SEARCH · Search PubMed

Results for “CHROMIUM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources

PubMed1992

[Biological monitoring in chromium-plating industry].

The purpose of the present investigation was to evaluate the role of biological monitoring as a means of surveillance of exposure in the Danish chromium-plating industry. We collected spot urine samples from 47 employees in five electro-plating plants near Aarhus and compared the results wide 40 non-exposed workers. We found no increase of chromium in urine during a work shift (mean = 0.11 nmol chromium/mmol creatinine, p = .46). The mean urine chromium value among the chromium workers was twice the mean value of the referent population (p = 0.001). There was, however, a considerable overlap between the two populations. All of the urine chromium values were much lower than the proposed American biological exposure indices. The results do not indicate any need for implementation of biological monitoring in the Danish chromium-plating industry, but longitudinal studies concerning possible accumulation of chromium at present occupational exposure levels should be carried out.

Adult↗

PubMed1991

Effect of chromium on oxygen free radical metabolism, inhibition of superoxide dismutase and enhancement of 6-hydroxydopamine oxidation.

The effect of chromium on superoxide dismutase activity (SOD) as well as on the rate of hydroxydopamine oxidation was studied in vitro, since chromium is known as an environmental and occupational carcinogen and oxygen free radicals are implicated in carcinogenic processes. Chromium is a strong inhibitor of SOD activity in this system. The degree of inhibition is directly proportional to the chromium concentration (tested chromium range 0.166-0.33 mg/L in reaction mixture), to reaction time (tested range up to 10 minutes), and to substrate concentration. Autoxidation of 6-hydroxydopamine was increased by chromium concentration of 15 mg/L. The combination of excessive oxygen free radical production and inhibition of their elimination by inhibition of SOD activity may contribute to the toxic effects of chromium.

Ascorbic Acid↗

PubMed1991

Effect of ascorbic acid on DNA damage, cytotoxicity, glutathione reductase, and formation of paramagnetic chromium in Chinese hamster V-79 cells treated with sodium chromate(VI).

The effect of pretreatment with ascorbic acid (vitamin C) on chromate-induced DNA damage, cytotoxicity, and enzyme inhibition as well as on the cellular reduction of chromium(VI) was investigated using Chinese hamster V-79 cells. Cellular pretreatment with nontoxic levels of 1 mM ascorbic acid for 24 h prior to exposure resulted in a significant increase (1.7-fold) in cellular levels of this vitamin. Alkaline elution assays demonstrated that this pretreatment decreased cellular levels of Na2CrO4-induced alkali-labile sites while the numbers of DNA-protein crosslinks produced by chromate increased. In colony-forming assays, pretreatment with ascorbic acid enhanced the cytotoxicity of chromate. However, the inhibition of glutathione reductase attributed to Na2CrO4 was attenuated by this pretreatment. Under the same experimental condition, the uptake of chromate in pretreated cells was found to increase. ESR studies revealed that cellular pretreatment with ascorbic acid reduced the level of chromium(V) intermediate and increased the level of chromium(III) complex, indicating that cellular reduction of chromium(VI) to chromium(III) was accelerated by this vitamin. These results suggest that ascorbic acid decreases chromate-induced alkali-labile sites and chromium inhibition of glutathione reductase, but it enhances DNA-protein cross-links and cytotoxicity caused by this metal through its ability to directly reduce chromium(VI).

Animals↗

PubMed1989

Influence of vitamin B2 on formation of chromium(V), alkali-labile sites, and lethality of sodium chromate(VI) in Chinese hamster V-79 cells.

