Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

The effect of adipose-derived mesenchymal stem cells against high fructose diet induced liver dysfunction and dysbiosis.

Mohammed MA., Hay NHA., Mohammed MT., Mahmoud HS., Ahmed MY., Abdelmenem A.

Animal Study on Type 2 Diabetes, published in Naunyn Schmiedebergs Arch Pharmacol (2024) — 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
Read the A–D evidence level guide

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
Animal Study
Journal
Naunyn Schmiedebergs Arch Pharmacol (2024)
Country
Germany
Reported sample size
—
Source database
PubMed
PMID
39500806
PMCID
PMC11978704
DOI
10.1007/s00210-024-03518-5
Citations
1

Abstract (original English)

High fructose diet (HFrD) has been approved to be involved in the pathogenesis of insulin resistance. Mesenchymal stem cells have a vital role in the treatment of various diseases including metabolic disturbances. We investigated the effect of Adipose-derived mesenchymal stem cells (ADMSCs) against HFrD-induced metabolic disorders and the molecular mechanisms for this effect. Rats were divided into 3 groups; control, HFrD, and combined HFrD with ADMSCs. We assessed liver functions, gut microbiota activity, oxidative stress, adiponectin, and IL10 levels. Also, we measured SREBP-1, IRS-1 expression using Western blot, and Malat1 expression using rt-PCR. ADMSCs antagonized metabolic abnormalities induced by HFrD in the form of improvement of liver functions and alleviation of oxidative stress. In addition, ADMSCs ameliorated gut microbiota activity besides the elevation of adiponectin and IL10 levels. ADMSCs attenuated insulin resistance through upregulation of IRS1 and downregulation of SREBP-1 and Malat1. ADMSCs can protect against HFrD-induced metabolic hazards.

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.

How we grade evidence
AnimalsMaleFructoseGastrointestinal MicrobiomeDysbiosisRatsMesenchymal Stem Cell TransplantationOxidative StressInsulin ResistanceAdipose Tissue

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