Evidence map›Paper›PMID 42754096›Full record

ArticleAdvances in nutrition (Bethesda, Md.)2026

The Incretin Mirage: Epigenetic Memory as a Potential Driver of Post-Treatment Weight Regain.

Ruslan Kubant, G Harvey Anderson

Abstract read
In one paragraph

Article in Advances in nutrition (Bethesda, Md.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Ruslan KubantDepartment of Nutritional Sciences, University of Toronto, Toronto, ON, Canada. Electronic address: ruslan.kubant@utoronto.ca.
G Harvey AndersonDepartment of Nutritional Sciences, University of Toronto, Toronto, ON, Canada; Department of Physiology, University of Toronto, Toronto, ON, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although incretin receptor agonists deliver profound weight loss, clinical data reveal a consistent challenge: treatment discontinuation routinely triggers rapid weight regain. We define this phenomenon as the "Incretin Mirage"-a state where pharmacologically induced weight reduction temporarily conceals the persistent metabolic and neuroendocrine adaptations established during chronic obesity. Despite a lower body mass, key drivers of the disease, including adipocyte dysfunction and altered appetite signaling, retain a molecular imprint of obesity driven by persistent epigenetic marks. To explain why the body aggressively resists sustained weight loss after treatment cessation, we introduce the "Epigenetic Detent." This novel conceptual mechanism links adipocyte epigenetic memory with neuroendocrine plasticity to preserve a high-adiposity set-point. Consequently, the moment pharmacological suppression is lifted, this persistently defended set-point serves as a potential driver of weight regain. Achieving a durable therapeutic response therefore requires moving beyond transient appetite suppression. We advocate for a coordinated, multitiered strategy that couples lifestyle and environmental restructuring with emerging epigenetic therapies aimed at erasing these cellular marks and achieving a complete cellular metabolic reset.

Indexed as

adipose tissue memoryEpigenetic DetentGLP-1/GIP receptor agonistsIncretin Mirageobesitytranslational medicineweight regain

Identifiers

PMID42754096
PMCPMC13676900

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.