Biomedical Engineering Reference
In-Depth Information
ADHESION MOLECULES AND METABOLIC SYNDROME
Metabolic syndrome (MetS) is the name given to a group of risk factors that
increase an individual's risk of CHD and other related problems including diabetes
and stroke. h ese include: abdominal adiposity (as dei ned by a large WHR); a
higher than normal triglyceride level; a lower than normal level of high density
lipoprotein cholesterol (HDL-cholesterol); a higher than normal blood pressure;
and a higher than normal fasting glucose level or insulin resistance. While the
World Health Organization and the National Cholesterol Education Program
Adult Treatment Panel III (NCEP-ATPIII) have slightly dif erent cut-of values
and diagnostic criteria (Haf ner 2007), in principle a diagnosis of MetS is made
when three or more of the i ve previously listed factors are present. Individuals
with MetS have an aggressive form of vascular disease that is characterized by
accelerated atherosclerosis and pro-inl ammatory changes (Haf ner 2007). h e
exact pathophysiology of MetS is unknown but is thought to be mediated through
insulin resistance and visceral obesity. Men with MetS, but not diabetes, have a
twofold increased CVD risk, which is increased to threefold in the presence of
diabetes. h is increased risk in the presence of diabetes is even more apparent
in women. In the absence of diabetes, women with MetS have a twofold greater
risk of CVD than women without MetS but in the presence of diabetes this risk
increases dramatically to eightfold (Haf ner 2007), highlighting the therapeutic
importance of addressing gender-specii c multiple risk factors.
h e relationship between WHR and adhesion molecules has been previously
examined and in the following section the relationship between adhesion molecule
levels and the other risk factors for MetS will be examined before looking at the
ef ect of combinations of these factors.
Adhesion Molecules and Serum Triglycerides
High serum levels of triglyceride-rich lipoproteins, which result either from the
diet or from an individual's genetic background, are linked to the development
of atherosclerosis. Unstable plaques are characterized by the presence of an
abundance of macrophages and other inl ammatory cells together with a paucity
of smooth muscle cells and a thin i brous cap. Triglyceride-rich lipoproteins, their
remnants and small LDL particles have a pro-inl ammatory action and, while this
appears to be mainly a result of their very high susceptibility to oxidation, other
studies have also indicated that they may have a direct ef ect on NF-κB, or the
ef ect may be mediated by tissue necrosis factor alpha (TNF-α) (Libby 2007).
Studies have demonstrated that adhesion molecules are related to serum
triglyceride levels (Rohde
et al.
1999, Miller
et al.
2003, Miller and Cappuccio
2006). Following a meal there is an increase in serum lipids and competition for
the endothelium-bound lipoprotein lipase (LPL) enzyme, which is responsible
