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Volume 211, Issue 1, Pages 303-307 (July 2010)


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Leptin is associated with the size of the apolipoprotein(a) particle in African tribal populations living on fish or vegetarian diet

Mikolaj Winnickibad, Massimo Puatoa, Virend K. Somersd, Alberto Zambona, Santica M. Marcovinac, Marcello Rattazzia, Bradley G. Phillipse, Paolo PaulettoaCorresponding Author Informationemail address

Received 10 July 2009; received in revised form 18 January 2010; accepted 27 January 2010. published online 02 March 2010.

Abstract 

Objective

Apolipoprotein(a) [or apo(a)] isoform size, which is strongly genetically determined, showed significant association with the cardiovascular risk. Subjects on a fish diet have lower lipoprotein(a) levels, larger apo(a) isoform sizes and lower leptin levels than their vegetarian diet counterparts. We hypothesized that leptin may contribute to a potential association between the type of diet and the size of apo(a) isoforms.

Methods

Anthropometric data, dietary nutrients, lipoprotein profile, plasma leptin levels, and apo(a) isoforms were evaluated in two related homogenous African tribal populations of Tanzania, one on a primarily freshwater fish diet (n=278), and the other on a vegetarian diet (n=326).

Results

We observed a strong negative association between leptin levels and size of each of the apo(a) isoforms in both fish and vegetable diet groups, and in both genders. However, leptin was not associated with levels of lipoprotein(a). In multivariate analysis, a strong and independent association between leptin and size of apo(a) isoforms was observed. The size of apo(a) isoforms was strongly associated with high and low leptin states. Subjects with low leptins had 30% larger sizes of apo(a) isoforms than their high leptin counterparts.

Conclusions

High leptin subjects have smaller, potentially more atherogenic, apo(a) isoform sizes than low leptin ones. We suggest that omega-3 rich diet can influence the levels of apo(a) and/or Lp(a) even though they are mainly genetically determined. These findings may have implications for understanding the interaction between leptin and cardiovascular risk.

a University of Padova, Italy

b Medical University of Gdansk, Poland

c University of Washington, Seattle, WA, United States

d Mayo Clinic, Rochester, MN, United States

e University of Iowa, Iowa City, IA, United States

Corresponding Author InformationCorresponding author at: Department of Clinical & Experimental Medicine, University of Padova, Via. Giustiniani 2, 35126 Padova, Italy. Tel.: +39 049 821 2278; fax: +39 049 875 4179.

PII: S0021-9150(10)00089-4

doi:10.1016/j.atherosclerosis.2010.01.041


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