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PubMed1995

Effects of dietary chromium picolinate supplementation on growth, carcass characteristics, and accretion rates of carcass tissues in growing-finishing swine.

An experiment was conducted to evaluate the effects of chromium picolinate (CrP) on growth performance, carcass composition, and tissue accretion rates in pigs from 27 to 109 kg BW. Seven littermate sets of Yorkshire-Hampshire barrows, individually penned, were fed a fortified, corn-soybean meal basal diet (.95% lysine from 27 to 55 kg; .80% lysine from 55 to 109 kg) supplemented with 0 or 200 micrograms/kg of Cr from CrP. Addition of CrP increased (P < .09) ADG but did not affect ADFI or feed:gain ratio. Average and 10th rib backfat and longissimus muscle area were not affected by Cr supplementation. The right side of the carcass was physically dissected into muscle, fat, bone, and skin. Additionally, five pigs were killed for determination of initial body composition. Dietary CrP addition increased (P < .02) the percentage of muscle and decreased (P < .06) the percentage of fat. Total gain of dissected bone and skin were not different between treatments, but CrP increased (P < .06) the total gain of dissected muscle and decreased (P < .02) the total gain of dissected fat. Also, CrP increased the daily accretion rates of muscle (P < .05) and bone (P < .03) and decreased the daily accretion rate of fat (P < .05). The left side of the carcass was ground for determination of water, protein, lipid, and ash. The addition of CrP to the diet increased the percentage (P < .09) and accretion rate (P < .09) of water and increased the percentage (P < .004), total gain (P < .02), and accretion rate (P < .02) of protein while decreasing (P < .04) the percentage of lipid. Pigs fed CrP also had a decreased (P < .004) percentage of lipid in the dissected carcass muscle. Water, protein, and ash from the dissected muscle were not different between treatments. These results suggest that CrP supplementation throughout the entire growing-finishing phase increases the total gain and accretion rate of muscle while decreasing the total gain and accretion rate of fat. This results in carcasses with an increased percentage of muscle and decreased percentage of fat.

Animals↗
PubMed1995

Dietary chromium picolinate additions improve gain:feed and carcass characteristics in growing-finishing pigs and increase litter size in reproducing sows.

Growth trials were conducted to determine the effects of Cr as chromium picolinate at various protein levels on performance of growing pigs. The effects of continued supplementation on sow fecundity and body weight changes through two parities also were examined. In Trial 1, 48 crossbred pigs (40.9 kg initial weight) were assigned to one of three diets (0, 250, or 500 ppb of added Cr). The only observed difference was an overall trend for an improvement in gain:feed when Cr was added to the diet (P < .10). In Trial 2, 105 crossbred pigs (14.5 kg initial weight) were assigned to one of seven treatments involving a combination of two factors: 1) lysine level at 100 or 120% of NRC (1988) requirement estimate and 2) added Cr level (0, 100, 200, 500, or 1,000 ppb). A Cr x lysine interaction (P < .02) for gain:feed existed that demonstrated that the addition of 200 ppb of Cr resulted in improved gain:feed at the 100% of requirement lysine level but not at the 120% of requirement lysine level. The addition of 200 ppb Cr also reduced backfat (P < .04) and increased longissimus muscle area (P < .04) regardless of lysine level in the diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1995

Effect of chromium picolinate on growth, body composition, and tissue accretion in pigs.

