Zinc deficiency has been associated with delayed wound healing. Because zinc deficiency may be common in the United States, foods rich in zinc, as well as all other essential nutrients, should be promoted in the diet of patients who are malnourished or at risk for malnutrition.
"Zinc is an essential trace element that is involved in numerous cellular enzymatic reactions and gene regulation through the modulation of several transcription factors . Zinc deficiency is associated with diverse disorders, such as impaired immunity , retarded growth, brain development disorders and delayed wound healing  . In adults, zinc deficiency has been associated with retarded skeletal development and development of osteoporosis  . "
[Show abstract][Hide abstract] ABSTRACT: Zinc is an essential trace element that is involved in diverse metabolic and signaling pathways. Zinc deficiency is associated with retardation of bone growth. Previous in vitro studies have suggested a direct effect of zinc on both the proliferation and differentiation of osteoblast-like cells. However, the mechanisms for uptake of zinc into osteoblasts have not been examined in detail. Several families of zinc transporters have previously been characterized in mammalian cells; such transporters function in the uptake, intracellular sequestration or efflux of zinc. In the current study, we examined zinc transport in osteoprogenitor cells and have attempted to define a functional role for a zinc transport mechanism in osteogenic differentiation. We identified at least two zinc transporters in both human mesenchymal stem cells (MSCs) and in osteoblastic cells--the ubiquitous zinc transporter, ZIP1, and LIV-1, which was previously characterized as a protein that is expressed in breast cancer cells. The subcellular localization of both these zinc transporters suggested distribution in both the plasma membrane and also diffusely in the cytoplasm. During the differentiation process of pluripotent MSCs into osteoblast-like cells, both zinc uptake and expression of the ZIP1 protein were increased. An adenoviral-mediated overexpression of ZIP1 in MSCs resulted in Alizarin-red-positive mineralization and also increased expression of specific osteoblast-associated markers, such as alkaline phosphatase, and of several osteoblast differentiation genes, including osteopontin, Cbfa1/Runx2, promyelocytic leukemia zinc finger and bone sialoprotein. An siRNA-mediated reduction of ZIP1 protein expression in MSCs caused decreased zinc uptake and inhibition of osteoblastic differentiation under osteogenic culture conditions. Finally, following overexpression of ZIP1 in MSCs, cDNA microarray analysis revealed differential regulation of several genes associated with the proliferation of osteoprogenitor cells and osteoblast differentiation. In conclusion, these studies provide important insights into the role of a plasma membrane zinc transporter in the initiation of an osteogenic lineage from MSCs.
Bone 03/2006; 38(2):181-98. DOI:10.1016/j.bone.2005.08.010 · 3.97 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Obesity continues to reach epidemic proportions in the United States, with more than 60% of Americans classified as obese. Correspondingly, the number of individuals undergoing bariatric surgery has increased dramatically. There are several bariatric procedures that may be performed, with laparoscopic adjusted gastric band (LABG) the newest. Following bariatric surgery and massive weight loss, patients may be left with problematic loose, hanging skin. The loose or redundant skin may occur on the abdomen, back, upper arms, and inner and outer thighs. Body-contouring surgery may be performed to correct the residual excess tissues. Prebariatric planning for plastic surgery to correct skin defects, as well as postoperative bariatric and body-contouring care, is discussed.
Plastic surgical nursing: official journal of the American Society of Plastic and Reconstructive Surgical Nurses 11/2006; 27(1):3-13; quiz 14-5. DOI:10.1097/01.PSN.0000264157.22882.d1
[Show abstract][Hide abstract] ABSTRACT: Changes in extracellular zinc concentration participate in modulating fundamental cellular processes such as proliferation, secretion, and ion transport in a mechanism that is not well understood. Here, we show that a micromolar concentration of extracellular zinc triggers a massive release of calcium from thapsigargin-sensitive intracellular pools in the colonocytic cell line HT29. Calcium release was blocked by a phospholipase-C inhibitor, indicating that formation of inositol 1,4,5-triphosphate is required for zinc-dependent calcium release. Zinc influx was not observed, indicating that extracellular zinc triggered the release. The Ca(i)2+ release was zinc specific and could not be triggered by other heavy metals. Furthermore, zinc failed to activate the Ca(2+)-sensing receptor heterologously expressed in HEK293 cells. The zinc-induced Ca(i)2+ rise stimulated the activity of the Na(+)/H(+) exchanger in HT29 cells. Our results indicate that a previously uncharacterized extracellular, G protein-coupled, Zn(2+)-sensing receptor is functional in colonocytes. Because Ca(i)2+ rise is known to regulate key cellular and signal-transduction processes, the zinc-sensing receptor may provide the missing link between extracellular zinc concentration changes and the regulation of cellular processes.
Proceedings of the National Academy of Sciences 10/2001; 98(20):11749-54. DOI:10.1073/pnas.201193398 · 9.67 Impact Factor
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