Paper
International Journal of Obesity (2005) 29, 85–92. doi:10.1038/sj.ijo.0802826 Published online 26 October 2004
Association of leptin levels with obesity and blood pressure: possible common genetic variation
G Livshits1, I Pantsulaia1,2 and L M Gerber3
- 1Human Population Biology Research Unit, Department of Anatomy and Anthropology, Sackler Faculty of Medicine, Tel Aviv University, Israel
- 2Department of Biomedicine, Institute of Medical Biotechnology, Georgian Academy of Sciences, Georgia
- 3Weill Medical College of Cornell University, New York, USA
Correspondence: Dr G Livshits, Human Population Biology Research Unit, Department of Anatomy and Anthropology, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv 69978, Tel Aviv, Israel. E-mail: gregl@post.tau.ac.il
Received 21 April 2004; Revised 30 August 2004; Accepted 5 September 2004; Published online 26 October 2004.
Abstract
OBJECTIVE:
To ascertain the extent to which relationships between obesity (OB) and blood pressure (BP) can be explained by an individual's leptin plasma levels.
DESIGN:
Pedigree-based cross-sectional study in an apparently healthy population of European origin.
SUBJECTS:
The study sample is comprised of 90 nuclear and more complex families totaling 210 male and 213 female subjects aged 18–75 y, randomly recruited in Bashkorstan Autonomic region, Russia.
MEASUREMENTS:
Various fatness and fat distribution traits (including nine circumferences (CRCs), and eight skinfolds (CKFs) by anthropometry), blood pressure, and plasma leptin levels (by ELISA kits).
RESULTS:
Adjustment for circulating leptin led to attenuation of the magnitude of correlations between OB and BP, regardless of trait pair and sex cohort. Some of these correlations became statistically nonsignificant. All familial effects were gone, and heritability estimates became virtually zero after adjustment of each of the OB traits and systolic blood pressure (SBP) in offspring for leptin values in parents.
CONCLUSION:
BP and OB covariation is substantially mediated by circulating leptin levels. As a result, body fat has only a weak independent effect on BP variation after adjustment for leptin levels. Our findings also strongly suggest that genetic variation in body mass index, SKFs, and even body CRCs, as well as of SBP is due to genetic variation of leptin. Genetic variation of diastolic blood pressure in the present sample, however, shared very little with that of leptin.
Keywords:
leptin, blood pressure, heritability
