AD2, APO-E, ApoE4, LDLCQ5, LPG}, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 2597] {aka G3PD, GAPD, HEL-S-162eP}, CP (ceruloplasmin) [NCBI Gene 1356] {aka AB073614, CP-2}, LPL (lipoprotein lipase) [NCBI Gene 4023] {aka HDLCQ11, LIPD}, APOB (apolipoprotein B) [NCBI Gene 338] {aka FCHL2, FLDB, LDLCQ4, apoB-100, apoB-48}, TREM2 (triggering receptor expressed on myeloid cells 2) [NCBI Gene 54209] {aka AD17, PLOSL2, TREM-2, Trem2a, Trem2b, Trem2c}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, LRP1 (LDL receptor related protein 1) [NCBI Gene 4035] {aka A2MR, APOER, APR, CD91, DDH3, IGFBP-3R}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}
- **Diseases:** metabolic syndrome (MESH:D024821), hyperglycemia (MESH:D006943), lipemia (MESH:D006949), Inflammation (MESH:D007249), injury to (MESH:D014947), coronary heart disease (MESH:D003327), atherogenesis (MESH:D050197), monocytic leukemia (MESH:D007951), cancer (MESH:D009369), gastrointestinal or metabolic disorders (MESH:D005767), diabetic (MESH:D003920), cardiovascular (MESH:D002318), Insulin Resistance (MESH:D007333), Obesity (MESH:D009765), type 2 diabetes (MESH:D003924), non-communicable diseases (MESH:D000073296), intestinal disturbances (MESH:D007410), metabolic (MESH:D008659), atherosclerotic plaques (MESH:D058226), visceral adiposity (MESH:D007418), hypertriglyceridemia (MESH:D015228), tissue injuries (MESH:D017695), TRL (MESH:C566031), lipotoxic damage (MESH:D020263)
- **Chemicals:** NaCl (MESH:D012965), alloxan (MESH:D000496), 16:1 n-7 (MESH:C008757), linoleic acid (MESH:D019787), methanol (MESH:D000432), olive oil (MESH:D000069463), fat (MESH:D005223), FA methyl esters (-), penicillin (MESH:D010406), PUFA (MESH:D005231), acids (MESH:D000143), hexane (MESH:D006586), silica (MESH:D012822), Nitrogen (MESH:D009584), butter (MESH:D002079), PMA (MESH:D013755), dichloromethane (MESH:D008752), coconut oil (MESH:D000074263), canola oil (MESH:D000074262), Fatty acid (MESH:D005227), carbohydrates (MESH:D002241), acetone (MESH:D000096), streptomycin (MESH:D013307), MUFA (MESH:D005229), cholesteryl ester (MESH:D002788), stearic acids (MESH:D013229), TG (MESH:D014280), CO2 (MESH:D002245), water (MESH:D014867), PL (MESH:D010743), Oil Red O (MESH:C011049), palm olein (MESH:D000073878), stearic acid (MESH:C031183), arachidonic acid (MESH:D016718), Lipid (MESH:D008055), chloroform (MESH:D002725), hydrogen (MESH:D006859), isopropanol (MESH:D019840), gondoic acid (MESH:C572289), alcohol (MESH:D000438), myristic acid (MESH:D019814), oleic acid (MESH:D019301), KCl (MESH:D011189), cholesterol (MESH:D002784), glucose (MESH:D005947)
- **Species:** Solanum lycopersicum (tomato, species) [taxon 4081], Mus musculus (house mouse, species) [taxon 10090], Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606], Nicotiana tabacum (American tobacco, species) [taxon 4097]
- **Mutations:** L90K
- **Cell lines:** THP-1 — Homo sapiens (Human), Childhood acute monocytic leukemia, Cancer cell line (CVCL_0006)

## Full text

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## Figures

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## References

68 references — full list in the complete paper: https://tomesphere.com/paper/PMC12943205/full.md

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Source: https://tomesphere.com/paper/PMC12943205