Chromium is an essential mineral in humans and is know to be necessary as a co-factor for the chromodulin complex in activation of the insulin receptor. In animal models chromium deficiency causes glucose intolerance and chromium supplementation is able to reverse this condition. Evidence suggests that chromium insufficiency is widespread in western nations due to a combination of high intakes of sugar and low concentrations of chromium in the diet. Randomised clinical trials administering chromium to humans have shown inconsistent results, possibly because the chromium status of the subjects is difficult to accurately assess. This is because serum levels of the mineral are very low (1 to 2 ng/mL) and because it difficult to accurately measure the chromium intake directly. The relationship between plasma chromium and glucose is important to consider because chromium is taken up by cells in response to a glucose load.
Researchers1 have investigated the effects of a glucose load on serum chromium levels in 27 healthy women. Subjects were divided into two groups based on the results of an oral glucose tolerance test and each group received 5g of brewers yeast containing 4µg of chromium daily for 3 months. Analysis of the data showed that following supplementation 67% of subjects showed a decreased in total glucose levels and 85% showed a decrease in total insulin levels. The authors calculated the relative chromium response (RCR) to illustrate the effects of a glucose load on serum chromium levels. This was defined as the chromium levels 1 hour post glucose load divided by the fasting chromium serum levels times by 100. Amongst the subjects 73 and 75% showed an improved RCR after supplementation, in the normal and hyperglycaemic group respectively. The increase RCR was associated with both the reduced glucose and reduced insulin levels.
In the normal subjects before supplementation the serum levels of chromium did not change significantly in response to a glucose load, possible suggesting adequate chromium status. However, post supplementation the serum levels increased from 1.43 to 1.86ng/mL 1 hour post glucose load. This may suggest that following binding to chromodulin, chromium was being released to the plasma. In the hyperglycaemic subjects before supplementation the serum levels of chromium decreased from a fasting level of 1.89 to 1.03ng/mL 1 hour post glucose load, but rose from 0.94 to 1.03ng/mL post supplementation. This suggests that the chromium status of the hyperglyaemic subjects may have been inadequate at baseline and that chromium levels in plasma decreased as chromium was transported into cells for binding to chromodulin. Post supplementation, the increase in plasma chromium 1 hour post glucose load may suggest an improved chromium status.
RdB
