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(Circulation Research. 2005;97:e52.)
© 2005 American Heart Association, Inc.

Letter to the Editor

Obesity and Endothelial Function

E.R. Duncan, A.M. Shah, M.T. Kearney

Cardiovascular Division, GKT School of Medicine, King’s College, London

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We read with interest the article by Molnar and colleagues¹ exploring the effect of dietary-induced obesity on endothelial function in mice. Molnar et al fed male C57BL/6 mice 1 of 2 high-fat diets from 9 weeks of age for 9 weeks. The investigators then studied endothelial function in femoral arteries using wire myography. Mice became obese, hyperglycemic, and hyperinsulinemic. They report that the mice fed the high-fat diet had lower plasma levels of triglycerides and free fatty acids than control animals.

These data differ from previous studies by Uysal et al² and by our own group.³ In our study, where mice were fed a high-fat diet from 4 weeks of age, free fatty acids measured at 8 weeks were 1.41±0.1 mmol/L in obese mice compared with 0.42±0.1 mmol/L in lean mice (P<0.01). A similar pattern was seen with triglycerides which were 5.4±0.1 in obese mice compared with 2.2±0.1 mmol/L in lean mice (P<0.01).

Molnar et al also reported that vasodilator responses to both acetylcholine and sodium nitroprusside (SNP) were blunted in obese mice although the constrictor response to phenylephrine was augmented.¹ Using a very similar feeding model (although we used only 1 diet; 5286 kcal/kg, Bioserve), we found that the vasodilator response to acetylcholine assessed in aortic rings ex vivo was preserved after both 4 and 8 weeks of high-fat feeding.³ (However, this was at least in part attributable to production of the reactive oxygen species hydrogen peroxide, which acted as a vasodilator . . . [Full Text of this Article]