The effect of vitamin B2 on the cellular reduction and cytotoxicity of chromate(VI) was studied using Chinese hamster V-79 cells. Electron spin resonance studies showed that incubation of cells with Na2CrO4 resulted in the formation of both chromium(V) and chromium(III) complex and that cellular pretreatment with riboflavin (Vitamin B2) for 24 h prior to exposure increased the level of chromium(V) complex, but the level of chromium(III) remained unchanged. Analysis of flavin derivatives revealed that pretreatment with vitamin B2 increased free riboflavin without altering flavin adenine dinucleotide and flavin mononucleotide. In addition, the level of the flavoenzyme glutathione reductase, which is capable of reducing chromate, was unaffected by pretreatment with vitamin B2. However, treatment of cells with vitamin B2 and Na2CrO4 augmented the inhibition of glutathione reductase attributable to Na2CrO4 alone. Using a colony-forming assay, pretreatment with vitamin B2 resulted in a decrease of cytotoxicity after exposure to the lethal concentration of chromate (15 microM) but did not affect the cytotoxicity at sublethal concentration of this metal (5-7.5 microM). Alkaline elution studies demonstrated that Na2CrO4 induced alkali-labile sites in the DNA of cells in a concentration-dependent manner (5-15 microM) and pretreatment with vitamin B2 resulted in an increase of these DNA lesions at all concentrations of Na2CrO4. The results, showing that vitamin B2 enhances chromate-induced alkali-labile lesions and chromium inhibition of glutathione reductase, might be due to an increase of chromium(V) species, possibly through its ability to directly reduce chromium(VI). The results also suggest that the extent of DNA lesions induced by chromate may not correlate directly with the cytotoxic effects of this metal.

Animals↗

PubMedDate not supplied

Quantitative determination of chromium and nickel in tumour and tumour-free human tissue.

Environmental pollution with carcinogenic substances, in addition to individual abuse, are discussed as important factors causing development of cancer. We must assume that certain nickel and chromium compounds, which are ubiquitous in our ecosystem, must have carcinogenic effects on humans too. The aim of this study is therefore to examine the extent to which the accumulation of the potentially carcinogenic metal ions nickel and chromium could be measured in tissue from tumour patients. We examined tumour and tumour-free tissue obtained from a total of 48 patients who had carcinomas of the stomach, bowel, or kidney. We also analyzed nickel and chromium content in whole blood and urine samples from these persons. The quantitative metal estimations were done using atomic absorption spectrophotometry. Differences between chromium and/or nickel content in tumour or tumour-free tissue were not observed. An accumulation of these metal ions in tumour tissue is therefore improbable. We were also unable to find differences in metal content with regard to chromium and nickel as related to the appearance of tumour in the organ. In contrast, tumour patients had a 5- to 7-fold increase over normal values for chromium and nickel in blood and urine. This was attributable to unavoidable contamination of tissue and body fluids with chromium- and nickel-containing instruments during major surgical procedures.

Adult↗

PubMed1987

[Toxicological and analytical lists: chromium and its compounds].

The main aspects of occupational exposure to chromium and chromium compounds are surveyed. Special attention is paid to the toxic action of this metal at the different target organs. The nutritional aspect of CrIII is examined preliminarily, and data detailing the metal contents in water and food are provided. As far the different working processes that entail occupational exposure to chromium are concerned, hygienic and environmental problems are discussed while identifying the average environment exposure to the different chemical forms of chromium (CrIII, CrIV, soluble and not soluble), as a function of the worker's tasks, and the relevant human response (total human Cr). Different hygienic and environmental standards in force in various countries and applicable to chromium compounds are compared. Additional information is given on the main aspects of chromium metabolism (absorption, distribution, excretion), and on the prevailing toxic actions, with specific reference to cancerogenesis. As far as biologic monitoring of the exposed people is concerned, the significance of Cr-U as dose-exposure indicator is discussed, also in the light of a critical review of the reference values. The report describes a series of analytical methods for the identification of chromium in aqueous and biologic matrices. The problems connected with health monitoring and fitness for work are eventually covered.

Chromium↗

PubMed1985

Prominent role of DT-diaphorase as a cellular mechanism reducing chromium(VI) and reverting its mutagenicity.

