Can Adipokine FAM19A5 Be a Biomarker of Metabolic Disorders?

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)

Aim One of the most critical functions of adipose tissue is the production of adipokines, ie, numerous active substances that regulate metabolism. One is the newly discovered FAM19A5, whose older name is TAFA-5. Purpose The study aimed to review the literature on the FAM19A5 protein. Methods The review was conducted in December 2023 using the PubMed (Medline) search engine. Sixty-four papers were included in the review. Results This protein exhibits the characteristics of an adipokine with positive features for maintaining homeostasis. The results showed that FAM19A5 was highly expressed in adipose tissue, with mild to moderate expression in the brain and ovary. FAM19A5 may also inhibit vascular smooth muscle cell proliferation and migration through the perivascular adipose tissue paracrine pathway. Serum levels of FAM19A5 were decreased in obese children compared with healthy controls. There are negative correlations between FAM19A5, body mass index, and fasting insulin. Serum FAM19A5 level is correlated with type 2 diabetes, waist circumference, waist-to-hip ratio, glutamic pyruvic transferase, fasting plasma glucose, HbA1c, and mean shoulder pulse wave velocity. FAM19A5 expression was reduced in mice with obesity. However, the data available needs to be clarified or contradictory. Conclusion Considering today's knowledge about FAM19A5, we cannot consider this protein as a bi

Evidence level

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

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