Animal experiments have shown that long-term consumption of some medicines can affect chromium absorption through affecting stomach acidity or gastrointestinal prostaglandins (Davis et al 1995, Kamath et al 1997). Animal experiments have shown that high phytate levels can reduce absorption (Chen et al 1973) although lower levels appear to have no effect (Keim et al 1987). Vitamin C appears to increase absorption (Davis et al 1995, Offenbacher 1994, Seaborn & Stoecker 1990). Most ingested chromium is excreted unabsorbed in the faeces (Mertz 1969, Offenbacher et al 1986) whilst absorbed chromium is excreted mainly in the urine (Anderson et al 1983). However, data from metabolic balance and urinary excretion studies suggest that only 0.4-2.5% of chromium is absorbed, the actual amount being determined by the environment of the gastrointestinal tract and ligands provided by foods (Clydesdale 1998).Ĭhromium is widely distributed through the food supply but the content within a given type of food can vary widely because of geochemical factors (Welch & Carey 1975). Research on chromium metabolism is limited by the lack of a good measure for establishing deficiency states in man. In man, chromium accumulates in liver, spleen, soft tissue and bone (Lim et al 1983). ![]() These studies have been reviewed by Anderson (1997), Mertz (1993), Offenbacher et al (1997) and Stoecker (1996). ![]() ![]() Chromium is involved in potentiating the action of insulin in vivo and in vitro (Mertz 1969, 1993, Mertz et al 1961) and several studies have shown beneficial effects of chromium on circulating glucose, insulin and lipids in humans, although not all studies were positive.
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