Abstract
Zinc deficiency is common in Japan, yet awareness on this disorder is lacking. The Japanese Society of Clinical Nutrition recently issued the Japan’s Practical Guideline for Zinc Deficiency 2018 setting forth criteria for diagnosing zinc deficiency, i.e., (a) one or more symptoms of zinc deficiency or low serum alkaline phosphatase, (b) ruling out other diseases, (c) low serum zinc, and (d) alleviation of symptoms upon zinc administration. Serum zinc <60 μg/dL and 60–80 μg/dL indicate zinc deficiency and marginal deficiency, respectively. Zinc deficiency symptoms vary and include dermatitis and taste disorders among others. Zinc administration improves taste in 50–82% of patients suffering from taste disorders (a common symptom of zinc deficiency). Effects of zinc administration do not appear immediately, and therapy should be continued for at least three months. Zinc deficiency often accompanies various diseases and conditions. Here, we focus on inflammatory bowel diseases and liver cirrhosis. As zinc deficiency enhances intestinal inflammation via macrophage activation, we discuss the pathological mechanism for inflammation and zinc deficiency in the context of IBD. Zinc deficiency can also lead to a nitrogen metabolic disorder in patients with liver cirrhosis. Zinc supplementation can improve not only the ammonia metabolism, but also the protein metabolism. We also discuss directions for future studies of zinc deficiency.
Highlights
Zinc deficiency is common in developing countries and affects over two billion people worldwide [1]
According to a multicenter hospital-based case–control study conducted in Japan, higher doses of zinc taken by patients one year before the study period were associated with a decreased odds ratio for ulcerative colitis (UC), indicating that high zinc intake can protect against UC [43]
We previously reported that that production of several inflammatory cytokines (TNF-α, IFN-γ, and IL-17) was significantly production of several inflammatory cytokines (TNF-α, IFN-γ, and IL-17) was significantly elevated elevated in peritoneal macrophages derived from MT-I/II knockout mice [45], and that dextran sulfate in peritoneal macrophages derived from MT-I/II knockout mice [45], and that dextran sulfate sodium sodium (DSS)-induced colonic inflammation as an animal model of UC was aggravated significantly in (DSS)-induced colonic inflammation as an animal model of UC was aggravated significantly in knockout mice [45]
Summary
Zinc deficiency is common in developing countries and affects over two billion people worldwide [1]. Wessells and Brown reported that the estimated percentage of the population with inadequate zinc intake in Japan in 1990, 1995, and 2000 was 14.7, 14.7, and 15.5%, respectively, indicating an increasing prevalence in zinc deficiency [2] One reason for this is the rapidly growing population of the elderly, who suffer from chronic diseases and are treated with medications. Another contributor is the lack of awareness among Japanese. Sci. 2020, 21, 2941 are treated with medications Another contributor is the lack of awareness among Japanese clinicians about zinc deficiency. Symptoms of many of these diseases are likely to improve with zinc therapy
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