Level D· Scientific groundwork from lab and animal studiesLaboratory StudyPubMed

Stress-coping phenotypes shape adipose tissue function and plasticity and modulate metabolic resilience.

Mehta SK., Ben-Shachar M., Govindaraj S., Sen S., Segev A., Rahimi O.

Laboratory Study, published in Transl Psychiatry (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
Transl Psychiatry (2026)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
42431893
DOI
10.1038/s41398-026-04260-7

Abstract (original English)

Our previous findings demonstrated that stress resilience confers metabolic protection in high-fat diet (HFD)-fed mice. Recognizing the central role of adipose tissue in the pathogenesis of obesity comorbidities, this study aimed to define how stress resilience shapes adipose tissue function. Stress-resilient (Dominant, Dom) and stress-vulnerable (Submissive, Sub) mice were examined under standard (STD) or HFD. Metabolic, molecular, and transcriptomic analyses were performed in epididymal and inguinal white adipose tissue (eWAT and iWAT), and the effects of PPARgamma activator (pioglitazone) and antidepressant (paroxetine) were investigated. Stromal vascular fraction (SVF) cells were isolated to assess adipogenic potential. Sub mice developed glucose intolerance under HFD, accompanied by impaired insulin-induced Akt phosphorylation, and reduced glucose uptake in WAT, whereas Dom mice remained metabolically protected. Sub WAT exhibited adipocyte hypertrophy, an unfavorable leptin-to-adiponectin ratio, and depot-specific suppression of BCAA catabolic enzymes. RNA sequencing revealed transcriptomic divergence between strains, with Sub mice showing downregulation of adipogenesis under STD conditions. Functional analyses confirmed reduced proliferative and adipogenic potential of SVF cells, derived from Sub mice under both dietary conditions. In contrast, Dom-derived adipocytes disp

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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