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Results for “PICOLINE”

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PubMed1994

Picolinic acid blocks the neurotoxic but not the neuroexcitant properties of quinolinic acid in the rat brain: evidence from turning behaviour and tyrosine hydroxylase immunohistochemistry.

Previous results suggest that the tryptophan metabolite, picolinic acid may have the unusual properties of antagonizing the neurotoxic but not the neuroexcitant effects of another tryptophan metabolite, quinolinic acid in the central nervous system. The present experiments tested this possibility utilizing behavioural and tyrosine hydroxylase immunohistochemical techniques. In the first series of experiments, rats received injections of relatively high concentrations of 6-hydroxydopamine (12 micrograms in 1 or 2 microliters), quinolinic acid (120 nmol in 0.5 microliters), picolinic acid (480 nmol in 0.5 microliters) or co-treatments (0.5 microliters) with quinolinic (120 nmol) plus picolinic acid (480 nmol) into the region of the substantia nigra. Results revealed that 6-hydroxydopamine and quinolinic acid alone produced a large loss of tyrosine hydroxylase-positive cells in the pars compacta of the substantia nigra. Behavioural results for all 6-hydroxydopamine (n = 10) and for some quinolinate-treated rats (n = 5) revealed ipsi- and contraversive circling following amphetamine (1 mg/kg, i.p.) and apomorphine (0.5 mg/kg, s.c.), respectively, consistent with unilateral loss of dopamine cells in the substantia nigra. The remaining quinolinate-treated rats (n = 9) circled ipsiversively following either stimulant suggesting damage to the pars reticulata. Groups treated with picolinic acid alone (n = 6) or co-injected (n = 6) showed no loss of tyrosine hydroxylase-positive cells in the substantia nigra and no circling response to the stimulants. In the second series of experiments, low concentrations of quinolinic acid (2.5, 5.0, 7.5 nmol), picolinic acid (10, 20, 30 nmol), or the two together (7.5 plus 30 nmol, respectively) were microinjected (0.5 microliter) into the dorsal striatum and circling behaviour evaluated. These results revealed dose-dependent contralateral circling with either quinolinate or picolinate; co-injection of the two tryptophan metabolites also produced contralateral circling. It was concluded that picolinic acid blocks the neurotoxic but not the neuroexcitant effects of quinolinic acid.

Animals↗

PubMed2006

Chromium-picolinate induced ocular changes: Protective role of ascorbic acid.

Chromium-picolinate (Cr-picolinate) is a popular nutritional supplement; however its safety has been questioned with regard to its ability to act as a clastogen. The aim of the present work was to evaluate the biochemical, histological and morphological changes in the cornea and lens following oral administration of Cr-picolinate and the possible protective effect of Vitamin C. Ninety male Sprague-Dawley rats were divided into five groups included the control group, the groups treated with Cr-picolinate (0.8 and 1.5 mg/100 g b.w.) alone or in combination with Vitamin C (0.5 mg/100 g b.w.) for 8 weeks. The results indicated that the high dose of Cr-picolinate induced a significant decrease in SOD, GSH, Na(+)-, K(+)-ATPase levels, and a significant increase in MDA level. Severe morphological and histological changes in the cornea and lens accompanied with a decrease in the total soluble protein of the lens homogenate and changes in the crystalline fractions in lens. Vitamin C supplementation succeeded to restore these changes to great extent. It could be concluded that consumption of Cr-picolinate for a long time induced several hazards to cornea and lens. Supplementation with extra amounts of Vitamin C may be useful to restrain the Cr-picolinate induced ocular changes.

Animals↗

PubMed2005

Chromium picolinate, rather than biotin, alleviates performance and metabolic parameters in heat-stressed quail.

