CCN1 induces adipogenic differentiation of fibro/adipogenic progenitors in a chronic kidney disease model.

Early human evidence such as case series or small samples is exploring possible benefits.

• 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)

Previous studies have shown that sarcopenic obesity is highly prevalent in patients with chronic kidney disease (CKD). Here, the association between CKD and sarcopenic obesity were investigated. The 5/6 nephrectomy was performed to establish CKD in mice. Fluorescence-activated cell sorting (FACS), quantitative real-time PCR, ELISA kits assay, immunohistochemistry, and cell proliferation assay were carried out to investigate the condition of muscle loss and fatty infiltration were in CKD mice and the origin of adipocytes. Muscle atrophy occurred and adipogenic gene expression, Perilipin and FABP4 were markedly increased in the hind limb muscle of CKD mice. Results indicated that fibro/adipogenic progenitors (FAPs) are the precursor of adipocytes in the muscle of CKD mice. Meanwhile, the content of extracellular matrix protein CCN1 was notably increased in serum of CKD patients with sarcopenic obesity which was also found in muscle and serum of CKD mice. CCN1 induced the differentiation of FAPs into adipocytes. These results suggest that CKD mice are susceptible to sarcopenic obesity. CCN1 may be a novel activator of the differentiation of FAPs in CKD muscle.

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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