Evidence map›Paper›PMID 34826585›Full record

ArticleBiochimica et biophysica acta. Molecular basis of disease2022

SNAP25 mutation disrupts metabolic homeostasis, steroid hormone production and central neurobehavior.

Xiao Hao, Bing Zhu, Pinglin Yang, Dachuan Dong, Peyman Sahbaie, Peter L Oliver, Wen-Jun Shen, Salman Azhar, Fredric B Kraemer

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta. Molecular basis of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 30% of its field
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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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 at 3 institutions in 3 countries.

Xiao HaoDivision of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States; Department of Endocrinology, First Affiliated Hospital of the Medical College of Zhengzhou University, Zhengzhou, China.
Bing ZhuDivision of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States; Department of Endocrinology and Metabolism, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Pinglin YangDivision of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States; Department of Orthopedics, Second Affiliated Hospital of Xi'an, Jiaotong University, Xi'an, Shaanxi, China.
Dachuan DongDivision of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States.
Peyman SahbaieGeriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States; Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, United States.
Peter L OliverMedical Research Council Harwell Institute, Harwell Campus, Oxfordshire, United Kingdom.
Wen-Jun ShenDivision of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States. Electronic address: wenjun@stanford.edu.
Salman AzharDivision of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States.
Fredric B KraemerDivision of Endocrinology, Gerontology and Metabolism, Stanford University School of Medicine, Stanford, CA, United States; Geriatric Research, Education, and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, CA, United States. Electronic address: fbk@stanford.edu.
VA Palo Alto Health Care System · USMary Lyon Centre at MRC Harwell · GBTongji University · CN

Funding

Stanford Islet Research CoreP30DK116074 · NIDDK · STANFORD UNIVERSITY · PI HASSAN CHAIB · 2017 to 2026
$19.5M
LipolysisI01BX000398 · VA · VETERANS ADMIN PALO ALTO HEALTH CARE SYS · PI KRAEMER, FREDRIC B. · 2009 to 2020
–
Role of Cholesterol in Age-related Decline in SteroidogenesisI01BX001923 · VA · VETERANS ADMIN PALO ALTO HEALTH CARE SYS · PI AZHAR, SALMAN · 2013 to 2020
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BLR&D Research Career Scientist Award ApplicationIK6BX004200 · VA · VETERANS ADMIN PALO ALTO HEALTH CARE SYS · PI AZHAR, SALMAN · 2018 to 2024
–
BLRD VA I01 BX000398BLRD VA I01 BX001923BLRD VA IK6 BX004200NIDDK NIH HHS P30 DK116074
6 · The paper itself

Abstract

objectiveSNAP-25 is one of the key proteins involved in formation of soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complexes that are at the core of hormonal secretion and synaptic transmission. Altered expression or function of SNAP-25 can contribute to the development of neuropsychiatric and metabolic disease. A dominant negative (DN) I67T missense mutation in the b-isoform of SNAP-25 (DN-SNAP25mut) mice leads to abnormal interactions within the SNARE complex and impaired exocytotic vesicle recycling, yet the significance of this mutation to any association between the central nervous system and metabolic homeostasis is unknown.

methodsHere we explored aspects of metabolism, steroid hormone production and neurobehavior of DN-SNAP25mut mice.

resultsDN-SNAP25mut mice displayed enhanced insulin function through increased Akt phosphorylation, alongside increased adrenal and gonadal hormone production. In addition, increased anxiety behavior and beigeing of white adipose tissue with increased energy expenditure were observed in mutants.

conclusionsOur results show that SNAP25 plays an important role in bridging central neurological systems with peripheral metabolic homeostasis, and provide potential insights between metabolic disease and neuropsychiatric disorders in humans.

Indexed as

Behavior, AnimalHomeostasisInsulin ResistanceMutationAnimalsFemaleGonadal Steroid HormonesMaleMetabolic DiseasesMiceMice, Inbred C3HSynaptic TransmissionSynaptosomal-Associated Protein 25Gonadal Steroid HormonesSnap25 protein, mouseSynaptosomal-Associated Protein 25Anxiety-like behaviorBeigeingBrown adipose tissueGlucose metabolismInsulin secretionNeurobehaviorSNAP25SteroidogenesisWhite adipose tissue

Identifiers

PMID34826585
PMCPMC8759409
OpenAlexW3216593054

What Socratic holds

Textmetadata
LicenceTDM
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.