Rat liver postmitochondrial (S-12) fractions accounted for the bulk of the activity of whole cell homogenates in reducing chromium(VI) and accordingly in decreasing its mutagenicity. Both cytosolic (S-105) and microsomal fractions concurred to this process, which in all subcellular preparations tested was selectively induced by phenobarbital and especially by Aroclor 1254, but not by 3-methylcholanthrene. Cytosolic fractions were markedly more efficient in reducing chromium(VI) than microsomal fractions recovered from the same amount of tissue (liver or lung), although the latter preparations had a higher specific activity. The microsomal activity was exclusively NADPH dependent. A minor part of the cytosolic reduction was determined by nonenzymatic components, notably by some electron donors and chiefly by reduced glutathione, which proved to reduce chromium(VI) at physiological concentrations. However, also in cytosolic fractions, the most important contribution to chromium reduction was enzyme catalyzed, as shown by the following properties: thermolability; requirement for exogenous NADH or NADPH [supplied as such or in the form of a NADPH-generating system (S-9 mix)]; and saturation by chromium(VI). The likely involvement of DT-diaphorase in this metabolic process is supported by several findings, including its sharp pH dependence and its partial suppression by known inhibitors of this enzyme protein, such as p-chloromercuribenzoate, L-thyroxine, and dicumarol (which conversely did not counteract the metabolic deactivation of the other direct-acting mutagens 2-methoxy-6-chloro-9-[3-(2-chloroethyl)aminopropylamino]acridine 2HCl and epichlorohydrin). Similarly, cytosolic reduction of chromium(VI) was partially inhibited by selective metabolic depletors of both coenzymes of DT-diaphorase, i.e., NADPH and NADH. Pretreatment of rats with enzyme inducers (phenobarbital and 3-methylcholanthrene) stimulated the activity of DT-diaphorase in liver cytosolic fractions. A dramatic stimulation (35 to 40 times over untreated controls) was produced by Aroclor 1254, which also coinduced the liver cytosolic activity of enzymes involved in the glucose 6-phosphate-dependent pathway of both nicotinamide-adenine-dinucleotide phosphate and glutathione reduction (glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and glutathione reductase). In the lung cytosol, a slight yet significant stimulation of some of these enzyme activities was determined by the daily intratracheal instillations of high doses of chromium(VI) itself for 4 weeks, a condition which has been found to enhance the pulmonary metabolism of this metal ion.

Animals↗

PubMed1985

Dietary chromium and manganese intakes of a selected sample of Canadian elderly women.

Energy, manganese and chromium intakes of a selected sample of 90 free-living Canadian women (mean age 66.2 +/- 6.2 years) living in a university community and consuming self-selected diets were assessed by chemical analyses of 24-h duplicate diets and via three-day dietary records, collected by the subjects. Mean gross energy intake (determined via bomb calorimetry) was 6.0 +/- 2.4 MJ (1435 +/- 580 kcal) and mean intake of manganese (determined via atomic absorption spectrophotometry) was 3.8 +/- 2.1 mg/day, respectively. Mean and median chromium intakes, analysed via instrumental neutron activation analysis were 96.4 and 77.4 micrograms/day, respectively. The manganese and chromium densities of these diets were higher compared to diets for pre-menopausal women studied earlier, attributed in part to the higher (P less than 0.0003) median intake of tea (360 g) vs 180 g for the pre-menopausal women. No significant differences between the pre and post-menopausal groups in mean intakes (in g) of any other food groups investigated, were found. Silver-plated cutlery may also be a source of adventitious chromium in the diets of these post-menopausal subjects. Nevertheless 22 per cent of the subjects had chromium intakes based on one day duplicate diets, below the US suggested safe limit, which if representative of their habitual chromium intakes, may result in chromium depletion.

Aged↗

PubMed1982

[Study of nickel-chromium alloys containing titanium for porcelain bonding (author's transl)].

In order to analyze the effects of titanium and chromium and to determine the best composition of nickel-chromium alloys containing titanium for porcelain bonding, the mechanical properties, the tarnish resistance, and the porcelain bond strength of each of sixteen experimental alloys which were composed of nickel (54 to 90 wt%), chromium (10 to 40 wt%), titanium (0 to 6 wt%) were studied. The values of tensile strength, proportional limit, and Vickers hardness number for the alloys ranged from 33.4 to 68.1 kgf/mm2, 9.2 to 67.6 kgf/mm2, and 109 to 504 respectively. The increasing amount of titanium and/or chromium tended to the increase of those values. The elongation was higher than 24% for the alloys containing no titanium, but decreased to 0.3% with the increase of titanium and/or chromium content. The tarnish resistance for the alloys which contained only 10% chromium was not good. The porcelain bond strength of the alloys increased very significantly as the titanium content and/or the chromium content increased. In this study, the compositions of 58 to 76% Ni - 20 to 40%Cr - 2 to 4%Ti were considered to be optimum for porcelain bonding.

Chromium Alloys↗

PubMed1994

Investigation of chromium (VI) tolerant bacteria.

