Chromium has an abundance of 0.033% in the Earth’s crust. It is a transition element that can occur in a number of valence states, with 0, +2, +3, and +6 being the most common. Trivalent chromium is the most stable form in biological systems. The principal ore is chromite. Chromium is used to harden steel, to manufacture stainless steel, and to form many useful alloys. It finds wide use as a catalyst. Hexavalent chro-mium is a strong oxidizing agent that comes primarily from industrial sources.
The human body contains only a small amount of chromium, less than 6 mg. The kidney, followed by the spleen, liver, lungs, heart, and skeletal muscle are the tissues with the greatest chromium concentrations.
Absorbed chromium is excreted primarily in urine and only small amounts of chromium are lost in the hair, sweat, and bile. Therefore, urinary chromium excretion can be used as an accurate estimation of absorbed chromium. At normal dietary chromium intakes (10–40 μg/day), chromium absorption is inversely related to dietary intake. Chromium intake is approximately 0.5% at a daily intake of 40 μg/day and increases to 2% when the intake drops to 10 μg/ day. The inverse relationship between chromium intake and absorption appears to be a basal control mechanism to maintain a minimal level of absorbed chromium. It is absorbed in the small intestine, pri-marily in the jejunum in humans. The mechanism is not well understood, but a nonsaturable passive dif-fusion process seems likely. Ascorbic acid promotes chromium absorption.
Chromium absorption in young and old subjects is similar, but insulin-dependent diabetic patients absorb two to four times more chromium than other apparently healthy subjects. Diabetic subjects appear to have an impaired ability to convert inorganic chro-mium to a usable form. Therefore, diabetic subjects require additional chromium and the body responds with increased absorption, but the absorbed chro-mium cannot be utilized effectively and is excreted in the urine. The chromium content of tissues of these patients is also lower.
Chromium is transported to the tissues primarily bound to transferrin, the same protein that transports iron. It has been hypothesized that iron interferes with the transport of chromium in hemochromatosis and that this may explain the high incidence of dia-betes in hemochromatosis patients, and which may be induced by chromium deficiency.
Chromium in the trivalent form is an essential nutrient that functions in carbohydrate, lipid, and nucleic acid metabolism. The essentiality of chromium was documented in 1977 when the diabetic signs and symptoms of a patient on total parenteral nutrition were reversed by supplemental chromium. Chromium functions primarily through its role in the regulation of insulin. Adequate dietary chromium leads to a nor-malization of insulin, with reductions in blood glucose concentration in subjects with elevated blood glucose levels, increases in subjects with low blood glucose levels, and no effect on subjects with near-optimal glucose tolerance. Improved insulin function is also associated with an improved lipid profile. Supplemental chromium also leads to increased insulin binding and increased insulin receptor numbers, and recent evi-dence suggests that chromium may be involved in the phosphorylation and dephosphorylation of the insulin receptor proteins.
The hallmark of marginal chromium deficiency is impaired glucose tolerance. In studies of patients whose total parenteral nutrition solutions contained no chromium or were supplemented with inadequate amounts of chromium, insulin requirements were reduced and glucose intolerance was reversed with chromium chloride supplementation. Two of these patients had weight loss that was restored with chro-mium supplementation. Peripheral neuropathy was seen in one of the patients and it too was reversed with chromium supplementation.
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