1. The effects of chromium picolinate and biotin supplementation alone and in combination on performance, carcase characteristics, malondialdehyde (MDA), vitamin C, vitamin E, glucose and cholesterol levels were evaluated in Japanese quail exposed to high ambient temperature. 2. Two hundred and forty quails (10d old) were assigned randomly to 4 dietary treatments at room temperature (22 degrees C; thermoneutral, TN) or ambient (34 degrees C for 8 h/d; heat stress, HS). Both TN and HS were fed either on a basal (control) diet or the basal diet supplemented with 400 microg of Cr/kg (Cr group), 0.5 mg of biotin/kg of diet (biotin group) or both (Cr + Biotin group). 3. Supplementing the diet of heat-stressed quails with chromium picolinate improved live weight gain, feed intake, feed efficiency and carcase traits. Biotin supplementation during TN and HS conditions did not have any beneficial effects on body weight gain, feed intake, feed efficiency or carcase traits. 4. Either in combination or alone, chromium picolinate increased serum concentrations of vitamins C and E, but decreased MDA, glucose and cholesterol concentrations in birds kept at high ambient temperature. There was no difference in vitamins C and E and MDA concentrations between birds given chromium picolinate and birds receiving chromium picolinate plus biotin, while glucose and cholesterol levels were significantly lower in all groups. The lowest concentrations of cholesterol and glucose were found in the combination group under both TN and HS conditions. An interaction between diet and temperature was detected for glucose and cholesterol concentrations. 5. Excretion rates for zinc, iron and chromium were lower in TN groups than in the corresponding HS groups. Supplementing diet with chromium picolinate and chromium picolinate plus biotin decreased excretion of minerals while biotin alone did not effect excretion of minerals. 6. Chromium supplementation, but not biotin supplementation, attenuated the decline in performance and antioxidant status resulting from heat stress.

Animals↗

PubMed1980

Zinc absorption in rats fed a low-protein diet and a low-protein diet supplemented with tryptophan or picolinic acid.

Zinc absorption was examined in rats fed a basal diet with 5% vitamin-free casein, in rats fed the 5% casein-based diet supplemented with tryptophan and in rats fed the 5% casein-based diet supplemented with picolinic acid. True, total daily zinc absorption was determined by an isotope dilution technique after the rats had been injected intramuscularly with carrier-free 65Zn. The zinc concentration of the kidneys from the rats fed the 5% casein diet was significantly less than that of the kidneys from rats fed the same diet supplemented with either tryptophan or picolinic acid. The specific activity of Zn in the kidneys from the rats fed the low-protein diet was significantly greater than that of the kidneys from rats fed the diet supplemented with either tryptophan or picolinic acid. The specific activity of Zn in the feces from rats fed the low-protein diet was significantly less than the specific activity of the feces from rats fed either supplemental tryptophan or supplemental picolinic acid. True, total daily zinc absorption in rats fed the low-protein diet was significantly less than the total daily zinc absorption in rats fed either supplemental tryptophan or supplemental picolinic acid. Since tryptophan is a metabolic precursor of picolinic acid, the results support the hypothesis that endogenous and exogenous picolinic acid facilitates zinc absorption.

Absorption↗

PubMed1985

Effect of dietary picolinic acid on the metabolism of exogenous and endogenous zinc in the rat.

The excretion of 65Zn was compared by metabolic balance studies in adult male rats fed purified diets containing 0.8 mmol Zn/kg diet, with and without 40 mmol picolinic acid per kilogram diet, after single intragastric (i.g.) and intraperitoneal (i.p.) doses of the isotope. In a third experiment picolinic acid was introduced for 3 d into the diet of rats prelabeled with 65Zn. The urinary excretion of total zinc was increased by the ingestion of picolinic acid in all three experiments. The urinary and fecal outputs of 65Zn were both consistently greater in picolinic acid-fed rats than in the corresponding control animals. This was particularly marked after i.p. injection of the tracer, and the specific activities of urine and feces from the treated rats were both increased. When picolinic acid was introduced into the diet of prelabeled rats there was a delay of 24 h in the urinary response and 48 h in the fecal response. The residual 65Zn levels were reduced in several tissues from the picolinic acid-fed rats, especially after i.p. administration of the isotope. These observations indicate that dietary picolinic acid increases the turnover of endogenous zinc in addition to enhancing the absorption and excretion of ingested metal, and this has implications for its use in cases of zinc deficiency.

