Evidence map›Paper›PMID 41495038›Full record

ArticleCell discovery2026

Prefrontal cortex-to-hypothalamic outputs orchestrate cue-potentiated palatable food consumption via AMPKβ2 signaling.

Jiakun Xiang, Minghong Shi, Jiajia Kang, Xingyuan Zhang, Jiankai Ling, Wei Zhan, Dianyi Li, Rongfeng K Hu, Zhi-Xiang Xu

Abstract read
In one paragraph

Article in Cell discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
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

9 authors.

Jiakun XiangShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Brain Function and Disorders and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China.
Minghong ShiShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Brain Function and Disorders and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China.
Jiajia KangShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Brain Function and Disorders and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China.
Xingyuan ZhangShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Brain Function and Disorders and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China.
Jiankai LingShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Brain Function and Disorders and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China.
Wei ZhanShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Brain Function and Disorders and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China.
Dianyi LiShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Brain Function and Disorders and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China.
Rongfeng K HuInstitute for Translational Brain Research, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science, Fudan University, Shanghai, China.ORCID http://orcid.org/0009-0000-0164-6215
Zhi-Xiang XuShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Brain Function and Disorders and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China. zhixiangxu@fudan.edu.cn.ORCID http://orcid.org/0000-0002-0962-7702

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cognitive factors critically influence appetite and food consumption, contributing to the increasing incidence of obesity in modern obesogenic environments. However, the cellular and molecular mechanisms underlying this phenomenon remain poorly understood. Here, using calcium imaging in freely moving mice, we found that neurons in the prelimbic cortex (PrL) underwent activity-dependent plasticity in response to learned environmental cues paired with a high-fat diet (HFD). The activity of these neurons reliably predicted the duration of food consumption. Transcriptomic analyses further revealed significant alterations in ATP metabolic processes in the PrL following HFD-associated learning. Notably, the depletion of AMPKβ2, a subunit of AMPK that senses ATP dynamics, abolished PrL plasticity during HFD associative learning and prevented the cue-driven overconsumption of palatable food. At the circuitry level, the activity of PrL

Identifiers

PMID41495038
PMCPMC12775431

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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.