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  4. Micronutrient risk with GLP-1 receptor and dual incretin agonists in obesity: Mechanistic pathways, clinical signals, and a monitoring framework
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Micronutrient risk with GLP-1 receptor and dual incretin agonists in obesity: Mechanistic pathways, clinical signals, and a monitoring framework

Journal
Obesity Pillars
ISSN
26673681
Date Issued
2026-09
Author(s)
Simancas Racines, Daniel  
CENTRO DE INVESTIGACIÓN DE EVIDENCIA, IMPLEMENTACIÓN Y TOMA DE DECISIONES EN SALUD  
Campuzano-Donoso, Martín
Rossetti, Gianluca
Cobellis, Luigi
Pilone, Vincenzo
Fascì-Spurio, Federica
Jima Gavilanes, Dolores
Soria, Carlos
Reytor González, Claudia  
CENTRO DE INVESTIGACIÓN DE EVIDENCIA, IMPLEMENTACIÓN Y TOMA DE DECISIONES EN SALUD  
Schiavo, Luigi
Type
Article
DOI
10.1016/j.obpill.2026.100290
URL
https://cris.indoamerica.edu.ec/handle/123456789/10159
Abstract
Background: Incretin-based pharmacotherapies, including GLP-1 receptor agonists and dual GIP/GLP-1 receptor agonists, have transformed obesity management by producing substantial weight loss through appetite suppression, reduced energy intake, and gastrointestinal effects. These mechanisms may also modify dietary intake, gastrointestinal physiology, and weight-loss–related metabolic adaptations, raising concern about micronutrient disturbances during long-term treatment. Methods: This narrative clinical review synthesizes evidence on mechanistic pathways, clinical signals, and monitoring considerations related to micronutrient risk during incretin-based obesity pharmacotherapy. Evidence was integrated from dietary studies, observational cohorts, mechanistic investigations, clinical trials, pharmacovigilance reports, and literature on obesity-related micronutrient physiology. Results: Micronutrient vulnerability appears to arise from the interaction between reduced food intake, lower dietary diversity, gastrointestinal intolerance, delayed gastric emptying, rapid weight loss, and baseline nutritional risk. The most relevant signals involve hematologic, fat-soluble, bone-related, trace element, and electrolyte domains, particularly iron, vitamin B12, vitamin D, calcium, magnesium, zinc, with additional context-dependent concerns involving thiamine, folate, vitamin A, other fat-soluble vitamins and potassium. Most abnormalities reported to date are subclinical or indirect, but clinically meaningful consequences may occur in susceptible individuals, including those with prior bariatric surgery, gastrointestinal disorders, poor baseline diet quality, older age, or prolonged nausea and vomiting. Conclusion: Micronutrient risk during incretin-based obesity pharmacotherapy is likely multifactorial and patient-specific. Individualized nutritional assessment and targeted laboratory monitoring should be considered for high-risk patients, while prospective studies are needed to define incidence, clinical relevance, and evidence-based monitoring strategies. © 2026 The Authors
Subjects

Glucagon-like peptide...

Incretin therapy

Micronutrient deficie...

Obesity pharmacothera...

Semaglutide

Tirzepatide

Investigación Indoamérica

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