An experiment was conducted to evaluate the effect of dietary chromium picolinate (CrP) on growth and body composition of pigs. Twenty-four barrows (three from each of eight litters) were randomly allotted within litter to one of three treatments: 1) basal (B) diet from 19.1 to 106.4 kg BW (Control); 2) B from 19.1 to 57.2 kg BW and then B + 200 ppb of chromium as CrP from 57.2 to 106.4 kg BW (CrP-F); and 3) B + 200 ppb of chromium as CrP from 19.1 to 106.4 kg BW (CrP- GF). Average daily gain and ADFI were reduced (P < .08) and first rib fat thickness was increased (P < .08) in pigs fed CrP-GF compared with pigs fed the Control diet. Specific gravity of the carcass was not affected (P > .10) by treatment. Tenth rib fat was reduced (P < .01) in pigs fed CrP-F compared with pigs fed CrP-GF, and percentage of muscle was increased in pigs fed CrP-F (P < .09) compared with pigs fed either the Control or CrP-GF diets. Leaf fat (P < .05) and lung weights (P < .08) were reduced in pigs fed CrP-F compared with pigs fed CrP-GF. As determined by physical-chemical separation, pigs fed CrP-GF had an increased (P < .07) percentage of intermuscular fat compared with pigs fed the Control or CrP-F diets. Pigs fed CrP-F had a lesser (P < .07) percentage of total fat and a greater (P < .07) percentage of muscle than pigs fed the Control or CrP-GF diets. As determined by mechanical-chemical separation, pigs fed CrP-F had a greater (P < .10) percentage of moisture than pigs fed the Control diet and a lesser (P < .10) percentage of fat and a greater (P < .06) percentage of ash than pigs fed the Control or CrP-GF diets. Pigs fed CrP-GF had an increased (P < .04) daily fat accretion compared with pigs fed CrP-F. Sensory and shear force values were not affected by CrP, with the exception that meat from pigs fed CrP-GF had a greater (P < .10) shear force value than meat from pigs fed CrP-F. These results suggest that dietary supplementation of CrP in the finishing phase of pig production may increase muscle and decrease fat deposition; however, not all measures of muscling or fatness were improved by CrP.

Animals↗
PubMed1997

Supplemental chromium picolinate influences nitrogen balance, dry matter digestibility, and carcass traits in growing-finishing pigs.

Four trials were conducted to determine the influence of feeding 200 ppb Cr as chromium picolinate (CrPic) on DM digestibility, N balance, and carcass traits of growing-finishing pigs. A 15% CP corn-soybean meal diet was fed during the grower phase, and a 13% CP corn-soybean meal diet was fed during the finisher phase. In each of three trials, crossbred barrows (six littermate pairs) were used for two N balance periods (end of grower, 61.3 kg; end of finisher, 98.9 kg). After the second balance period, all the barrows were killed and carcass data were collected. Initial and final BW were 23.5 and 104.9 kg, respectively. Growth rate was similar for control and CrPic-fed pigs in all trials. The rate of N absorption was increased by feeding CrPic (P < .05), but N retention was increased only numerically (P = .14). Dry matter digestibility was also increased by feeding CrPic (P < .02). Dressing percentage and backfat thickness at the 10th and last rib did not differ between treatment groups. Longissimus muscle area was larger (P < .05) for pigs fed CrPic. In Trial 4, crossbred barrows (six littermate pairs; initial BW, 82.0 kg) were used in a switch-back design with an extra period. Digestibility of DM (P < .02) and absorption of N (P < .06) were improved with only a numerical increase (P = .22) in N retention. No carryover effect was observed. These findings show that pigs fed 200 ppb Cr from CrPic can have larger longissimus muscle areas and that Cr supplementation improved N absorption and DM digestibility.

Absorption↗
PubMed1999

Efficacy of chromium picolinate on performance and tissue accretion in pigs with different lean gain potential.

We conducted two experiments to determine whether the efficacy of chromium picolinate (CrP) on growth performance, carcass composition, and tissue accretion rates is dependent on the lean gain potential of the pigs. In Exp. 1, 40 barrows (20 from each of two genetic backgrounds; two pigs per pen, five pens per treatment) were fed a fortified, corn-soybean meal basal diet (.95% lysine from 19 to 55 kg BW; .80% lysine from 55 to 109 kg BW) without or with 200 microg/kg of Cr from CrP. The addition of Cr had no effect on performance, carcass measurements, or accretion rates of carcass protein or lipid, regardless of the lean gain potential of the pigs. In Exp. 2, 60 group-penned pigs (three pigs per pen; five pens per treatment) were fed a fortified, corn-soybean meal basal diet without or with 200 microg/kg of Cr from CrP from 21 to 104 kg BW. Within the dietary Cr treatments, half of the pigs received daily injections of 3 mg of porcine somatotropin (pST) from 54 to 104 kg BW. The pST administration resulted in faster growth rates (P < .007), improved feed efficiency (P < .001), increased longissimus area (P < .001), and decreased 10th-rib backfat (P < .001). Administration of pST also increased the percentage and accretion rate of carcass protein (P < .001) and decreased the percentage and accretion rate of carcass lipid (P < .001). The addition of CrP to the diet had no effect on any variable measured in either the untreated or pST-treated pigs. In these studies, Cr was ineffective at altering the composition of the carcass and its effects were not dependent on the pig's potential for lean gain.

