Response to Insulin Resistance and Obesity in a Mouse Model of Systemic Lupus Erythematosus
We thank Perciaccante et al1 for their interest in our recent study.2 They correctly noted that little is known or has been reported about the incidence and importance of insulin resistance in patients with systemic lupus erythematosus (SLE), particularly with regard to SLE-associated hypertension. This gap in knowledge may be because of the diversity of SLE populations studied and the highly variable nature of SLE severity in humans. Although, to our knowledge, there have not been studies to determine whether autonomic function is altered in the NZBWF1 mouse model of SLE that we used for our studies, other investigators have suggested that autonomic dysfunction is more prevalent in patients with SLE. There have also been suggestions of increased sympathetic nerve activity in SLE,3 although the mechanisms that mediate the increased sympathetic activity are unknown. The explanation for the insulin resistance in the NZBWF1 model of SLE is also not clear. We have proposed as 1 possible mechanism a role for chronic inflammation. This would be consistent with a growing body of literature suggesting that metabolic syndrome is associated with inflammation. We agree with Perciaccante et al1 that the current study does not exclude the possibility that autonomic changes promote insulin resistance in this model and that this may be an important question to pursue in the future.
Perciaccante A, Fiorentini A, Tubani L. Insulin resistance and obesity in a mouse model of systemic lupus erythematosus. Hypertension. 2007; 49: e12.
Ryan MJ, McLemore GR Jr, Hendrix ST. Insulin resistance and obesity in a mouse model of systemic lupus erythematosus. Hypertension. 2006; 48: 988–993.