Absorption↗

PubMed1997

Efficacy of chromium picolinate and chromium chloride as potential carcass modifiers in swine.

We conducted two experiments to evaluate the effects of chromium picolinate and chromium chloride (CrCl3) on growth performance, carcass composition, percentages and accretion rates of carcass tissues and chemical components, and blood metabolites in pigs. In Exp. 1, 35 individually penned pigs were fed a fortified, corn-soybean meal basal diet (.95% lysine) supplemented with 0, 200, or 400 micrograms/kg of Cr from chromium picolinate or 5,000 or 25,000 micrograms/ kg of Cr from CrCl3. Each diet was fed to seven pigs for 35 d (19.6 to 43.2 kg BW). Addition of 200 micrograms/kg of Cr from chromium picolinate increased ADG (P < .07) and ADFI (P < .03) but did not affect feed:gain ratio. Backfat measurements and longissimus muscle area were not affected by either source of Cr. The percentages of muscle, fat, bone, and skin from the right ham and the percentages of water, protein, lipid, and ash from the left carcass were not significantly altered by Cr. The addition of 200 micrograms/kg Cr from chromium picolinate increased (P < .07) the accretion rate of lipid in the carcass. In Exp. 2, 42 individually penned pigs (three from each of 14 litters) were fed a fortified, corn-soybean meal basal diet (.95% lysine from 19 to 55 kg; .80% lysine from 55 to 109 kg) without or with 200 micrograms/kg of Cr from chromium picolinate or 5,000 micrograms/kg of Cr from CrCl3. Dietary Cr addition had no effect on the performance or backfat measurements of the pigs; however, both sources of Cr increased (P < .07) longissimus muscle area. The percentages and accretion rates of muscle tissue were increased (P < .001) and the percentages of fat tissue were decreased (P < .001) in pigs fed Cr, with chromium picolinate being more effective than CrCl3 (P < .05). The percentages (P < .01) and accretion rates (P < .07) of carcass protein were increased and the percentages and accretion rates of carcass lipid were decreased (P < .04) in pigs fed Cr. No changes in blood metabolites occurred as a result of supplemental Cr in either experiment. These results suggest that chromium picolinate is more effective than CrCl3 and that Cr must be supplemented throughout the growing-finishing period to improve the carcass composition.

Animals↗

PubMedDate not supplied

Oral chromium picolinate and control of glycemia in insulin-treated diabetic dogs.

Chromium is an essential dietary trace mineral involved in carbohydrate and lipid metabolism. Chromium is required for cellular uptake of glucose, and chromium deficiency causes insulin resistance. Chromium supplementation may improve insulin sensitivity and has been used as adjunct treatment of diabetes mellitus in humans. In this study, 13 dogs with naturally acquired diabetes mellitus were treated with insulin for 3 months, then with insulin and chromium picolinate for 3 months. Dogs weighing <15 kg (33 lb: n = 9) were administered 200 microg of chromium picolinate PO once daily for I month, then 200 microg of chromium picolinate twice daily for 2 months. Dogs weighing >15 kg (n = 4) received 200 microg of chromium picolinate once daily for 2 weeks, then 200 microg twice daily for 2 weeks, then 400 microg twice daily for 2 months. Type of insulin, frequency of insulin administration, and diet were kept constant, and insulin dosage was adjusted, as needed, to maintain optimal control of glycemia. Mean body weight, daily insulin dosage, daily caloric intake, 10-hour mean blood glucose concentration, blood glycated hemoglobin concentration, and serum fructosamine concentration were not markedly different when dogs were treated with insulin and chromium picolinate, compared with insulin alone. Adverse effects were not identified with chromium picolinate administration. Results of this study suggest that, at a dosage range of 20-60 microg/kg/d, chromium picolinate caused no beneficial or harmful effects in insulin-treated diabetic dogs.

Administration, Oral↗

PubMedDate not supplied

Antiviral, cytotoxic and apoptotic activities of picolinic acid on human immunodeficiency virus-1 and human herpes simplex virus-2 infected cells.