Pseudomonas strains were isolated from a heavy metal contaminated sludge. Some of the strains grew on chromium (VI) containing medium, and others were inhibited in their growth. Cells were able to remove chromium from the medium. This ability was independent of the rate of their growth. The concentration of chromium (VI) of the media decreased with 15-20 ppm in presence of 10(9) cells. The chromium (VI) was converted into a reduced form of chromium by bacteria. The reduced form of chromium was bound in the cell wall. The bound form of chromium could be recovered more or less with different chemicals. The best percentages of recovery were achieved with NaOH solution.

Biological Transport, Active↗

PubMed1995

Chromium(III) picolinate produces chromosome damage in Chinese hamster ovary cells.

Chromium(III) complexes currently being sold as dietary supplements were tested for their ability to cause chromosomal aberrations in Chinese hamster ovary cells. Complexes were tested in soluble and particulate forms. Chromium picolinate was found to produce chromosome damage 3-fold to 18-fold above control levels for soluble doses of 0.050, 0.10, 0.50, and 1.0 mM after 24 h treatment. Particulate chromium picolinate doses of 8.0 micrograms/cm2 (corresponding to a 0.10 mM solublized dose) and 40 micrograms/cm2 (0.50 mM) produced aberrations 4-fold and 16-fold above control levels, respectively. Toxicity was measured as a decrease in plating efficiency relative to controls. The above treatments produced > or = 86% survival for all doses except 1.0 mM chromium picolinate, which produced 69 +/- 10% survival. Chromium nicotinate, nicotinic acid, and chromium(III) chloride hexahydrate did not produce chromosome damage at equivalent nontoxic doses. Damage was inferred to be caused by the picolinate ligand because picolinic acid in the absence of chromium was clastogenic. Data are evaluated in terms of their relevance to human exposure based on pharmacokinetic modeling of tissue accumulation and are discussed in terms of literature reporting toxic effects of picolinic acid.

Animals↗

PubMed1996

Cobalt and chromium concentrations in patients with metal on metal total hip replacements.

There has been a resurgence of interest in the use of metal on metal bearings in total hip arthroplasty. Although the use of metal on metal bearing couples would eliminate or substantially reduce particulate polyethylene generation (depending on the presence or absence of polyethylene in the implant system), there is concern about the potential for increased particulate and ionic metal generation in comparison with polyethylene on metal bearings. These metallic degradation products may be transported away from the implant site and distributed systemically. Chromium concentrations in the serum and urine and cobalt concentrations in the serum were measured in subjects with cobalt chromium alloy metal on metal total hip replacements and in controls without implants. Eight subjects with long term (> 20 years) McKee-Farrar total hip replacements had 9-fold elevations in serum chromium, 35-fold elevations in urine chromium, and at least 3-fold elevations in serum cobalt concentrations in comparison with controls. Six subjects with short term (< 2 years) metal on metal surface replacement arthroplasties had 3-fold elevations in serum chromium, 4-fold elevations in urine chromium, and 4-fold elevations in serum cobalt concentrations in comparison with subjects with McKee-Farrar implants. Although the toxicologic importance of these trace metal elevations has not been established, serum and urine metal concentrations may be useful markers for the tribologic performance of metal on metal bearings.

Adult↗

PubMed2003

Asymmetric synthesis of axially chiral biaryls: inversion of planar chirality vs axial isomerization and functionalization at the side chain of biaryl chromium complexes.

Axially chiral syn-biaryl chromium complexes having a coordinating heteroatom substituent at the benzylic position gave anti-biaryl chromium complexes 5 with inversion of the planar chirality by heating in a nonaromatic solvent, while syn-biaryl chromium complexes with an o-methyl or formyl substituent afforded axially isomerized anti-biaryl chromium complexes under heating in an aromatic solvent. syn-biaryl and both enantiomeric anti-biaryl chromium complexes with the o-formyl group were stereoselectively prepared from an identical planar chiral arene chromium complex as chiral source. The formyl group of the axially chiral chromium complexes was functionalized by radical cyclization and beta-lactam formation, and hetero-Diels-Alder reaction.

Journal Article↗

PubMed2001

Effects of dietary chromium picolinate supplementation on performance and plasma concentrations of insulin and corticosterone in laying hens under low ambient temperature.

