Trivalent chromium inhibits protein glycosylation and lipid peroxidation in high glucose-treated erythrocytes.

Epidemiological studies have shown lower levels of chromium among men with diabetes and cardiovascular disease (CVD) compared with healthy control subjects. The mechanism by which chromium may decrease the incidence of CVD and insulin resistance is not known. Using erythrocytes as a model, this study demonstrates that chromium inhibits the glycosylation of proteins and oxidative stress, both risk factors in the development of CVD. Erythrocytes were treated with high levels of glucose (mimicking diabetes) in the presence or absence of chromium chloride in the medium at 37 degrees C for 24 hours. Chromium supplementation prevented the increases in protein glycosylation and oxidative stress caused by the high levels of glucose in erythrocytes. This study demonstrates for the first time that chromium supplementation inhibits protein glycosylation in erythrocytes exposed to high glucose medium, which appears to be mediated by its antioxidative effect. This provides evidence for a novel mechanism by which chromium supplementation may decrease incidence of CVD in diabetic patients.

Protective effects of 17beta-estradiol and trivalent chromium on interleukin-6 secretion, oxidative stress, and adhesion of monocytes: relevance to heart disease in postmenopausal women.

Postmenopausal diabetic women are at greater risk for heart disease compared with men of similar age and with other risk factors. We examined the hypothesis that 17beta-estradiol and trivalent chromium inhibit secretion of the pro-inflammatory cytokine interleukin (IL)-6 and oxidative stress in monocytes exposed to high glucose (HG). U937 human monocytes were cultured with HG (30 mM) with and without 17beta-estradiol (0-1000 nM) and chromium chloride (Cr(3+), 0-10 muM) at 37 degrees C for 24 h. Results show that 17beta-estradiol inhibits IL-6 and adhesion to endothelial cells (p <. 05) by HG-treated monocytes. Treatment with 17beta-estradiol+Cr(3+) required a significantly lower dose of estradiol-17beta compared with 17beta-estradiol alone for IL-6 inhibition. 17beta-Estradiol+Cr(3+) also inhibited lipid peroxidation and the adhesivity to human endothelial cells in HG-treated monocytes. Thus, 17beta-estradiol+Cr(3+) inhibits oxidative stress, IL-6 secretion, and monocytic adhesion to endothelial cells, risk factors in the development of heart disease. The female body requires E but studies on some patients indicate side effects with increased amounts of 17beta-estradiol-supplementation. The potential benefit of a lower estrogen dose in combination with chromium is novel and needs to be explored in postmenopausal diabetic women.

Progesterone, but not 17beta-estradiol, increases TNF-alpha secretion in U937 monocytes.

The Women Health Initiative Clinical trial results suggest that post-menopausal women receiving estrogen + progesterone are at risk for heart disease compared with estrogen alone supplemented women. We examined the hypothesis that progesterone but not 17beta-estradiol (E) increases the secretion of pro-inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha. U937 human monocytes were cultured with normal or high glucose in the presence and absence of estrogen or progesterone at 37 degrees C for 24 h. Results show that estrogen inhibits IL-6 but not TNF-alpha secretion (p < 0.05) in monocytes activated by lipopolysaccharide (LPS) or high glucose. In addition, progesterone increased the TNF-alpha secretion in activated monocytes. Thus, progesterone supplementation along with estrogen may increase blood levels of pro-inflammatory cytokine TNF-alpha and thus risk of heart disease in post-menopausal women.