The antiviral, cytotoxic and apoptotic effects of picolinic acid against human immunodeficiency virus-1 (HIV-1) and human herpes simplex virus-2 (HSV-2) infected cells were evaluated in cultured cells using in vitro assays. Picolinic acid was tested at several concentrations (from 0.15 to 3 mM) against one input dilution of the viruses to determine if the agent had any antiviral activity against HIV-1 or HSV-2. The results showed that picolinic acid at 1.5 mM (185 ug/mL) and 3 mM (369 ug/mL) was active against HIV-1 and HSV-2-infected cells, causing cytotoxicity which resulted in apoptosis and lack of viral replication. In parallel control experiments with non-infected cells, picolinic acid also caused cytotoxicity and apoptosis, which was more prominent at 3 mM than at 1.5 mM. Thus, infected cells appear to be slightly more sensitive to the cytotoxic and apoptotic effects of picolinic acid. The overlapping of the antiviral profile with the cytotoxic profile of picolinic acid indicates that, in vitro, the most likely sequence of events is that picolinic acid initially causes cytotoxicity which in turn results in apoptosis of cells infected with HIV-1 or HSV-2 and thus reduces the amount of viral replication.

Anti-HIV Agents↗

PubMed1994

Regulation of nitric-oxide synthase mRNA expression by interferon-gamma and picolinic acid.

Picolinic acid, a catabolite of L-tryptophan, is a potent co-stimulatory agent for the induction of tumoricidal activity and the production of L-arginine-dependent reactive nitrogen intermediates (RNI) in murine macrophages. We studied whether picolinic acid could affect nitric-oxide synthase (NOS) expression at the gene level in the macrophage cell line ANA-1. NOS mRNA was neither constitutively expressed nor induced by treatment with picolinic acid alone. However, low levels of NOS mRNA were induced by interferon (IFN)-gamma alone. In contrast, a major increase of NOS mRNA expression was observed after treatment with IFN-gamma plus picolinic acid. The synergism was already detectable after 5-6 h and increased up to 20 h of treatment. The ability of picolinic acid to augment IFN-gamma-dependent NOS mRNA expression was associated with a parallel increase in transcription, as demonstrated by nuclear run-on experiments. Protein synthesis was required for the induction of NOS mRNA because addition of cycloheximide dramatically reduced IFN-gamma plus picolonic acid-induced NOS mRNA expression. Finally, interleukin-4 significantly decreased IFN-gamma plus picolinic acid-induced NOS mRNA expression and NOS transcription. These data provide evidence of a molecular event connecting arginine and tryptophan metabolic pathways in the generation of RNI, and they indicate that picolinic acid can induce transcriptional activation of gene expression.

Amino Acid Oxidoreductases↗

PubMed2006

Exposure of pregnant mice to chromium picolinate results in skeletal defects in their offspring.

BACKGROUND: Chromium(III) picolinate, [Cr(pic)(3)], is a widely marketed dietary supplement. However, Cr(pic)(3) has been associated with oxidative damage to DNA in rats and mutations and DNA fragmentation in cell cultures. In isolated case reports, Cr(pic)(3) supplementation has been said to cause adverse effects, such as anemia, renal failure, liver dysfunction, and neuronal impairment. To date, no studies have been published regarding the safety of chromium picolinate supplementation to a developing fetus, although Cr(pic)(3) has been recommended for pregnant women who are diagnosed with gestational diabetes. METHODS: From gestation days (GD) 6-17, pregnant CD-1 mice were fed diets containing either 200 mg/kg Cr(pic)(3), 200 mg/kg CrCl(3), 174 mg/kg picolinic acid, or the diet only to determine if Cr(pic)(3), CrCl(3), or picolinic acid could cause developmental toxicity. Dams were sacrificed on GD 17, and their litters were examined for adverse effects. RESULTS: The incidence of bifurcated cervical arches was significantly increased in fetuses from the Cr(pic)(3) group as compared to the diet-only group. Fetuses in the picolinic acid-treated group had an incidence double that of the control group; however, this increase was not statistically significant. Fetuses in the CrCl(3) group did not differ from the controls in any variable examined. No maternal toxicity was observed in any of the treatment groups. CONCLUSIONS: High maternal oral exposures to chromium picolinate can cause morphological defects in developing offspring of mice.