This experiment was conducted to evaluate the effects of chromium (chromium picolinate) on performance and plasma concentrations of insulin and corticosterone of laying hens (Ross Brown) under a low ambient temperature (6.9 degrees C). One hundred and twenty laying hens (46 weeks old) were divided into four groups, 30 hens per group. The laying hens were fed either a control diet containing 710.3 p.p.b. chromium or the control diet supplemented with 100, 200 or 400 microg chromium/kg diet. Increasing supplemental chromium increased live weight change (p < or = 0.001, linear) and egg production (p < or = 0.001, linear) and also improved feed efficiency linearly (p < or = 0.001). Live weight change and egg production also had quadratic responses (p < or = 0.001) to increasing chromium supplementation. Plasma insulin concentration increased linearly (p < or = 0.001), whereas corticosterone concentration decreased linearly (p < or = 0.001) as dietary chromium supplementation increased. The results of this study indicate that supplemental dietary chromium, 200 p.p.b. in particular, had a positive effect on performance and increased the plasma insulin concentration of laying hens under cold stress.

Animals↗

PubMed2006

The effect of chromium picolinate and biotin supplementation on glycemic control in poorly controlled patients with type 2 diabetes mellitus: a placebo-controlled, double-blinded, randomized trial.

BACKGROUND: Preclinical studies have shown that the combination of chromium picolinate and biotin significantly enhances glucose uptake in skeletal muscle cells and enhances glucose disposal. The present pilot study was conducted to determine if supplementation with chromium picolinate and biotin can improve glycemic control in patients with type 2 diabetes mellitus with suboptimal glycemic control despite use of oral antihyperglycemic agents. METHODS: Forty-three subjects with impaired glycemic control (2-h glucose >200 mg/dL; glycated hemoglobin >or=7%), despite treatments with oral antihyperglycemic agents, were randomized to receive 600 microg of chromium as chromium picolinate and biotin (2 mg/day) (Diachrome(, Nutrition 21, Inc., Purchase, NY) in addition to their prestudy oral antihyperglycemic agent therapy. Measurements of glycemic control and blood lipids were taken at baseline and after 4 weeks. RESULTS: After 4 weeks, there was a significantly greater reduction in the total area under the curve for glucose during the 2-h oral glucose tolerance test for the treatment group (mean change -9.7%) compared with the placebo group (mean change +5.1%, P < 0.03). Significantly greater reductions were also seen in fructosamine (P < 0.03), triglycerides (P < 0.02), and triglycerides/ high-density lipoprotein cholesterol ratio (P < 0.05) in the treatment group. No significant adverse events were attributed to chromium picolinate and biotin supplementation. CONCLUSIONS: This pilot study demonstrates that supplementation with a combination of chromium picolinate and biotin in poorly controlled patients with diabetes receiving antidiabetic therapy improved glucose management and several lipid measurements. Chromium picolinate/ biotin supplementation may represent an effective adjunctive nutritional therapy to people with poorly controlled diabetes with the potential for improving lipid metabolism.

Adult↗

PubMed1986

Chromium(III)ATP inactivating (Na+ + K+)-ATPase supports Na+-Na+ and Rb+-Rb+ exchanges in everted red blood cells but not Na+,K+ transport.

