Adipose gene expression profiles related to metabolic syndrome using microarray analyses in two different models

Area of Science:

• Metabolic Syndrome Research
• Adipokine Signaling Pathways
• Obesity Pathogenesis

Background:

• Metabolic syndrome involves complex genetic and environmental factors.
• Peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists influence metabolic pathways.
• Otsuka Long-Evans Tokushima Fatty (OLETF) rats model metabolic syndrome.

Purpose of the Study:

• Identify genes dysregulated in metabolic syndrome.
• Investigate overlapping gene expression changes induced by PPAR-γ agonists and in OLETF rats.
• Validate the role of lipocalin-2 in metabolic syndrome.

Main Methods:

• Microarray analysis comparing PPAR-γ agonist-treated db/db mice with controls.
• Microarray analysis comparing OLETF rats with Long-Evans Tokushima Otsuka (LETO) rats.
• Real-time reverse transcription polymerase chain reaction (RT-PCR) for gene expression validation.

Main Results:

• Lipocalin-2 expression decreased in PPAR-γ agonist-treated mice visceral adipose tissue.
• Lipocalin-2 expression increased in OLETF rats visceral adipose tissue.
• Lipocalin-2 expression significantly elevated in obese human visceral adipose tissue, correlating with BMI, IL-6, FABP, and WBC count.

Conclusions:

• Lipocalin-2 is a key adipokine influenced by PPAR-γ agonists and obesity.
• Lipocalin-2 expression is significantly increased in obese human visceral adipose tissue.
• Elevated lipocalin-2 correlates with systemic inflammation markers in humans.