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Biochemical and Molecular Actions of Nutrients

Zinc Deficiency Increases Plasma Lipids and Atherosclerotic Markers in LDL-Receptor–Deficient Mice¹

Gudrun Reiterer^*,, Ruth MacDonald^**,2, Jim D. Browning^**, Jason Morrow, Sergey V. Matveev, Alan Daugherty, Eric Smart, Michal Toborek^# and Bernhard Hennig^,3

^* Graduate Center for Nutritional Sciences Molecular and Cell Nutrition Laboratory, College of Agriculture, Departments of Pediatrics Cardiovascular Medicine, and ^# Surgery, University of Kentucky, Lexington, KY 40546; ^** Department of Food Sciences, University of Missouri-Columbia, Columbia, MO 65211; and Department of Medicine, Vanderbilt University, Nashville, TN 37232

³To whom correspondence should be addressed. E-mail: bhennig{at}uky.edu.

Low zinc concentration can be associated with an increased risk of cardiovascular diseases. In the current study, we hypothesize that zinc deficiency can increase and zinc supplementation can decrease proatherosclerotic events in LDL receptor knock-out (LDL-R–/–) mice fed a moderate-fat diet. Mice were fed either a zinc-deficient (0 µmol Zn/g), a control (0.45 µmol Zn/g), or a zinc-supplemented (1.529 µmol Zn/g) diet for 4 wk. Mice fed the zinc-deficient diet had significantly increased concentrations of cholesterol and triacylglycerides in the VLDL and HDL fractions. Zinc supplementation decreased these lipid variables compared with control mice. We detected significantly higher concentrations of glutathione reductase mRNA in the thoracic aortae of zinc-deficient mice. Furthermore, inflammatory markers, such as nuclear factor-B and vascular cell adhesion molecule-1, were significantly increased in zinc-deficient mice compared with mice of the control or supplemented groups. In addition, zinc deficiency significantly reduced the DNA binding activity of peroxisome proliferator activate receptors (PPARs) in liver extracts. Interestingly, mRNA expression levels of PPAR were significantly increased in thoracic aortae of zinc-deficient mice, indicating an adaptation process to decreased PPAR signaling. These data provide in vivo evidence of zinc deficiency inducing proinflammatory events in an atherogenic mouse model. These data also suggest that adequate zinc may be a critical component in protective PPAR signaling during atherosclerosis.

KEY WORDS: • zinc deficiency • atherosclerosis • inflammation • PPAR • lipoproteins

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