Zinc-deficiency linked to CV disease, animal study
cardiovascular disease through inflammation and a decreased level
of compounds that protect against atherosclerosis, indicates a new
study in mice.
Atherosclerosis is the process whereby fatty substances such as cholesterol and calcium form plaque on the inner lining of an artery, causing them to harden. If enough builds up the plaque can reduce blood flow through the artery, and if it ruptures blood clots can form, which can block the flow of blood to the heart and cause a heart attack.
Atherosclerosis occurs naturally in humans as part of the aging process, but certain factors including high blood cholesterol, smoking, high blood pressure, obesity and diabetes increase the risk. Inflammation in the circulating blood, causing the formation of blood clots, is also believed to increase the risk of heart attack.
The researchers from the University of Kentucky set out to investigate whether zinc deficiency can increase and zinc supplementation decrease factors leading to atherosclerosis.
Over a four-week period, the researchers fed the mice one of three different moderate-fat diets: the zinc-deficiency diet contained no zinc; the control diet contained 0.45 micro mol of zinc per gram; and the zinc-supplemented diet 1.529 micro-mol of zinc per gram.
They found that the mice fed the zinc deficient diet had significantly higher concentrations of both VLDL ('bad' low density lipoprotein) and HDL ('good' high density lipoprotein) cholesterol and triacylglycerides compared to the control mice.
In the zinc supplemented mice, these lipid variables were decreased.
The researchers also noted that the zinc-deficient mice experienced an increase in inflammatory markers compared to the control and supplemented groups. The concentrations of glutathione reductase mRNA in their thoracic aortae were also higher, and the DNA binding activity of peroxisome proliferator activate receptors (PPARs) in liver extracts was reduced.
"These data provide in vivo evidence of zinc deficiency inducing proinflammatory events in an atherogenic mouse model," wrote the researchers in the September issue of the Journal of Nutrition (vol 135, pp2114-2118).
"These data also suggest that adequate zinc may be a critical component in protective PPAR signaling during atherosclerosis," they concluded.
