The Effect of Chromium supplementation on Glucose and Lipid Metabolism in Type II Diabetics

Animal studies conducted in the 1950's, first suggested that chromium played a role in glucose metabolism. Experiments that restricted chromium intake in monkeys and rats were able to induce a state of glucose intolerance. This condition, similar to diabetes, was readily reversible with chromium supplementation. Clinical relevance were reported in the late 1970's when several cases of patients receiving long term hyperalimentation developed poor glucose tolerance with pronounced insulin resistance. Intravenous supplementaion with chromium almost immediately restored normal insulin sensitivity and action. The exact mechanism of chromium's action is unknown. It is proposed that chromium potentiates the action of insulin. Some studies have suggest that chromium increases the number of insulin receptors, others proposed that chromium enhances the affinity of insulin for its receptors. In one study, chromium was also seen to increase the volume of pancreatic Beta cell. This implied that chromium may increase insulin secretion. Chromium's function in lipid metabolism was observed in animal studies during the same time. Animals deficient in chromium exhibited abnormal lipid profiles. Several animal studies linked chromium deficiency to development CAD. One study even found that chromium supplementation in rabbits was able to reverse formed atherosclerotic plaques. Early clinical correlation came from several human autopsy series that linked low chromium level with death from heart disease. The mechanism behind chromium's effect on lipids is even less well defined. Again it is thought to be mediated by chromium's action on insulin sensitivity. Human studies since the afore mentioned studies have been carried out by a small group of investigators. Most were observational trials with optimistic results but inadequate controls. The few randomized trials published have shown more equivocal results; however, some have documented significant increases in HDL, improvement in total cholesterol, and improved response to oral glucose tolerance test. Beneficial evidence for improvement in triglyceride value and fasting glucose values has been weaker. Many factors have made the interpretation of the data from these trials difficult. These trials are usually composed of a small group of patients, most averaging less than 30 patients. Different chromium formulations at different doses were used. Very different population of patients were also studied. Typically the duration of these trials generally were short; most less than 3 months. An agent like chromium that may improve both glucose metabolism and lipid profile deserves further investigation. Diabetic dyslipidemia is felt to be a major risk factor for early morbidity and mortality from the disease. Atherosclerotic disease in NIDDM is responsible for over 50% of hospital admissions and 80% of all mortality. If proven even to be mildly efficacious, the low cost and benign nature of chromium would make it an ideal adjuvant therapeutic agent.