Evidence map›Paper›PMID 42778065›Full record

ArticleJournal of lipid research2026

Prohibitin-1 cysteine-69 plays a sex-dependent role in fatty acid metabolism.

Katherine J Bernier, Zhanguo Gao, Yeshika Bhatia, Niloofar Beheshti Dehkordi, Fatemeh Nasiri, Alexes C Daquinag, Renata Pasqualini, Wadih Arap, Mikhail G Kolonin, Suresh Mishra

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Article in Journal of lipid research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

10 authors.

Katherine J BernierDepartment of Physiology and Pathophysiology, Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.
Zhanguo GaoBrown Foundation Institute of Molecular Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Yeshika BhatiaDepartment of Physiology and Pathophysiology, Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.
Niloofar Beheshti DehkordiDepartment of Physiology and Pathophysiology, Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.
Fatemeh NasiriDepartment of Internal Medicine, Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.
Alexes C DaquinagBrown Foundation Institute of Molecular Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Renata PasqualiniDivision of Cancer Biology, Rutgers Cancer Institute, Newark, NJ, USA; Division of Cancer Biology, Department of Radiation Oncology, Rutgers New Jersey Medical School, Newark, NJ, USA.
Wadih ArapDivision of Cancer Biology, Rutgers Cancer Institute, Newark, NJ, USA; Division of Hematology and Oncology, Department of Medicine, Rutgers New Jersey Medical School, Newark, NJ, USA.
Mikhail G KoloninBrown Foundation Institute of Molecular Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, USA. Electronic address: Mikhail.G.Kolonin@uth.tmc.edu.
Suresh MishraDepartment of Physiology and Pathophysiology, Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Internal Medicine, Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada. Electronic address: suresh.mishra@umanitoba.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic diseases are caused by dysregulation of glucose and lipid homeostasis, which relies on the function of adipose tissues (ATs). This regulation and the associated pathologies differ between sexes, which remain incompletely understood. Prohibitin-1 (PHB1) has multifaceted tissue-specific functions converging on metabolism. Here, we investigated the role of PHB1's evolutionarily conserved cysteine-69 by replacing it with an alanine in a knock-in (Phb1-KI) mouse model. We show that Phb1-KI mice lack cell surface localization of PHB1 and display sex-biased AT alterations in relative sizes of visceral and subcutaneous depots and their adipocyte sizes, expression of lipid metabolism effectors, and adipokine secretion. Phb1-KI adipocytes are defective in long-chain fatty acid uptake and mobilization, and their mitochondrial abnormalities and reduced oxidative capacity result in defective lipid metabolism. In compensation, Phb1-KI have increased glycolysis and Phb1-KI mice display improved glucose disposal and increased insulin sensitivity. Attributes of this phenotype manifested differently in males and females of Phb1-KI mice. Our results demonstrate the importance of cysteine-69 in sex-related function of PHB1 in integrative physiology and systemic metabolism.

Indexed as

brown adipose tissuefatty acid transportglucose metabolismmitochondriasex differenceswhite adipose tissue

Identifiers

PMID42778065

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