Chromium: Functions

A biologically active form of chromium participates in glucose metabolism by enhancing the effects of insulin. Insulin is secreted by specialized cells in the pancreas in response to increased blood glucose levels, for example, after a meal. Insulin binds to insulin receptors on the surface of cells, activating those receptors and stimulating glucose uptake by cells. Through its interaction with insulin receptors, insulin provides cells with glucose for energy and prevents blood glucose levels from becoming elevated. In addition to its effects on carbohydrate (glucose) metabolism, insulin also influences the metabolism of fat and protein. A decreased response to insulin or decreased insulin sensitivity may result in impaired glucose tolerance or type 2 diabetes, also known as non-insulin dependent diabetes mellitus (NIDDM). Type 2 diabetes is characterized by elevated blood glucose levels and insulin resistance.

The precise structure of the biologically active form of chromium is not known. Recent research suggests that a low-molecular-weight chromium-binding substance (LMWCr) may enhance the response of the insulin receptor to insulin. The following is a proposed model for the effect of chromium on insulin action. First, the inactive form of the insulin receptor is converted to the active form by binding insulin. The binding of insulin by the insulin receptor stimulates the movement of chromium into the cell and results in binding of chromium to apoLMWCr, a form of the LMWCr that lacks chromium. Once it binds chromium the LMWCr binds to the insulin receptor and enhances its activity. The ability of the LMWCr to activate the insulin receptor is dependent on its chromium content. When insulin levels drop due to normalization of blood glucose levels, the LMWCr may be released from the cell in order to terminate its effects.

Nutrient interactions

Iron: Chromium competes for one of the binding sites on the iron transport protein, transferrin. However, supplementation of older men with 925 mcg of chromium/day for 12 weeks did not significantly affect measures of iron nutritional status. A study of younger men found an insignificant decrease in transferrin saturation with iron after supplementation of 200 mcg of chromium/day for 8 weeks, but no long-term studies have addressed this issue. Iron overload in hereditary hemochromatosis may interfere with chromium transport by competing for transferrin binding. This has led to the hypothesis that decreased chromium transport might contribute to the diabetes associated with hereditary hemochromatosis.

Vitamin C: Chromium uptake is enhanced in animals when given at the same time as vitamin C. In a study of three women, administration of 100 mg of vitamin C together with 1 mg of chromium resulted in higher plasma levels of chromium than 1 mg of chromium without vitamin C.

Carbohydrates: Diets high in simple sugars (e.g., sucrose), compared to diets high in complex carbohydrates (e.g., whole grains), increase urinary chromium excretion in adults. This effect may be related to increased insulin secretion in response to the consumption of simple sugars compared to complex carbohydrates.

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