Harnessing adipogenesis to prevent obesity

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

Abstract (original English)

Obesity and associated metabolic complications, including diabetes, cardiovascular and hepatic diseases, and certain types of cancers, create a major socioeconomic burden. Obesity is characterized by excessive expansion of white adipose tissue resulting from increased adipocyte size, and enhanced adipocyte precursor cells proliferation and differentiation into mature adipocytes, a process well-defined as adipogenesis. Efforts to develop therapeutically potent strategies to circumvent obesity are impacted by our limited understanding of molecular mechanisms regulating adipogenesis. In this review, we discuss recently discovered molecular mechanisms restraining adipogenesis. In this perspective, the discoveries of white adipose tissue endogenous adipogenesis-regulatory cells (Aregs) that negatively regulate adipocyte differentiation, platelet-derived growth factor receptor isoform α (PDGFRα) activation and downstream signaling that hinder adipocyte precursors differentiation, and a group of obesity-associated non-coding RNAs (ncRNAs) that regulate adipogenesis open up promising therapeutic avenues to prevent and/or treat obesity.

Evidence level

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

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