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Published on: February 25, 2016
The adipose tissue gene expression in mice with different nitric oxide availability
U Razny1, B Kiec-Wilk, A Polus
1Department of Clinical Biochemistry, Jagiellonian University Medical College, Cracow, Poland. urazny@cm-uj.krakow.pl
Summary
Endothelial nitric oxide synthase (eNOS) knockout mice exhibit metabolic syndrome symptoms. Reduced NO impairs energy metabolism, while increased NO via DDAH enhances it, highlighting NO
Area of Science:
- Metabolic Syndrome Research
- Adipose Tissue Biology
- Nitric Oxide Signaling
Background:
- Endothelial nitric oxide synthase (eNOS) knockout (ko) mice mimic human metabolic syndrome.
- Nitric oxide (NO) regulates energy substrate metabolism, blood flow, and angiogenesis.
- Asymmetric dimethylarginine (ADMA) inhibits NO production; dimethylarginine dimethylaminohydrolase (DDAH) degrades ADMA, increasing NO bioavailability.
Purpose of the Study:
- To compare adipose tissue gene expression in eNOS ko mice (decreased NO) and DDAH-overexpressing mice (increased NO).
- To investigate the role of endogenous NO in regulating energy substrate metabolism and adipose tissue characteristics.
Main Methods:
- Gene expression analysis (microarray) in brown (BAT) and white (WAT) adipose tissue.
- Comparison of physiological parameters (weight, glucose, insulin, lipids) in age-matched mice models.
- Assessment of angiogenic activity.
Main Results:
- eNOS ko mice showed lower weight, higher glucose, insulin, leptin, and cholesterol.
- DDAH-overexpressing mice exhibited increased angiogenic activity compared to eNOS ko mice.
- Microarray analysis revealed activated adipogenesis genes in WAT of eNOS ko mice, contrasting with inhibition in DDAH overexpressing mice. Angiogenesis genes were downregulated in both models versus wild-type.
Conclusions:
- Endogenous NO plays a crucial role in maintaining energy substrate metabolism homeostasis.
- Altering NO generation impacts adipogenesis and angiogenic pathways in adipose tissue.
- NO bioavailability is a key factor in metabolic regulation.