Animal Feed↗
PubMed1987

Influence of picolinic acid on the uptake of 65zinc-amino acid complexes by the everted rat gut.

Three hundred fifty rats were used in three experiments to: 1) validate the everted gut procedure as an in vitro technique for estimating Zn absorption, 2) determine the effect of increasing ratios of picolinic acid (PA) to Zn on Zn absorption and 3) determine the effect of PA on absorption of Zn and amino acid complexes at pH 6, 7 and 8. In the first experiment the time delay between tissue collection with subsequent storage in ice-cold saline and start of tissue incubation was 0, 10, 20 or 30 min. A linear decrease was observed for 65Zn uptake with increasing delay time. Lysine absorption was not affected by delay time. In the second experiment, molar ratios of PA:Zn of 0, .5, 1.0, 1.5, 2.0 and 2.5 with Zn held constant were evaluated. A linear decrease in 65Zn absorption from 65ZnCl2 occurred as the molar ratio of PA to Zn increased. In the third experiment, 0 and 5 molar ratios of PA to a constant Zn level were evaluated using 65ZnCl2, 65Zn-14C-methionine (ZnMet) and 65Zn-3H-lysine (ZnLys) at pH 6, 7 and 8. The addition of PA decreased Zn absorption regardless of Zn source. The data suggest that the Zn sources used were of similar biological value. The data do not support the theory that PA facilitates Zn absorption.

Animals↗
PubMed1983

Effects of dietary picolinate on mice deprived of tryptophan, niacin and vitamin B-6.

Tryptophan (Trp) is usually catabolized to CO2, H2O and urea in mammals. Quantitatively, minor branches from this pathway lead to the production of picolinate (PA) and NAD+. Although niacin is a required nutrient when NAD+ synthesis from Trp is insufficient, it is not known if dietary PA is beneficial in such conditions. Two kinds of experiment were used to investigate the effects of dietary PA. First, mice were fed on a diet deficient in Trp for six weeks to diminish endogenous PA synthesis and stores. After this time the body mass of the mice was reduced by approximately 30%. Tryptophan-deficient mice subsequently fed a nutritionally complete diet gained weight more rapidly during the first but not subsequent week(s) of recovery when PA was added to their food. Second, mice were fed on a diet deficient in Trp, niacin and vitamin B-6 during the preimplantation period of pregnancy in an attempt to acutely lower PA synthesis and perhaps alter the embryos thus produced. The rate at which preimplantation blastocysts formed trophoblastic outgrowths when cultured in vitro was stimulated by dietary PA only if these blastocysts came from mice fed on a nutritionally deficient diet. The results suggest that PA serves as a beneficial nutrient under some conditions where its endogenous synthesis may be diminished.

Animals↗
PubMed2000

Macrophage control of mycobacterial growth induced by picolinic acid is dependent on host cell apoptosis.

The effects of picolinic acid (PA) on the intramacrophagic growth of Mycobacterium avium were studied. PA reduced M. avium growth inside mouse macrophages and led to a complete control of mycobacterial growth when added together with IFN-gamma. The mechanism involved did not require TNF-alpha, NO, or the respiratory burst, and was not dependent on either iron or zinc withholding. The mycobacteriostatic activity of the macrophages was associated with the induction of morphological changes that culminated in apoptosis at day 4 of treatment. PA alone induced apoptosis in macrophages, and this effect was increased by IFN-gamma treatment. Apoptosis at day 4 of infection was reduced by inhibiting macrophage activation with the prostaglandin 15 deoxy-prostaglandin J2 or by treating the cells with the antioxidant N-acetylcysteine. Mycobacterial growth was partially restored in macrophages treated with PA and IFN-gamma when 15 deoxy-prostaglandin J2 was added, concomitant with a delay in apoptosis. N-Acetylcysteine or glutathione could also completely revert the mycobacteriostatic effects of PA or PA plus IFN-gamma.