Abnormalities, Drug-Induced↗

PubMed1992

Action of picolinic acid and structurally related pyridine carboxylic acids on quinolinic acid-induced cortical cholinergic damage.

Picolinic acid, a pyridine monocarboxylic acid derived from tryptophan metabolism by the kynurenine pathway, was shown to block cortical cholinergic neurotoxicity induced by quinolinic acid (QUIN), a pyridine dicarboxylic acid yielded by the same pathway. This study examined the specificity of the anti-toxic effect of picolinic acid by comparing its effect with several structurally related mono- and dicarboxylic acids, and by evaluating its potential to influence cholinergic neurotoxicity produced by kainic, ibotenic and quisqualic acid. Picolinic acid or related agents were injected alone or in combination with a fixed dose of QUIN into the right nucleus basalis magnocellularis (nbM) of rats anesthetized with halothane. Cholinergic neurotoxicity was assessed 7 days post injection by measuring choline acetyltransferase (ChAT) activity in the frontoparietal cortex on the injected and uninjected side. In picolinate experiments, the staining of nbM neurons by acetylcholinesterase (AChE) histochemistry was also examined. Focal injections of QUIN depleted cortical ChAT activity and staining of AChE in the nbM. Co-injection of picolinic acid with QUIN attenuated the decline in these two cholinergic neuron markers. Isonicotinate (4-pyridine monocarboxylate), but not nicotinate (3-pyridine monocarboxylate), significantly attenuated QUIN's effect on cortical ChAT activity. Among several dicarboxylic acids examined, only dipicolinate (2,6-pyridine dicarboxylate) showed activity. It produced a modest QUIN-like effect, but in co-injection experiments it attenuated the QUIN-induced decrease in cortical ChAT. When co-injected into the nbM with a neurotoxic dose of kainic, ibotenic or quisqualic acid which produced a neurotoxic response comparable to that of QUIN, picolinic acid attenuated kainic acid-induced neurotoxicity, but not ibotenate or quisqualate neurotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Mutagenicity of chromium picolinate and its components in Salmonella typhimurium and L5178Y mouse lymphoma cells.

Chromium picolinate is one of the most commonly used chromium dietary supplements available in the United States, and it has been marketed to consumers for use in weight loss, increasing muscle mass, and lowering serum cholesterol. Chromium picolinate is a synthetic compound that provides a bioavailable form of Cr(III) that is absorbed better than dietary chromium. However, there are several reports that it can have adverse effects. In order to study the mechanism of observed cellular toxicity and mutagenicity, chromium picolinate and its component compounds, chromium (III) chloride and picolinic acid, were evaluated in Salmonella typhimurium and L5178Y mouse lymphoma cells. Neither chromium picolinate nor chromium chloride induced a mutagenic response in S. typhimurium. However, in the L5178Y mouse lymphoma mutation assay, chromium picolinate induced mutagenic responses without and with the addition of S9.

Animals↗

PubMed2006

Multinuclear NMR spectroscopic and theoretical study on the interactions between diperoxovanadate complex and picoline-like ligands.

To understand the substituting effects of organic ligands on the reaction equilibrium, the interactions between diperoxovanadate complex [OV(O(2))(2)(H(2)O)](-) and a series of picoline-like ligands in solution were explored using 1D multinuclear ((1)H, (13)C, and (51)V) magnetic resonance, 2D diffusion ordered spectroscopy (DOSY), and variable temperature NMR in 0.15 mol/l NaCl ionic medium for mimicking the physiological conditions. The order of reactive capability of the picoline-like ligands with [OV(O(2))(2)(H(2)O)](-) is found to be picolinamide>N-methylpicolinamide>methyl picolinate>ethyl picolinate approximately propyl picoliniate>isopropyl picolinate. The substituting group influences the reactivity by either steric effect or electron-donating effect. Competitive coordination interactions result in a series of new seven-coordinated peroxovanadate species [OV(O(2))(2)L](-) (L=picoline-like ligands). Their coordination ways were confirmed by density functional calculations.

