Level B· Emerging clinical evidence with positive signalsRandomized Controlled TrialPubMed

Modulation of glucose and lipid metabolism by porcine adiponectin receptor 1-transgenic mesenchymal stromal cells in diet-induced obese mice.

Lin YY., Chen CY., Lin Y., Chiu YP., Chen CC., Liu BH.

Randomized Controlled Trial, published in Cytotherapy (2013) — summary generated from the PubMed abstract.

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Level B· Emerging clinical evidence with positive signalsEvidence level of this study

Several human studies show positive signals, while research methods and sample sizes continue to develop.

  • 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
Randomized Controlled Trial
Journal
Cytotherapy (2013)
Country
England
Reported sample size
—
Source database
PubMed
PMID
23732048
DOI
10.1016/j.jcyt.2013.03.008

Abstract (original English)

Obesity and its associated diseases demand better therapeutic strategies. Regenerative medicine combined with gene therapy has emerged as a promising approach in various clinical applications. Adiponectin (ApN) and its receptors have been demonstrated to play beneficial roles in modulating glucose and lipid homeostasis. In the current study, we tested such an approach by transplanting mesenchymal stromal cells (MSCs) from porcine ApN receptor (pAdipoR) 1-transgenic mice into high-fat/sucrose diet (HFSD)-fed mice. Twenty 6-week-old Friend virus B/NJNarl male mice were randomly assigned into four groups with the control fed a chow diet (chow) and others HFSD for 10 months. The HFSD groups were then intraperitoneally injected once per week for 8 weeks with placebo (200 μL phosphate-buffered saline), wild-type MSC (WT-MSC, 2 × 10(6) cells/200 μL phosphate-buffered saline) or pAdipoR1-transgenic MSC (pR1-tMSC, 2 × 10(6) cells/200 μL phosphate-buffered saline), respectively. Body weights, blood samples, tissue histology, and gene expression and protein levels of metabolism-associated genes were analyzed. Both WT-MSC and pR1-tMSC transplantations restored the messenger RNA expression of AdipoR1, with those of glucose transporter 4 and 5'-adenosine monophosphate-activated protein kinase catalytic subunit α-1 and protein levels of pyruvate kinase induced by pR1-tMSC in the muscles of HF

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

Evidence level

Several human studies show positive signals, while research methods and sample sizes continue to develop.

How we grade evidence
Adipose TissueAnimalsAnimals, Genetically ModifiedBlood GlucoseCell- and Tissue-Based TherapyFatty Acid Synthase, Type IGenetic TherapyGlucoseGlucose Transporter Type 4Hepatocytes

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