Hepatic metabolic reprogramming after metabolic and bariatric surgery: Gene-nutrition interactions and precision nutrition
7 affiliations
- 1Center for Evidence Ecosystems, Implementation Science, and Decision-Making (CIDES), Facultad de Ciencias de la Salud y Bienestar Humano, Universidad Tecnológica Indoamérica, Ambato, 180150, Ecuador
- 2Facultad de Ciencias Médicas, de la Salud y la Vida, Universidad Internacional del Ecuador UIDE, Quito, 170411, Ecuador
- 3Escuela de Medicina, Universidad Espíritu Santo, Samborondón, 0901952, Ecuador
- 4General and Bariatric Surgery Unit, Abano Terme Policlinic, Padova, 35031, Italy
- 5Unit of General Surgery, Casa Di Cura “Prof. Dott. Luigi Cobellis”, Vallo della Lucania, 84078, Italy
- 6Public Health Department, University of Naples Federico II, Naples, 80131, Italy
- 7Department of Medicine, Surgery and Dentistry “Scuola Medica Salernitana”, University of Salerno, Baronissi, 84081, Italy
Abstract
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent among individuals with obesity evaluated for metabolic and bariatric surgery (MBS) and may persist or recur despite substantial postoperative weight loss. This review examines the postoperative state as a dynamic model of hepatic metabolic reprogramming and gene–nutrition interaction, integrating surgical anatomy, dietary intake, nutrient absorption, metabolic response, weight trajectory, and inherited susceptibility.
Methods: This was a narrative clinical review informed by a structured literature search of MEDLINE (via PubMed), the Cochrane Library, and Epistemonikos (final search, August 3, 2026). Human evidence on hepatic outcomes after MBS, genetic determinants of liver disease, and postoperative nutritional exposures was prioritized; mechanistic and non-surgical human studies were considered only where direct postoperative evidence was limited.
Results: MBS rapidly reduces hepatic fat and improves insulin sensitivity, whereas resolution of metabolic dysfunction-associated steatohepatitis (MASH) and regression of fibrosis follow slower and partly dissociated trajectories. Genetic variants affecting hepatic lipid storage, lipid export, glucose-driven lipogenesis, and fibrogenesis may contribute to residual hepatic risk, but no study has jointly assessed genotype, repeated postoperative dietary exposure, and direct liver outcomes. Current evidence supports adequate protein intake, procedure-specific micronutrient supplementation, sustained dietary quality, metabolic risk control, alcohol assessment, and phenotype-guided liver surveillance regardless of genotype. Pharmacotherapy with demonstrated histological efficacy in MASH may be considered for residual MASH or weight recurrence, although it has not been evaluated specifically after MBS.
Conclusions: Genetic information may refine the interpretation of residual hepatic risk, but genotype-guided procedure selection, dietary patterns, macronutrient targets, or supplement doses are not supported. Prospective, adequately powered, multi-ancestry studies integrating longitudinal nutrition, genetic susceptibility, and direct hepatic outcomes are needed to determine whether genotype-informed nutrition improves outcomes beyond high-quality phenotype-guided care.
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BibTeX
@article{reytorgonzalez2026hepatic,
title = {{Hepatic metabolic reprogramming after metabolic and bariatric surgery: Gene-nutrition interactions and precision nutrition}},
author = {Claudia Reytor-González and Náthaly Mercedes Román-Galeano and Dolores Jima Gavilanes and Gianluca Rossetti and Luigi Cobellis and Vincenzo Pilone and Daniel Simancas-Racines and Luigi Schiavo},
journal = {Obesity Pillars},
year = {2026},
month = oct,
doi = {10.1016/j.obpill.2026.100348},
url = {https://doi.org/10.1016/j.obpill.2026.100348},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Hepatic metabolic reprogramming after metabolic and bariatric surgery: Gene-nutrition interactions and precision nutrition
AU - Claudia Reytor-González
AU - Náthaly Mercedes Román-Galeano
AU - Dolores Jima Gavilanes
AU - Gianluca Rossetti
AU - Luigi Cobellis
AU - Vincenzo Pilone
AU - Daniel Simancas-Racines
AU - Luigi Schiavo
PY - 2026
DA - 2026/10/15
JO - Obesity Pillars
DO - 10.1016/j.obpill.2026.100348
UR - https://doi.org/10.1016/j.obpill.2026.100348
AB - Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent among individuals with obesity evaluated for metabolic and bariatric surgery (MBS) and may persist or recur despite substantial postoperative weight loss. This review examines the postoperative state as a dynamic model of hepatic metabolic reprogramming and gene–nutrition interaction, integrating surgical anatomy, dietary intake, nutrient absorption, metabolic response, weight trajectory, and inherited susceptibility. Methods: This was a narrative clinical review informed by a structured literature search of MEDLINE (via PubMed), the Cochrane Library, and Epistemonikos (final search, August 3, 2026). Human evidence on hepatic outcomes after MBS, genetic determinants of liver disease, and postoperative nutritional exposures was prioritized; mechanistic and non-surgical human studies were considered only where direct postoperative evidence was limited. Results: MBS rapidly reduces hepatic fat and improves insulin sensitivity, whereas resolution of metabolic dysfunction-associated steatohepatitis (MASH) and regression of fibrosis follow slower and partly dissociated trajectories. Genetic variants affecting hepatic lipid storage, lipid export, glucose-driven lipogenesis, and fibrogenesis may contribute to residual hepatic risk, but no study has jointly assessed genotype, repeated postoperative dietary exposure, and direct liver outcomes. Current evidence supports adequate protein intake, procedure-specific micronutrient supplementation, sustained dietary quality, metabolic risk control, alcohol assessment, and phenotype-guided liver surveillance regardless of genotype. Pharmacotherapy with demonstrated histological efficacy in MASH may be considered for residual MASH or weight recurrence, although it has not been evaluated specifically after MBS. Conclusions: Genetic information may refine the interpretation of residual hepatic risk, but genotype-guided procedure selection, dietary patterns, macronutrient targets, or supplement doses are not supported. Prospective, adequately powered, multi-ancestry studies integrating longitudinal nutrition, genetic susceptibility, and direct hepatic outcomes are needed to determine whether genotype-informed nutrition improves outcomes beyond high-quality phenotype-guided care.
SN - 2667-3681
ER -