The obesity-linked human lncRNA AATBC stimulates mitochondrial function in adipocytes

Area of Science:

• Metabolic regulation and adipocyte biology.
• Molecular mechanisms of energy balance.

Background:

• Adipocyte dysfunction is central to obesity-related diseases.
• Thermogenic adipocytes promote cardiometabolic health.
• Adipocyte plasticity, the ability to switch between white and thermogenic phenotypes, is key to metabolic adaptation.

Purpose of the Study:

• To identify novel regulators of adipocyte plasticity.
• To investigate the role of the lncRNA AATBC in human adipocyte function.
• To explore the link between AATBC, metabolism, and obesity.

Main Methods:

• Comparative transcriptional profiling of human adipose tissues and cultured adipocytes.
• Functional studies using primary and immortalized human adipocytes.
• In vivo studies in mice expressing AATBC in adipose tissue.
• Correlation analysis in human subjects.

Main Results:

• AATBC is enriched in thermogenic conditions and enhances the thermogenic adipocyte phenotype.
• AATBC promotes increased cellular respiration and mitochondrial fragmentation.
• AATBC expression in mouse adipose tissue reduces plasma leptin levels.
• Human adipose tissue AATBC levels inversely correlate with plasma leptin, BMI, and metabolic health markers.

Conclusions:

• AATBC is a human-specific regulator of adipocyte plasticity.
• AATBC influences mitochondrial function and thermogenesis.
• AATBC is a novel obesity-linked factor impacting human metabolic health.