REVIEW article
Front. Cardiovasc. Med.
Sec. Lipids in Cardiovascular Disease
Volume 12 - 2025 | doi: 10.3389/fcvm.2025.1655889
This article is part of the Research TopicPostprandial dysmetabolism - A chronic stressor of the cardiometabolic systemView all articles
From Meal to Malfunction: Exploring Molecular Pathways, Biomarkers and Interventions in Postprandial Cardiometabolic Health
Provisionally accepted- 1Facultad de Ciencias de Facultad de Ciencias de la Salud Eugenio Espejo, Centro de Investigación en Salud Pública y Epidemiología Clínica (CISPEC), Universidad UTE, Quito, Ecuador
- 2Facultad de Ciencias de la Ingeniería e Industrias, Centro de Investigación de Alimentos (CIAL), Universidad UTE, Quito, Ecuador
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Cardiometabolic diseases—including type 2 diabetes, cardiovascular disease, and metabolic dysfunction–associated steatotic liver disease—are increasingly driven by near-continuous aftermeal exposure to glucose and lipid surges that traditional fasting tests often miss. This review prioritizes human studies from 2020–2025 and uses earlier work only as foundational anchors; non-English reports were excluded and preclinical findings are cited solely for mechanistic context. Evidence converges on six processes that amplify risk within hours after eating: impaired insulin signaling, delayed clearance of dietary lipids, mitochondrial and oxidative stress, loss of endothelial nitric oxide, inflammasome-mediated inflammation, and microbiome–hormone interactions. Dynamic, after-meal markers and simple composites such as the triglyceride–glucose index outperform fasting measures for identifying risk and guiding care. Practical strategies to shorten the "damage window" include Mediterranean-style meals with low glycemic index swaps and unsaturated fats, earlier distribution of daily energy and early time-restricted eating, a small pre-meal protein portion, and brief post-meal walking. Fast-acting medicines—glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide receptor agonists, rapid-acting insulin analogues, sodium–glucose cotransporter 2 inhibitors taken before meals, and proprotein convertase subtilisin/kexin type 9 inhibitors—further blunt peaks, while continuous glucose monitoring with algorithmic feedback enables timing-aware, person-specific adjustments. A tiered workflow— screen, stratify, and personalize—reframes prevention and treatment around after-meal physiology, with particular relevance to settings where resources are limited.
Keywords: postprandial dysmetabolism, Metaflammation, Insulin Resistance, Cardiometabolic Health, precision medicine, healthcare
Received: 28 Jun 2025; Accepted: 23 Sep 2025.
Copyright: © 2025 Reytor-González, Cevallos-Fernández, Jácome and Simancas-Racines. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Daniel Simancas-Racines, claudiareytor@gmail.com
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.