Chronic elevation of human C-reactive protein in transgenic rats caused adult-onset obesity, resulting in a 6- to 9-fold higher total fat mass compared to non-transgenic controls.
Does chronic elevation of human CRP cause adult-onset obesity in a transgenic rat model?
Chronic elevation of human CRP causes adult-onset obesity in a transgenic rat model, suggesting CRP is a causal factor rather than merely a marker of inflammation.
Effect estimate: 6- to 9-fold higher
Obesity is characterized by low-grade chronic inflammation. As an acute-phase reactant to inflammation and infection, C-reactive protein (CRP) has been found to be the strongest factor associated with obesity. Here we show that chronic elevation of human CRP at baseline level causes the obesity. The obesity phenotype is confirmed by whole-body magnetic resonance imaging (MRI), in which the total fat mass is 6- to 9- fold higher in the CRP rats than the control rats. Univariate linear regression analysis showed different growth rates between the CRP rats and the control rats, and that the difference appears around 11 weeks old, indicating that they developed adult-onset obesity. We also found that chronic elevation of CRP can prime molecular changes broadly in the innate immune system, energy expenditure systems, thyroid hormones, apolipoproteins, and gut flora. Our data established a causal role of CRP elevation in the development of adult-onset obesity.
Li et al. (2020) studied Adult-onset obesity (n=30). Human CRP transgene vs. Non-transgenic littermates was evaluated on Total fat mass by MRI (6- to 9-fold higher). Chronic elevation of human C-reactive protein in transgenic rats caused adult-onset obesity, resulting in a 6- to 9-fold higher total fat mass compared to non-transgenic controls.