The chromium(III) complex of ATP, an MgATP complex analogue, inactivates (Na+ + K+)-ATPase by forming a stable chromo-phosphointermediate. The rate constant k2 of inactivation at 37 degrees C of the beta, gamma-bidentate of CrATP is enhanced by Na+ (K0.5 = 1.08 mM), imidazole (K0.5 = 15 mM) and Mg2+ (K0.5 = 0.7 mM). These cations did not affect the dissociation constant of the enzyme-chromium-ATP complex. The inactive chromophosphoenzyme is reactivated slowly by high concentrations of Na+ at 37 degrees C. The half-maximal effect on the reactivation was reached at 40 mM NaCl, when the maximally observable reactivation was studied. However, 126 mM NaCl was necessary to see the half-maximal effect on the apparent reactivation velocity constant. K+ ions hindered the reactivation with a Ki of 70 microM. Formation of the chromophosphoenzyme led to a reduction of the Rb+ binding sites and of the capacity to occlude Rb+. The beta, gamma-bidentate of chromium(III)ATP (Kd = 8 microM) had a higher than the alpha, beta, gamma-tridentate of chromium(III)ATP (Kd = 44 microM) or the cobalt tetramine complex of ATP (Kd = 500 microM). The beta, gamma-bidentate of the chromium(III) complex of adenosine 5'-[beta, gamma-methylene]triphosphate also inactivated (Na+ + K+)ATPase. Although CrATP could not support Na+, K+ exchange in everted vesicles prepared from human red blood cells, it supported the Na+-Na+ and Rb+-Rb+ exchange. It is concluded that CrATP opens up Na+ and K+ channels by forming a relatively stable modified enzyme-CrATP complex. This stable complex is also formed in the presence of the chromium complex of adenosine 5'-[beta, gamma-methylene]triphosphate. Because the beta, gamma-bidentate of chromium ATP is recognized better than the alpha, beta, gamma-tridentate, it is concluded that the triphosphate site recognizes MgATP with a straight polyphosphate chain and that the Mg2+ resides between the beta- and the gamma-phosphorus. The enhancement of inactivation by Mg2+ and Na+ may be caused by conformational changes at the triphosphate site.

Adenosine Triphosphate↗

PubMed1998

Chromium picolinate toxicity.

OBJECTIVE: To describe a case of toxicity secondary to chronic ingestion of 6-12 times the recommended daily allowance of over-the-counter (OTC) chromium picolinate. CASE SUMMARY: A 33-year-old white woman presented with weight loss, anemia, thrombocytopenia, hemolysis, liver dysfunction (aminotransferase enzymes 15-20 times normal, total bilirubin 3 times normal), and renal failure (serum creatinine 5.3 mg/dL; blood urea nitrogen 152 mg/dL). She had ingested chromium picolinate 1200-2400 microg/d for the previous 4-5 months to enhance weight loss. The patient had chromium plasma concentrations 2-3 times normal. Thrombotic thrombocytopenic purpura and hemolytic uremic syndrome were ruled out by clinical findings, peripheral blood smears, and a bone marrow biopsy. The patient was managed with supportive measures and received blood product transfusions and hemodialysis. Hemolysis stabilized and liver function improved over 6 days. Liver function returned to normal prior to discharge. Renal function began to return on day 12 and her serum creatinine on discharge was 1.3 mg/dL. One year later, all laboratory values were within normal limits. DISCUSSION: Trivalent chromium is an essential trace element that is considered safe when ingested in normal quantities. Trivalent chromium compounds are used by patients to enhance weight loss, increase lean body mass, and/or improve glycemic control. Information regarding the toxicity of chromium picolinate is limited. CONCLUSIONS: Chromium supplements may cause serious renal impairment when ingested in excess. Medication histories should include attention to the use of OTC nutritional supplements often regarded as harmless by the public and lay media.

Acute Kidney Injury↗

PubMed1994

Beneficial effect of chromium supplementation on serum triglyceride levels in NIDDM.

OBJECTIVE: To investigate the effect of chromium picolinate supplementation on the lipid profile of the predominantly Hispanic population of non-insulin-dependent diabetes mellitus (NIDDM) patients in San Antonio, Texas. RESEARCH DESIGN AND METHODS: A prospective, double-blind, placebo-controlled, crossover study was performed on 14 men and 16 women. Initially, each patient was randomly assigned to receive either chromium picolinate or placebo for 2 months. This initial treatment phase was followed by a 2-month washout period. Subjects were then crossed-over and received the alternate capsule for an additional 2 months. Fasting blood glucose, HbA1c, and serum lipids were compared at the end of each treatment phase. RESULTS: Twenty-eight of the originally enrolled 30 patients completed the study. There were no adverse reactions to chromium reported. There were no differences noted between the control and chromium-treated subjects in glucose control, high-density lipoprotein cholesterol levels, or low-density lipoprotein cholesterol levels. Triglyceride (TG) levels were reduced significantly (17.4%; P < 0.05) during the 2 months of chromium supplementation. CONCLUSIONS: Ours is the first report of a significant reduction in serum TGs in a group of NIDDM patients treated with chromium. The low cost and excellent safety profile of chromium make it an attractive lipid-lowering agent for this population. Long-term studies are needed to determine if the short-term changes in plasma lipids can be sustained.

Administration, Oral↗