Deficiency chromium

Metabolic Functions. Chromium (ITT) potentiates the action of insulin and may be considered a cofactor for insulin (137,138). In in vitro tests of epididymal fat tissue of chromium-deficient rats, Cr(III) increases the uptake of glucose only in the presence of insulin (137). The interaction of Cr(III) and insulin also is demonstrated by experimental results indicating an effect of Cr(III) in translocation of sugars into ceUs at the first step of sugar metaboHsm. Chromium is thought to form a complex with insulin and insulin receptors (136). 

There appears to be a chromium pool in individuals who are not chromium deficient (136). When there is an increase in level of cHculating insulin in response to a glucose load, an increase in circulating chromium occurs over a period of 0.5—2 h. This is foUowed by a decline and excretion of chromium in urine increases. Chromium deficiency is indicated when no increase or a small increase in blood chromium level or urine chromium occurs. 

Attempts to isolate GTF from brewer s yeast have resulted in production of very active concentrates, but the substance is too labile to be obtained in the soHd state (136). However, it has been shown that GTF is a Cr(III) complex containing two coordinated nicotinate radicals and other amino acid anions (146). Active preparations containing similar complexes have been synthesi2ed (147). Chromium deficiency may also lead to atherosclerosis and peripheral neuropathy. 

Chromium deficiency may be related to the glucose tolerance factor (Herold and Fitzgerald 1994). The determination of this deficiency, however, is questioned, because the lack of accuracy of the Cr determination in the earlier publications. 

Chromium has proved effective in counteracting the deleterious effects of cadmium in rats and of vanadium in chickens. High mortality rates and testicular atrophy occurred in rats subjected to an intraperitoneal injection of cadmium salts however, pretreatment with chromium ameliorated these effects (Stacey et al. 1983). The Cr-Cd relationship is not simple. In some cases, cadmium is known to suppress adverse effects induced in Chinese hamster (Cricetus spp.) ovary cells by Cr (Shimada et al. 1998). In southwestern Sweden, there was an 80% decline in chromium burdens in liver of the moose (Alces alces) between 1982 and 1992 from 0.21 to 0.07 mg Cr/kg FW (Frank et al. 1994). During this same period in this locale, moose experienced an unknown disease caused by a secondary copper deficiency due to elevated molybdenum levels as well as chromium deficiency and trace element imbalance (Frank et al. 1994). In chickens (Gallus sp.), 10 mg/kg of dietary chromium counteracted adverse effects on albumin metabolism and egg shell quality induced by 10 mg/kg of vanadium salts (Jensen and Maurice 1980). Additional research on the beneficial aspects of chromium in living resources appears warranted, especially where the organism is subjected to complex mixtures containing chromium and other potentially toxic heavy metals. 

Frank, A., V. Galgan, and L.R. Petersson. 1994. Secondary copper deficiency, chromium deficiency and trace element imbalance in the moose (Alces alces L.) effect of anthropogenic activity. Ambio 23 315-317. 

Chromium was recognized as an essential trace element in 1955.1190 Rats fed a chromium-deficient diet developed an impaired tolerance for intravenous glucose, which could be reversed by an insulin-potentiating factor present in brewer s yeast, meat and various other foods. The insulin-potentiating factor was found to be a complex of chromium(IH)1191 and such substances have been termed Glucose Tolerance Factor(s) (GTFs). Chromium was demonstrated to be essential for humans in 1975.1192 There are several reviews of the chemistry of chromium(III) and its relationship to glucose tolerance.1193-1196... 

Most forms of Cr(III) are not absorbed and utilized by the body. For this reason, and because of the increased use of sucrose and other refined foods, a marginal human chromium deficiency may be widespread.604 605 This may result not only in poor utilization of glucose but also in other effects on lipid and protein metabolism.597 However, questions have been raised about the use of chromium picolinate as a dietary supplement. High concentrations have been reported to cause chromosome damage606 and there may be danger of excessive accumulation of chromium in the body.607... 

Chromium levels in biological matter have been studied extensively. In contrast to findings with other metals, chromium concentrations in the United States population ate highest at the time of birth, with a pronounced decline during the lifetime, whereas they appear to remain high in some other countries, such as Thailand and the Philippines. These findings suggest Ihe possibility of a relative chromium deficiency in the United States. The relationship of this to disturbances of carbohydrate metabolism in humans, while under study, remains to be established. 

