Author + information
- Received December 16, 2009
- Revision received February 22, 2010
- Accepted March 9, 2010
- Published online August 17, 2010.
- Abel Romero-Corral, MD, MS⁎,
- Fatima H. Sert-Kuniyoshi, PhD⁎,
- Justo Sierra-Johnson, MD, PhD‡,
- Marek Orban, MD⁎,
- Apoor Gami, MD⁎,
- Diane Davison, RN⁎,
- Prachi Singh, PhD⁎,
- Snigdha Pusalavidyasagar, MD⁎,
- Christine Huyber⁎,
- Susanne Votruba, PhD†,
- Francisco Lopez-Jimenez, MD, MSc⁎,
- Michael D. Jensen, MD† and
- Virend K. Somers, MD, PhD⁎,⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. Virend K. Somers, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, Minnesota 55905
Objectives The aim of this study was to determine the impact of fat gain and its distribution on endothelial function in lean healthy humans.
Background Endothelial dysfunction has been identified as an independent predictor of cardiovascular events. Whether fat gain impairs endothelial function is unknown.
Methods A randomized controlled study was conducted to assess the effects of fat gain on endothelial function. Forty-three normal-weight healthy volunteers were recruited (mean age 29 years; 18 women). Subjects were assigned to gain weight (approximately 4 kg) (n = 35) or to maintain weight (n = 8). Endothelial function (brachial artery flow-mediated dilation [FMD]) was measured at baseline, after fat gain (8 weeks), and after weight loss (16 weeks) for fat gainers and at baseline and follow-up (8 weeks) for weight maintainers. Body composition was measured by dual-energy X-ray absorptiometry and abdominal computed tomographic scans.
Results After an average weight gain of 4.1 kg, fat gainers significantly increased their total, visceral, and subcutaneous fat. Blood pressure and overnight polysomnography did not change after fat gain or loss. FMD remained unchanged in weight maintainers. FMD decreased in fat gainers (9.1 ± 3% vs. 7.8 ± 3.2%, p = 0.003) but recovered to baseline when subjects shed the gained weight. There was a significant correlation between the decrease in FMD and the increase in visceral fat gain (rho = −0.42, p = 0.004), but not with subcutaneous fat gain (rho = −0.22, p = 0.15).
Conclusions In normal-weight healthy young subjects, modest fat gain results in impaired endothelial function, even in the absence of changes in blood pressure. Endothelial function recovers after weight loss. Increased visceral rather than subcutaneous fat predicts endothelial dysfunction. (Fat Gain and Cardiovascular Disease Mechanisms; NCT00589498)
Continuing Medical Education (CME) is available for this article.
Dr. Romero-Corral was supported by a postdoctoral fellowship from the American Heart Association (Dallas, Texas). Dr. Sert-Kuniyoshi was supported by grant 09-20069G from the American Heart Association. Dr. Sierra-Johnson was partially supported by faculty funds from the Board of Post-Graduate Education of Karolinska Institutet (KID Award) and by the European Foundation for the Study of Diabetes (Düsseldorf, Germany) through a research fellowship, and is an employee of Eli Lilly Company. Dr. Singh was supported by grant 0725787Z from the American Heart Association. Dr. Lopez-Jimenez is a recipient of a Clinical Scientist Development Award from the American Heart Association. Dr. Somers was supported by grants R01 HL73211 and R21 DK81014 from the National Institutes of Health (Bethesda, Maryland) and is working with Mayo Health Solutions on intellectual property related to obesity and cardiovascular disease. Drs. Romero-Corral, Lopez-Jimenez, and Somers are recipients of a grant from Select Research (Suckley, United Kingdom) for separate work related to the measurement of obesity. Drs. Orban, Gami, Pusalavidyasagar, Votruba, and Jensen and Ms. Davison and Huyber report that they have no relationships to disclose.
- Received December 16, 2009.
- Revision received February 22, 2010.
- Accepted March 9, 2010.
- American College of Cardiology Foundation