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

**Authors:** Marwa Abdeltawab Mohammed, Nesma Hussein Abel Hay, Maha Tarek Mohammed, Hoda Sayed Mahmoud, Manar Yehia Ahmed, Ahmed Abdelmenem, Dina Sayed Abdelrahim

PMC · DOI: 10.1007/s00210-024-03518-5 · 2024-11-05

## TL;DR

Adipose-derived stem cells help protect the liver and gut from the harmful effects of a high fructose diet by reducing oxidative stress and improving metabolic functions.

## Contribution

This study demonstrates that ADMSCs can counteract high fructose diet-induced liver dysfunction and gut dysbiosis through specific molecular mechanisms.

## Key findings

- ADMSCs improved liver function and reduced oxidative stress in rats on a high fructose diet.
- ADMSCs increased adiponectin and IL10 levels while modulating IRS1 and SREBP-1 expression.
- ADMSCs ameliorated gut microbiota activity and attenuated insulin resistance.

## Abstract

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.

## Linked entities

- **Genes:** SREBF1 (sterol regulatory element binding transcription factor 1) [NCBI Gene 6720], IRS1 (insulin receptor substrate 1) [NCBI Gene 3667], MALAT1 (metastasis associated lung adenocarcinoma transcript 1) [NCBI Gene 378938]
- **Species:** Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** SREBF1 (sterol regulatory element binding transcription factor 1) [NCBI Gene 6720] {aka HMD, IFAP2, SREBP1, bHLHd1}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, MALAT1 (metastasis associated lung adenocarcinoma transcript 1) [NCBI Gene 378938] {aka HCN, LINC00047, NCRNA00047, NEAT2, PRO2853, miPEP-52}, IRS1 (insulin receptor substrate 1) [NCBI Gene 3667] {aka HIRS-1}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}
- **Diseases:** metabolic disturbances (MESH:D024821), metabolic abnormalities (MESH:D008659), insulin resistance (MESH:D007333), liver dysfunction (MESH:D017093)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11978704/full.md

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Source: https://tomesphere.com/paper/PMC11978704