Evidence map›Paper›PMID 41959671›Full record

ArticleiScience2026

Alpha-ketoglutarate alleviates acute pancreatitis by restoring energy metabolism.

Peng Li, Chunfeng Shi, Hangshi Wang, Shiyang Zhan, Jiahui Zhang, Dongyao Xu, Yuxun Lv, Furong Yan, Shaobin Xu, Jin Chen and 1 more

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Peng LiDepartment of Hepatobiliary and Pancreatic Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China.
Chunfeng ShiDepartment of Hepatobiliary and Pancreatic Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China.
Hangshi WangDepartment of Orthopedics, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China.
Shiyang ZhanDepartment of Hepatobiliary and Pancreatic Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China.
Jiahui ZhangDepartment of Hepatobiliary and Pancreatic Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China.
Dongyao XuDepartment of Hepatobiliary and Pancreatic Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China.
Yuxun LvClinical Center for Molecular Diagnosis and Therapy, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China.
Furong YanClinical Center for Molecular Diagnosis and Therapy, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China.
Shaobin XuDepartment of Hepatobiliary and Pancreatic Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China.
Jin ChenClinical Center for Molecular Diagnosis and Therapy, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China.
Wei WangDepartment of Hepatobiliary and Pancreatic Surgery, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute pancreatitis (AP) lacks specific therapies. This study identified dysregulated metabolites in AP and investigated the therapeutic potential of α-ketoglutaric acid (AKG). Metabolomic profiling of human serum revealed 76 AP-specific metabolites compared to acute cholecystitis and normal control, with AKG significantly elevated and correlated with disease severity. In a severe AP mouse model, oral AKG supplementation attenuated pancreatic injury, systemic inflammation, and multi-organ damage. Mechanistically, AKG restored pancreatic energy metabolism and mitochondrial structure while reactivating the Nrf2 antioxidant and adenosine monophosphate-activated protein kinase signaling pathways. These findings highlight AKG as a specific metabolic signature of AP and a promising therapeutic agent for alleviating mitochondrial dysfunction and organ injury.

Indexed as

health sciences

Identifiers

PMID41959671
PMCPMC13059122

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.