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Publications

Journal Article Review Epublish 3 citations

PubMed: 42382663 DOI: 10.1016/j.obpill.2026.100290

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

Obes Pillars 19:100290

Authors: Daniel Simancas-Racines, Martín Campuzano-Donoso, Gianluca Rossetti, Luigi Cobellis, Vincenzo Pilone, Federica Fascì-Spurio, Dolores Jima Gavilanes, Carlos Soria, Claudia Reytor-González, Luigi Schiavo

Affiliations

  • Facultad de Ciencias de la Salud y Bienestar Humano, Universidad Tecnológica Indoamérica, Ambato, 180150, Ecuador.
  • General and Bariatric Surgery Unit, Abano Terme Policlinic, Padova, 35031, Italy.
  • Unit of General Surgery, Casa Di Cura "Prof. Dott. Luigi Cobelli", Vallo della Lucania, 84078, Italy.
  • Public Health Department, University of Naples Federico II, Naples, 80131, Italy.
  • Gastroenterology Unit, Ospedale dell'Angelo, Venice, Italy.
  • Escuela de Medicina, Universidad Espíritu Santo, Samborondón, 0901952, Ecuador.
  • Hospital de Lima Este Vitarte, Ctra. Central KM 7.5, Ate, 15491, Peru.
  • Department of Medicine, Surgery and Dentistry, "Scuola Medica Salernitana", University of Salerno, Baronissi, 84081, Italy.

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.

MeSH

Glucagon-Like Peptide 1, Physiology, Glucagon-Like Peptide-1 Receptor, Vitamins, Drug Therapy, Diet, Micronutrients, Vitamin B 12, Obesity, Incretins, Weight Loss