[Chromium and insulin resistance].
ABSTRACT Since as early as the 50s of the last century, it has been known that chromium is essential for normal glucose metabolism. Too little chromium in the diet may lead to insulin resistance. However, there is still no standard against which chromium deficiency can be established. Nevertheless, chromium supplements are becoming increasingly popular. Various systematic reviews have been unable to demonstrate any effects of chromium on glycaemic regulation (possibly due partly to the low dosages used), but there is a slight reduction in body weight averaging 1 kg. In a double-blind randomised placebo-controlled trial in a Chinese population with type-2 diabetes mellitus, supplementation with 1000 micrograms of chromium led to a fall in the glycosylated haemoglobin level (HbA1c) by 2%. Toxic effects of chromium are seldom seen; recently, however, the safety of one of the dosage forms of chromium, chromium picolinate, has been questioned. One should be aware that individual patients with type-2 diabetes mellitus may have an increased risk of hypoglycaemic episodes when taking chromium supplements as self-medication.
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ABSTRACT: Chromium supplementation has been proposed to promote the action of insulin and the lowering of blood glucose levels in diabetic patients. However, the molecular mechanism by which chromium increases insulin sensitivity is not known. Using U937 monocytes as a cell culture model, this study demonstrates that chromium inhibits the secretion of TNF-alpha, a cytokine known to inhibit the sensitivity and action of insulin. U937 cells were cultured with high levels of glucose (mimicking diabetes) in the presence or absence of chromium chloride in the medium at 37 degrees C for 24 h. This study demonstrates that chromium supplementation prevents the increase in TNF-alpha levels and oxidative stress caused by the high levels of glucose in cultured U937 monocytic cells. Similarly, chromium supplementation prevented elevated TNF-alpha secretion and lipid peroxidation levels in H(2)O(2)-treated U937 cells. This study demonstrates for the first time that chromium supplementation inhibits TNF-alpha secretion in U937 monocytes cultured in high-glucose medium, which appears to be mediated by its antioxidative effect. This provides evidence for a novel molecular mechanism by which chromium supplementation may increase insulin sensitivity and glycemic control in diabetic patients.Biochemical and Biophysical Research Communications 01/2002; 289(3):687-91. · 2.41 Impact Factor
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ABSTRACT: Chromium is involved in normal glucose metabolism. To test whether chromium is also associated with the exercise-induced increases in glucose utilization, urinary chromium excretion, serum glucose, insulin, and glucagon of nine male runners (23-46 yr) were evaluated. Blood samples were taken prior to, immediately following, and 2 h after a strenuous 6-mile run. Urine samples were also taken at these times, and total daily urine collections were made the day of the run and the following day. Mean serum glucose for all runners immediately after running was 185 +/- 19 mg/dl compared with 90 +/- 1 mg/dl (mean +/- SE) prior to running. Mean serum glucagon immediately after running was significantly elevated compared with that observed prior to or 2 h after running; serum insulin levels were not altered significantly. Mean urinary chromium concentration was increased nearly five-fold 2 h after running; similar results were obtained when chromium concentration was expressed per mg of creatinine. Total daily urinary Cr excretion was approximately two times higher the day of running compared with the following nonrun day. Daily urinary excretion of sodium, potassium, and calcium were measured to determine if exercise had a general nonspecific effect on renal function; daily urinary excretion of these was not changed by exercise. These data demonstrate that accompanying the exercise-induced changes associated with increased glucose utilization, there is a significant increase in chromium excretion.Diabetes 04/1982; 31(3):212-6. · 7.90 Impact Factor
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ABSTRACT: Chromium (Cr) is essential for the regulation of insulin action, and Cr supplementation has been studied as a potential therapy of insulin resistance and lipid abnormalities. Corticosteroid treatment is well known to cause the abnormality of carbohydrate metabolism. Recently, it has been reported that corticosteroid increases urinary loss of Cr, and Cr supplementation recovers steroid-induced diabetes mellitus. In this experiment, rats were treated daily with dexamethasone (DEX) (0.2 mg/kg, intraperitoneal [IP]) for the first 7 days and were further treated with DEX plus either chromium picolinate (CrP, 30 mg/kg/d) orally or a placebo for a period of 14 days. At the end of experiment (D21), the control rats, which were treated only with DEX weighed 320 g (80% of initial weight) on average, but CrP-treated rats weighed 364 g (91% of initial weight. P <.05). Glucose tolerance tests (GTTs) and insulin sensitivity tests were conducted. During insulin sensitivity tests, the area under the curve (AUC(0-->120)) of the time-glucose concentrations curves in CrP-treated group were decreased compared with those in the control group (271.4 +/- 74.9 v 1,097.4 +/- 722.2 mmol/L/min, P <.01). Fasting serum insulin levels in CrP-treated rats were clearly decreased by 46.9% compared with those in the control group (0.52 +/- 0.19 v 0.98 +/- 0.36 nmol/L, P <.05). During the GTTs, the AUC(0-->120) for time-glucose concentrations curves in CrP-treated group was not significantly different from the control group, but the AUC(0-->120) of serum insulin concentrations in the CrP-treated group were 55.8% lower than those in the control group (123.1 +/- 42.5 v 278.2 +/- 59.1 nmol/L/min, P <.01). The mean AUC(0-->120) of time-cholesterol concentration curves during GTTs did not significantly differ between the 2 groups (867.6 +/- 155.2 v 827.7 +/- 94.3 mmol/L/h, P = not significant [NS]). In contrast, 1-hour and 2-hour plasma triglycerides were significantly lower in the CrP-treated group, and the mean AUC of the time-triglyceride curve was significantly lower in CrP-treated group than in the control group (3.4 +/- 0.5 v 5.9 +/- 1.3 mmol/L/h, P <.05). We suggest that Cr supplementation in DEX-treated rats can relatively reverse a catabolic state and increase insulin sensitivity. Our results support the hypothesis that Cr supplementation can be considered to improve carbohydrate and lipid metabolism in patients receiving corticosteroid treatment.Metabolism 05/2002; 51(5):589-94. · 3.10 Impact Factor