Chromium steroid induced diabetes

In photoallergic dermatitis, sunlight and exposure to the offending substance usually affect the face and arms, but the sun-shaded area under the chin is generally spared. Although sunlight is essential for the initiation of photosensitization, the dermatitis may continue long after the photoallergy is eliminated (a condition known as a “persistent light eruption”). 9 Common photoallergic substances include fruits and vegetables (., limes, celery, parsnips), hydrocarbons (., coal tar, pitch, asphalt, anthracene), and drugs (., tetracycline, thiazide diuretics, phenothiazines, sulfonamides) and fluorescein dye. 3

4-HNE was first discovered in 60s [ 54 ]. Later, in 80s 4-HNE was reported as a cytotoxic product originating from the peroxidation of liver microsomal lipids [ 40 ]. 4-Hydroxyalkenals produced in the course of biomembrane lipids peroxidation, elicited either by free radicals or by chemicals, might exert a genotoxic effect in humans [ 55 ]. The 4-hydroxyalkenals are the most significant products because they are produced in relatively large amounts, and they are very reactive aldehydes that act as “second messengers of free radicals.” In particular 4-HNE, which has been subjected to intense scientific scrutiny in 90s [ 49 ], is considered as “one of the major toxic products generated from lipid peroxides” [ 49 ]. 4-HNE high toxicity can be explained by its rapid reactions with thiols and amino groups [ 56 ]. Reactive aldehydes, especially 4-HNE, act both as signaling molecules ( see below 4-HNE as signaling molecule ) and as cytotoxic products of lipid peroxidation causing long-lasting biological consequences, in particular by covalent modification of macromolecules ( see below 4-HNE biomolecular adducts ). 4-HNE is considered as “second toxic messengers of free radicals,” and also as “one of the most physiologically active lipid peroxides,” “one of major generators of oxidative stress,” “a chemotactic aldehydic end-product of lipid peroxidation,” and a “major lipid peroxidation product” [ 57 ]. Thus, it is not a surprise that 4-HNE is nowadays considered as major bioactive marker of lipid peroxidation and a signaling molecule involved in regulation of several transcription factors sensible to stress such as nuclear factor erythroid 2-related factor 2 (Nrf2), activating protein-1 (AP-1), NF- κ B, and peroxisome-proliferator-activated receptors (PPAR), in cell proliferation and/or differentiation, cell survival, autophagy, senescence, apoptosis, and necrosis ( see below 4-HNE as signaling molecule ).

Corticosteroid treatment leads to decreased insulin sensitivity, impaired glucose tolerance, and/or diabetes as well as increased losses of the essential nutrient, chromium [Ravina et al., Diabetes Med, 1999]. Since supplemental chromium leads to improved glucose levels and increased insulin sensitivity in subjects with impaired glucose tolerance and diabetes, we supplemented 50 patients with steroid-induced diabetes with supplemental chromium, 200 μg of Cr as chromium picolinate three times per day. Within 1 week of supplemental chromium, blood glucose values of 47 of 50 patients with uncontrolled steroid-induced diabetes decreased from > mmol L −1 (250 mg dL −1 ) to < mmol L −1 (150 mg dL −1 ). Oral hypoglycemic medications and/or insulin were reduced one-half in patients prior to the initiation of supplemental chromium. These data demonstrate that chromium may be beneficial in the control of steroid-induced diabetes. J. Trace Elem. Exp. Med. 12:375–378, 1999. Published 1999 Wiley-Liss, Inc.

Oral curcumin administration has been found to inhibit the development of chemically-induced cancer in animal models of oral (58, 59) , stomach (60, 61) , liver (62) , and colon (63-65) cancer. Apc Min/+ mice have a mutation in the Apc (adenomatous polyposis coli) gene similar to that in humans with familial adenomatous polyposis , a genetic condition characterized by the development of numerous colorectal adenomas ( polyps ) and a high risk for colorectal cancer . Oral curcumin administration has been found to inhibit the development of intestinal adenomas in Apc Min/+ mice (66, 67) . Despite promising results in animal studies, there is presently little evidence that high intakes of curcumin or turmeric are associated with decreased cancer risk in humans. A 30-day phase II clinical trial in 40 smokers with at least eight rectal aberrant crypt foci (ACF; precancerous lesions) found that the number of ACF was significantly lower with a daily supplementation with 4 g/day of curcumin compared to 2 g/day (68) . Several controlled clinical trials in humans designed to evaluate the effect of oral curcumin supplementation on precancerous colorectal lesions, such as adenomas, are under way (69) .

Chromium steroid induced diabetes

chromium steroid induced diabetes

Oral curcumin administration has been found to inhibit the development of chemically-induced cancer in animal models of oral (58, 59) , stomach (60, 61) , liver (62) , and colon (63-65) cancer. Apc Min/+ mice have a mutation in the Apc (adenomatous polyposis coli) gene similar to that in humans with familial adenomatous polyposis , a genetic condition characterized by the development of numerous colorectal adenomas ( polyps ) and a high risk for colorectal cancer . Oral curcumin administration has been found to inhibit the development of intestinal adenomas in Apc Min/+ mice (66, 67) . Despite promising results in animal studies, there is presently little evidence that high intakes of curcumin or turmeric are associated with decreased cancer risk in humans. A 30-day phase II clinical trial in 40 smokers with at least eight rectal aberrant crypt foci (ACF; precancerous lesions) found that the number of ACF was significantly lower with a daily supplementation with 4 g/day of curcumin compared to 2 g/day (68) . Several controlled clinical trials in humans designed to evaluate the effect of oral curcumin supplementation on precancerous colorectal lesions, such as adenomas, are under way (69) .

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