Adjuvants, Immunologic↗
PubMed2000

The tryptophan catabolite picolinic acid selectively induces the chemokines macrophage inflammatory protein-1 alpha and -1 beta in macrophages.

We previously found that the tryptophan catabolite picolinic acid (PA) is a costimulus for the activation of macrophage effector functions. In this study, we have investigated the ability of PA to modulate the expression of chemokines in macrophages. We demonstrate that PA is a potent activator of the inflammatory chemokines MIP (macrophage inflammatory protein)-1 alpha and MIP-1 beta (MIPs) mRNA expression in mouse macrophages in a dose- and time-dependent fashion and through a de novo protein synthesis-dependent process. The induction by PA occurred within 3 h of treatment and reached a peak in 12 h. The stimulatory effects of PA were selective for MIPs because other chemokines, including monocyte chemoattractant protein-1, RANTES, IFN-gamma-inducible protein-10, MIP-2, and macrophage-derived chemokine, were not induced under the same experimental conditions and were not an epiphenomenon of macrophage activation because IFN-gamma did not affect MIPs expression. Induction of both MIP-1 alpha and MIP-1 beta by PA was associated with transcriptional activation and mRNA stabilization, suggesting a dual molecular mechanism of control. Iron chelation could be involved in MIPs induction by PA because iron sulfate inhibited the process and the iron-chelating agent, desferrioxamine, induced MIPs expression. We propose the existence of a new pathway leading to inflammation initiated by tryptophan catabolism that can communicate with the immune system through the production of PA, followed by secretion of chemokines by macrophages. These results establish the importance of PA as an activator of macrophage proinflammatory functions, providing the first evidence that this molecule can be biologically active without the need for a costimulatory agent.

Adjuvants, Immunologic↗
PubMed2000

Systemic contact dermatitis caused by oral chromium picolinate.

Although nickel is the metal most commonly implicated in systemic contact dermatitis, other metals such as chromate have also been known to cause dermatitis when ingested. Chromium picolinate has been espoused as a nutritional supplement. Allegedly, it helps control blood sugar in diabetes and may reduce cholesterol and blood pressure levels.

Administration, Oral↗
PubMed2001

The effect of chromium picolinate on muscular strength and body composition in women athletes.

Fifteen women softball athletes were randomly divided into 2 groups, the chromium treatment group (n = 8) and the placebo control group (n = 7) to examine the effect of chromium, in the form of chromium picolinate (CrPic) supplementation, on muscular strength, body composition (body weight, percent body fat, and lean body mass), and urinary excretion. The CrPic supplementation consisted of a 500 ug dosage taken once per day. All participants trained 3 times per week with 2-3 sets of 8-12 repetitions at 80% of 1 repetition maximum (1RM) using variable resistance machines and free weights. No significant (p < 0.05) differences in muscular strength or body composition were found after 6 weeks of resistance training. In addition, chromium excretion (microg per 24 every hours) was examined and increased significantly with the treatment group after the 6-week period.

Adolescent↗
PubMed2002

Blood glucose lowering and toxicological effects of zinc (II) complexes with maltol, threonine, and picolinic acid.

The blood glucose lowering effects in KK-Ay mice with type 2 diabetes mellitus (DM) receiving daily an intraperitoneal (i.p.) administration of Zn(II) complexes with maltol, L-threonine, and picolinic acid for 14 days were estimated under the same conditions, and dose-dependent blood glucose lowering effects in the dose range of 0.2-3.0 mg Zn/kg body weight were found. Among them, the bis(maltolato)Zn(II) complex exhibited the highest blood sugar lowering effect at the dose of 3.0 mg Zn/kg. The improvement of DM was confirmed with oral glucose tolerance tests as well as blood HbA1c levels after the administration of the three Zn(II) complexes at the dose of 3.0 mg Zn/kg. For the purpose of the clinical trial of the complexes in the future, we examined the toxic effects of these three Zn(II) complexes in regard of the LD50 values and hepatic cytochrome P450 levels. The LD50 values of the three Zn(II) complexes exhibited high values compared with that of ZnCl2. No changes of both CYP1A1 and CYP2E1 levels in the liver of KK-Ay mice treated with the three Zn(II) complexes were observed. The obtained results will be important when the complexes are tried for clinical use.

