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20-06-2010 | Cardiometabolic | Article

Raised apoB may drive atherogenicity in the metabolic syndrome

Abstract

Free abstract

MedWire News: Multiple biomarkers are associated with the presence of and future risk for the metabolic syndrome in young adults, clinical trial data suggest.

Importantly, the new analysis of The Cardiovascular Risk in Young Finns Study suggests that atherogenicity of the metabolic syndrome in this population is “substantially mediated” by elevated apolipoprotein (apo) B levels.

Noora Mattsson (University of Turku, Finland) and team used data from an ongoing study into atherosclerosis risk factors in the Finnish population. A total of 3596 boys and girls aged 3–18 years were recruited in 1980; of these, 2283 were re-assessed in 2001 and 2200 were re-assessed in 2007.

At the 2001 follow-up examination, 325 (14.5%) participants had the metabolic syndrome. These individuals tended to have higher levels of apoB, C-reactive protein (CRP), and type II secretory phospholipase (sPL)A2, and lower levels of apoA-1 than those without the metabolic syndrome, report Mattsson and colleagues in the journal Arteriosclerosis, Thrombosis, and Vascular Biology.

Among the 1587 individuals who were assessed in both 2001 and 2007, those with the metabolic syndrome in 2001 were significantly more likely to have increased carotid intima-media thickness (IMT), a marker for subclinical atherosclerosis, or carotid plaque in 2007.

Similarly, high apoB levels in 2001 predicted increased carotid IMT (>90th percentile) or plaque in 2007.

Interestingly, the longitudinal association between the metabolic syndrome and future carotid atherosclerosis was attenuated by approximately 40% after adjusting for apoB. By contrast, the association between apoB and carotid atherosclerosis was not altered after adjusting for multiple biomarkers including CRP and sPLA2.

Mattsson et al say their findings suggest that elevated apoB is an “integral part” of the metabolic syndrome in young adults and may contribute to its atherogenicity.

Conversely, CRP and sPLA2 do not appear to play a significant role in explaining the increased atherogenicity associated with the syndrome.

“Individuals with the metabolic syndrome and high apoB had more than three times the relative risk of incident high IMT compared with those without metabolic syndrome and normal apoB,” the researchers write.

“Thus, from a clinical standpoint, apoB may have an important role as a marker to assess those subjects with metabolic syndrome and increased burden of future atherosclerosis, because young adults with both metabolic syndrome and high apoB seem susceptible to develop atherosclerosis later in life.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010

By Joanna Lyford