FAT/CD36 expression is not ablated in spontaneously hypertensive rats

Area of Science:

• Metabolic research
• Cardiovascular science
• Animal models

Background:

• Spontaneously hypertensive rats (SHR) are widely used in hypertension research.
• There is ongoing debate regarding the expression of fatty acid translocase (FAT/CD36) in the North American strain of SHR.
• Understanding FAT/CD36 expression is crucial for interpreting metabolic studies in this model.

Purpose of the Study:

• To investigate the expression and function of FAT/CD36 in the heart, muscle, liver, and adipose tissue of the North American SHR strain.
• To determine if SHR are a natural null model for FAT/CD36.
• To assess the impact of altered FAT/CD36 expression on fatty acid transport and insulin resistance.

Main Methods:

• Quantitative analysis of FAT/CD36 mRNA transcripts (2.9, 3.8, and 5.4 kb) in various tissues.
• Western blot analysis to determine FAT/CD36 protein expression levels.
• Assessment of plasmalemmal FAT/CD36 content.
• Measurement of fatty acid transport rates in isolated tissues.
• Evaluation of insulin resistance in skeletal muscle.

Main Results:

• Skeletal muscle in SHR exhibited insulin resistance.
• Aberrant FAT mRNA expression was observed, with the major 2.9 kb transcript absent but 3.8 and 5.4 kb transcripts present.
• FAT/CD36 protein was expressed in all examined tissues, though with significant tissue-specific reductions (26-85%).
• Fatty acid transport was decreased in adipose tissue (-50%) and increased in the liver (+47%).
• Normal fatty acid transport rates in heart and muscle were potentially due to compensatory upregulation of fatty acid binding protein (FABPpm).

Conclusions:

• The North American strain of SHR is not a natural FAT/CD36 null model.
• SHR express FAT/CD36 protein, but at reduced levels in key metabolic tissues.
• Altered FAT/CD36 expression influences tissue-specific fatty acid transport and may contribute to metabolic dysfunction in SHR.