Evidence map›Paper›PMID 40790268›Full record

ArticleNature neuroscience2025

A pancreas-hippocampus feedback mechanism regulates circadian changes in depression-related behaviors.

Yao-Nan Liu, Qiu-Wen Wang, Xin-Yu She, Li-Jun Li, Bing Wang, Ruilan Yang, Qian Li, Si-Yao Lu, Ying-Han Wang, Wei Shen and 9 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

19 authors.

Yao-Nan Liu *State Key Laboratory of Membrane Biology, IDG/McGovern Institute for Brain Research, School of Life Sciences, Tsinghua University, Beijing, China.ORCID http://orcid.org/0009-0003-2498-0568
Qiu-Wen Wang *Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA, USA.
Xin-Yu She *State Key Laboratory of Membrane Biology, IDG/McGovern Institute for Brain Research, School of Life Sciences, Tsinghua University, Beijing, China.ORCID http://orcid.org/0000-0003-2877-8175
Li-Jun Li *Department of Neuropsychiatry, Behavioral Neurology and Clinical Psychology, Beijing Tiantan Hospital, Capital Medical University, China National Clinical Research Centre for Neurological Diseases, Beijing, China.
Bing WangState Key Laboratory of Membrane Biology, IDG/McGovern Institute for Brain Research, School of Life Sciences, Tsinghua University, Beijing, China.
Ruilan YangThe Affiliated Brain Hospital, Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou Medical University, Guangzhou, China.
Qian LiChina National Center for Bioinformation, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, China.
Si-Yao LuState Key Laboratory of Membrane Biology, IDG/McGovern Institute for Brain Research, School of Life Sciences, Tsinghua University, Beijing, China.
Ying-Han WangState Key Laboratory of Membrane Biology, IDG/McGovern Institute for Brain Research, School of Life Sciences, Tsinghua University, Beijing, China.
Wei ShenState Key Laboratory of Membrane Biology, IDG/McGovern Institute for Brain Research, School of Life Sciences, Tsinghua University, Beijing, China.
Chong-Lei FuState Key Laboratory of Membrane Biology, IDG/McGovern Institute for Brain Research, School of Life Sciences, Tsinghua University, Beijing, China.ORCID http://orcid.org/0000-0002-1082-2783
Dan LiState Key Laboratory of Membrane Biology, IDG/McGovern Institute for Brain Research, School of Life Sciences, Tsinghua University, Beijing, China.
Lan YiState Key Laboratory of Membrane Biology, IDG/McGovern Institute for Brain Research, School of Life Sciences, Tsinghua University, Beijing, China.
Chun-Xue WangDepartment of Neuropsychiatry, Behavioral Neurology and Clinical Psychology, Beijing Tiantan Hospital, Capital Medical University, China National Clinical Research Centre for Neurological Diseases, Beijing, China.
Wei ShiKey Laboratory for Biomechanics and Mechanobiology of Ministry of Education, School of Engineering Medicine, Beihang University, Beijing, China.
Xin ChengState Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Liping CaoThe Affiliated Brain Hospital, Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou Medical University, Guangzhou, China.
Shuangli MiChina National Center for Bioinformation, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, China.ORCID http://orcid.org/0000-0001-8883-3215
Jun YaoState Key Laboratory of Membrane Biology, IDG/McGovern Institute for Brain Research, School of Life Sciences, Tsinghua University, Beijing, China. jyao@mail.tsinghua.edu.cn.ORCID http://orcid.org/0000-0002-4916-3412

Funding

National Science Foundation of China | National Natural Science Foundation of China-Yunnan Joint Fund (NSFC-Yunnan Joint Fund) 32371008
6 · The paper itself

Abstract

Individuals with neuropsychiatric disorders often show metabolic symptoms. However, the mechanisms underlying this co-occurrence remain unclear. Here we show that induced pluripotent stem cell-derived pancreatic islets from individuals with bipolar disorder have insulin secretion deficits caused by increased expression of RORβ, a susceptibility gene for bipolar disorder. Enhancing RORβ expression in mouse pancreatic β cells induced depression-related behaviors in the light phase and mania-like behaviors in the dark phase. Pancreatic RORβ overexpression in the light phase reduced insulin release from islets, inducing hippocampal hyperactivity and depression-like behaviors. Furthermore, this hippocampal hyperactivity in the light phase had the delayed effect of promoting insulin release in the dark phase, resulting in mania-like behaviors and hippocampal neuronal hypoactivity. Our results in mice point to a pancreas-hippocampus feedback mechanism by which metabolic and circadian factors cooperate to generate behavioral fluctuations and which may play a role in bipolar disorder.

Indexed as

Bipolar DisorderCircadian RhythmDepressionFeedback, PhysiologicalHippocampusPancreasAnimalsHumansInsulinInsulin SecretionMaleMiceMice, Inbred C57BLMice, TransgenicInsulin

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.