ReviewObesity pillars2026
Hepatic metabolic reprogramming after metabolic and bariatric surgery: Gene-nutrition interactions and precision nutrition.
Review in Obesity pillars, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.