Carbon↗

PubMed1997

Induction of cytochromes P450 2B and 2E1 in rat liver by isomeric picoline N-oxides.

Pyridine derivatives are widely used solvents and precursors for the synthesis of chemicals of industrial importance. Oxidized metabolites have been implicated in the observed toxicity of pyridines and are known to induce drug-metabolizing enzymes in rat liver. In this study the three isomeric picoline (methylpyridine) N-oxides, as major oxidized metabolites of 2-, 3- and 4-picoline, were evaluated as inducers of cytochrome P450 (CYP) enzymes in rat liver. After a single dose of 100 mg/kg 24 h before sacrifice the 3- and 4-isomers were effective inducers of microsomal substrate oxidations associated with the phenobarbital-inducible CYPs 2B; upregulation of CYP2B protein was confirmed by immunoblotting. In contrast, the 2-isomer did not increase CYP2B protein or activity in rat liver but CYP2E1 protein expression was upregulated by the isomers to 160-200% of control. The three chemicals increased aniline 4-hydroxylation activity in rat liver, which is consistent with induction of CYPs 2B or 2E1 and 4-nitrophenol 2-hydroxylation activity was increased in microsomal fractions from 3- and 4-picoline N-oxide-treated rats. The activities of several other CYPs were also determined and CYP1A-dependent 7-ethylresorufin O-deethylation was increased (to approximately 6- and 2-fold of control) by the 3- and 4-isomer, respectively, whereas the activity of CYP3A-mediated androstenedione 6beta-hydroxylation was decreased by the agents--most notably by the 2-isomer. During NADPH-supported oxidation of CCl4, lipid peroxidation was increased in microsomes from 3- and 4-picoline N-oxide-pretreated rats and was modulated in vitro by the CYP2B inhibitor orphenadrine, but not by the CYP2E1 inhibitor 4-methylpyrazole. These findings establish that particular isomers of picoline N-oxide rapidly upregulate CYP2B or, to a lesser extent, CYP2E1 and implicate CYP2B in the enhanced lipid peroxidation observed in microsomes from rats treated with 3- and 4-picoline N-oxides. Such induction process may contribute to the hepatotoxicity of pyridines by enhancing the capacity for microsomal lipid peroxidation.

Animals↗

PubMed1995

Effect of intracellular iron depletion by picolinic acid on expression of the lactoferrin receptor in the human colon carcinoma cell subclone HT29-18-C1.

A lactoferrin receptor has been found on the brush-border membrane of intestinal epithelial cells of several species, including humans. A role for this receptor in intestinal iron absorption, which is well regulated in response to body iron stores, has been proposed. We have investigated the effect of intracellular iron depletion by picolinic acid, an iron chelator, on the cell surface binding of human lactoferrin to human enterocytes and its intracellular uptake, using HT29-18-C1 cells, an enterocyte-like differentiable cell line. The confluent cells exhibited 5.8 x 10(6) specific binding sites per cell for diferric human 125I-labelled lactoferrin with relatively low affinity (Kd 8.4 x 10(-7) M). The addition of picolinic acid to the culture medium resulted in a concentration- and time-dependent increase in lactoferrin binding that was correlated with a decrease in intracellular iron content. The maximum effect of picolinic acid on lactoferrin binding (approx. 2-fold increase), which appeared between 12 and 18 h after its addition, was obtained at a picolinic acid concentration of 2 mM. Scatchard analysis showed that the enhanced lactoferrin binding resulted from an increase in the number of lactoferrin receptors rather than an alteration in the binding affinity for lactoferrin. The time-dependent effect of picolinic acid was completely abolished in the presence of 1 microM anisomycin, a protein synthesis inhibitor, indicating that ongoing protein synthesis is involved in this effect. The enhanced lactoferrin binding induced by picolinic acid produced an increase of approx. 30% in the uptake of lactoferrin-bound 59Fe, indicating the existence of functional receptors. These results suggest that biosynthesis of lactoferrin receptors in intestinal epithelial cells can be regulated in response to the levels of intracellular chelatable iron, consistent with intestinal iron absorption dependent on body iron stores.

