microRNA miR-27b impairs human adipocyte differentiation and targets PPARgamma.
Karbiener M., Fischer C., Nowitsch S., Opriessnig P., Papak C., Ailhaud G.
Animal Study on Type 2 Diabetes, published in Biochem Biophys Res Commun (2009) — summary generated from the PubMed abstract.
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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- Study type
- Animal Study
- Journal
- Biochem Biophys Res Commun (2009)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 19800867
- DOI
- 10.1016/j.bbrc.2009.09.098
Abstract (original English)
Obesity has emerged as a global health problem with more than 1.1 billion adults to be classified as overweight or obese, and is associated with type 2 diabetes, cardiovascular disease, and several cancers. Since obesity is characterized by an increased size and/or number of adipocytes, elucidating the molecular events governing adipogenesis is of utmost importance. Recent findings indicate that microRNAs (miRNAs) - small non-protein-coding RNAs that function as post-transcriptional gene regulators - are involved in the regulatory network of adipogenesis. Whereas only a single human miRNA is known so far to be functional in adipogenesis as pro-adipogenic, several mouse miRNAs have been identified very recently as adipogenic regulators, thereby stimulating demand for studying the functional role of miRNAs during adipogenesis in human. Here, we demonstrate that miR-27b abundance decreased during adipogenesis of human multipotent adipose-derived stem (hMADS) cells. Overexpression of miR-27b blunted induction of PPARgamma and C/EBPalpha, two key regulators of adipogenesis, during early onset of adipogenesis and repressed adipogenic marker gene expression and triglyceride accumulation at late stages. PPARgamma has a predicted and highly conserved binding site in its 3'UTR and was indeed confirmed to be a direct target of miR-27b. Thus, these results suggest that the anti-adipogenic
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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