Chromium deficiency is characterized by glucose intolerance but also may include neuropathy, increased free fatty acid concentrations, and a low respiratory quotient. Chromium deficiency has been identified in the setting of long-term, chromium-free parenteral nutrition. 

Urinary excretion rates have been measured in humans after oral exposure to several chromium compounds (Finley et al. 1996b). A group of four male and two female volunteers ingested capsules containing chromium(ni) picolinate at a dose of 200 pg/day for 7 days, to ensure that chromium deficiency was not a confounding factor. They then ingested 0.005 mg/kg/day chromium(VI) as potassium chromate (3 days), and 1.0 mg/kg/day chromium(III) as chromic oxide (3 days), with 3 days... 

In animals, severe chromium deficiency has resulted in hyperglycemia, decreased weight gain, elevated serum cholesterol levels, aortic plaques, corneal opacities, impaired fertility and lethality. 

The Committee on Dietary Allowances, Food and Nutrition of the National Research Council has recommended an estimated safe and adequate daily dietary intake of 50-200 pg/day for adults based on the absence of chromium-deficiency signs in the major part of the U.S. population consuming an average of 50 pg chromium/day (NRC 1989). ATSDR has adopted the upper range of the estimated safe and adequate daily dietary intake of 200 pg/day as provisional guidance for oral exposure to chromium(VI) and chromium(III). 

Jeejeebhuoy KN, Chu RC, Marliss EB, et al. 1977. Chromium deficiency, glucose intolerance, and neuropathy reversed by chromium supplementation in a patient receiving long-term total parenteral nutrition. Am J Clin Nutr 30 531-538. 

Penefsky ZJ, Elwood JC. 1996. Mechanical responses of chromium-deficient developing rat heart. Comp Biochem Physiol 114A(2) 175-187. 

Verhage AH, Cheong WK, Jeejeebhoy KN. 1996. Neurological symptoms due to possible chromium deficiency in long-term parenteral nutrition that closely mimic metronidazole-induce syndromes. J Parenter Enter Nutr 20(2) 123-127. 

Chromium is a trivalent cption that occurs as A typical daily intake isO-5 3-8 jimoJ (25-200 ig/day). After absorption from the diet, chromium occurs bound to transferrin. A safe and adequate intake of 50 to 200 ffg Cr/day has been established. Chromium appears to participate in glucose metabolism. The ion may play a part in mediating the hormonal effects of insulin. Chromium deficiency results in abnormally high glucose tolerance curves and impaired clearance of plasma glucose. Chromium deficiency can be induced in animals. There is evidence that... 

Tsuda K, Yokoyama Y, Morita M, Nakazawa Y, Onishi S. Selenium and chromium deficiency during long-term home total parenteral nutrition in chronic idiopathic intestinal pseudoobstruction. Nutrition 1998 14(3) 291-5. 

Chromium is an element with two faces, as far as health effects are concerned. Small amounts of chromium are essential for the health of plants and animals. In humans, a chromium deficiency leads to diabetes-like symptoms. Diabetes is a disease that develops when the body does not use sugar properly. Chromium seems to play a role in helping the body use sugar. 

It is generally accepted that chromium is an essential element for humans. World Health Organization has estimated that the minimum chromium requirement is 33pgday . Some investigators have proposed that chromium deficiency may cause postnatal growth retardation and impaired glucose tolerance. There are no reports documenting chromium deficiency in human reproduction. 

These cases, although rare, influenced the U.S. Food and Nutrition Board to designate chromium as an essential trace element. It is not dear why there have been so few cases of clinical chromium deficiency in comparison with zinc. 

A beneficial response of glucose-intolerant patients to chromium supplementation is presently the only means of confirming chromium deficiency. No practicable method of assessing intracellular chromium depletion is yet available and there is no consistently reliable animal model for chromium deficiency. Furthermore, it has been known from early animal experiments that circulating chromium is not in equihbrium with physiologically important reserves. It has been shown in late pregnancy that serum chromium concentration does not correlate with glucose intolerance, insuhn resistance, or serum hpids. ... 

Brown RO, Forloines-Lynn S, Cross RE, Heizer WD. Chromium deficiency after long-term total parenteral nutrition. Dig Dis Sci 1986 31 661-4,... 

Freund H, Ataraian S, Fischer JE. Chromium deficiency during total parenteral nutrition. JAMA 1979 241 496-8. 

Schroeder HA, Nason AP, Tipton IH. Chromium deficiency as a factor in atherosclerosis. J Chronic Dis 1970 23 123-42. 

---