Biological Transport↗

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↗

PubMed2005

Use of chromium picolinate and biotin in the management of type 2 diabetes: an economic analysis.

This paper addresses the potential economic benefits of chromium picolinate plus biotin (Diachrome) use in people with Type 2 diabetes (T2DM). The economic model was developed to estimate the impact on health care systems' costs by improved HbA1C levels with chromium picolinate plus biotin (Diachrome). Lifetimes cost savings were estimated by adjusting a benchmark from the literature, using a price index to adjust for inflation. The cost of diabetes is highly dependent on the HbA1C level with higher initial levels and higher annual increments increasing the cost. Improvement in glycemic control has proven to be cost-effective in delaying the onset and progression of T2DM, reducing the risk for diabetes-associated complications and lowering utilization and cost of care. Chromium picolinate plus biotin (Diachrome) showed greater improvement of glycemic control in poorly controlled T2DM patients (HbA(1C) > or = 10%) compared to their better controlled counterparts (HbA(1C) < 10%). This improvement was additive to that achieved by oral hypoglycemic medications and correlates to calculated levels of cost savings. Average 3-year cost savings for chromium picolinate plus biotin (Diachrome) use could range from 1,636 dollars for a poorly controlled patient with diabetes without heart diseases or hypertension, to 5,435 dollars for a poorly controlled patient with diabetes, heart disease, and hypertension. Average 3-year cost savings was estimated to be between 3.9 billion dollars and 52.9 billion dollars for the 16.3 million existing patients with diabetes. Chromium picolinate plus biotin (Diachrome) use among the 1.17 million newly diagnosed patients with T2DM each year could deliver lifetime cost savings of 42 billion dollars, or 36,000 dollars per T2DM patient. Affordable, safe, and convenient, chromium picolinate plus biotin (Diachrome) could prove to be a cost-effective complement to existing pharmacological therapies for controlling T2DM.

Biotin↗

PubMed1997

Chromium picolinate supplementation and resistive training by older men: effects on iron-status and hematologic indexes.

Chromium competes with iron for binding to transferrin, and high-dose chromium supplementation has been hypothesized to adversely affect iron status. This study examined the effects of chromium picolinate supplementation on hematologic indexes and selected indexes of iron status in 18 men aged 56-69 y who participated in an introductory resistive training program. The men were randomly assigned (double-blind design) to groups (n = 9) that consumed either 17.8 mumol Cr/d (924 micrograms Cr/d) as chromium picolinate or a low-chromium placebo for 12 wk while engaging in resistive training twice weekly (3 sets of 8-12 repetitions at 80% of one repetition maximum for 5 exercises). Hematocrit, hemoglobin, red blood cell (erythrocyte) count, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, red blood cell distribution width, platelet count, and mean platelet volume were within normal clinical ranges and were unchanged by either chromium picolinate supplementation or resistive training. Resistive training decreased total-iron-binding capacity from 38.4 +/- 9.3 to 27.3 +/- 5.6 mumol/L (P < 0.0001) and increased transferrin saturation from 35.7 +/- 16.3% to 45.4 +/- 16.9% (P = 0.050). Chromium picolinate supplementation did not influence these responses. Serum iron concentrations and serum ferritin concentrations were unchanged by either resistive training or chromium picolinate supplementation. These data suggest that high-dose chromium picolinate supplementation for 12 wk did not influence hematologic indexes or indexes of iron metabolism or status in older men. The decrease in total-iron-binding capacity and increase in transferrin saturation (%) with resistive training are largely opposite to changes associated with iron depletion and suggest a novel effect of resistive training on iron transport.

Aged↗