PTRF acts as an adipokine contributing to adipocyte dysfunctionality and ectopic lipid deposition

Area of Science:

• Metabolic research
• Endocrinology
• Cell biology

Background:

• Obesity leads to adipose tissue (AT) dysfunction and ectopic lipid deposition.
• Polymerase I and transcription release factor (PTRF) may impair adipocyte precursor function.
• The secretion of PTRF by adipocytes into circulation is unknown.

Purpose of the Study:

• Investigate PTRF presence in human plasma.
• Examine the effect of recombinant PTRF (rPTRF) on adipocyte-hepatocyte interactions.
• Determine the relationship between circulating PTRF and visceral adipose tissue.

Main Methods:

• Quantification of PTRF in human plasma, including exosomal fractions.
• In vitro treatment of 3T3-L1 adipocytes with rPTRF.
• Assessment of adipocyte hypertrophy, senescence, and lipid accumulation in co-cultured hepatocytes.
• Correlation analysis between plasma PTRF and visceral fat PTRF concentration.

Main Results:

• PTRF is detectable in human plasma, partly carried by exosomes.
• rPTRF treatment induced hypertrophy and senescence in 3T3-L1 adipocytes.
• rPTRF-treated adipocytes promoted lipid accumulation in hepatocytes.
• A positive correlation exists between circulating PTRF and visceral fat PTRF levels.

Conclusions:

• Dysfunctional visceral adipose tissue in obesity may secrete PTRF.
• Circulating PTRF acts as an adipokine, potentially contributing to obesity-related metabolic dysfunction.
• PTRF may play a role in the detrimental effects of visceral fat accumulation.