Animals↗
PubMed1989

[Selenazoles. XII. (1) Reaction of 4-(p-tolyl)-selenosemi-carbazides of acetic, benzoic, isonicotinic, nicotinic and picolinic acid with omega-acetophenone].

The cyclization of 4-(p-tolyl)-selenosemicarbazides of acetic, benzoic, isonicotinic, nicotinic and picolinic acids (Ia-e) with omega-bromoacetophenone was investigated in the medium of methanol (Method A) or in methanol in the presence of anhydrous sodium acetate (Method B). Acid hydrolysis of compounds IIf-i and IVa-c, e was studied. Results of UV and IR spectrometric measurements and of the in vitro microbiological studies are presented. In contradistinction to corresponding thiosemicarbazides, the change in N4 nitrogen atom basicity of the parent selenosemicarbazide I (pKa of p-toluidine = 5.1), in comparison to that of 4-phenyl-selenosemicarbazide (pKa of aniline = 4.63), proved to influence the equilibrium of the reaction with omega-bromoacetophenone only in the methanol medium without addition of anhydrous sodium acetate (Method A).

Acetates↗
PubMed1989

Preclinical antitumor activity of an alpha-picoline derivative, penclomedine (NSC 338720), on human and murine tumors.

Penclomedine, a synthetic alpha-picoline derivative, was identified as a potential antitumor agent in the P388 leukemia prescreen of the National Cancer Institute. Upon further evaluation in the National Cancer Institute in vivo tumor panel, the compound demonstrated good activity against two breast tumors. A single i.p. dose or five daily doses caused partial regressions of advanced-stage s.c. implanted mouse CD8F1 mammary adenocarcinomas. Also, penclomedine administered i.p. on Days 1,5, and 9 caused regression of the human MX-1 mammary carcinoma implanted under the renal capsule of athymic mice. In contrast, penclomedine demonstrated only marginal to moderate activity against the i.p. implanted L1210 leukemia and M5076 sarcoma and was inactive in three additional non-breast tumor models (i.p. B16 melanoma, i.v. Lewis lung carcinoma, and s.c. colon adenocarcinoma 38). Penclomedine administered p.o. and i.p. was equally effective against the subrenal capsule MX-1. Doses given p.o. every fourth day caused complete regression of 39 of 40 advanced-stage s.c. implanted MX-1 tumors but were much less effective against human H82 small cell lung carcinomas (13 of 80 complete regressions). Penclomedine p.o. also inhibited growth of the human MCF-7 and mouse 16/C breast adenocarcinomas. Further studies to support the development of penclomedine to clinical trial are in progress.

Animals↗
PubMed1989

[The effect of picolinic acid and iron ions on the proliferation of SPEV cells].

The effect of picolinic acid (PA) on SPEV cell proliferation is found to be different from that on normal and virus transformed NRC cells, and on spontaneously transformed CHO cells. It is shown that SPEV cells are arrested by PA at the end of G1-phase and at the beginning of S-phase and probably in G2-phase of the cell cycle. Ferrous ions remove the G1/S block induced by PA to permit the cell transfer through S-phase. On the one hand, PA chelates ferrous ions from the cells, and on the other one it inhibits the replicative DNA synthesis. It can be suggested that PA may arrest the SPEV cell growth affecting the iron-depend stable radical formation which is introduced into the active centre of ribonucleotiDE reduCTase. This results in the lower enzyme activity.

Animals↗
PubMed1987

Antiproliferative activity of picolinic acid due to macrophage activation.

Activation and subsequent enhancement of cytotoxicity of mouse peritoneal macrophages (M phi) by picolinic acid (PLA) in vivo have been reported previously by the authors' group. The optimum dose was found to be 100 mg/kg. PLA-stimulated M phi lysed different tumor targets in vitro, MBL-2 lymphoma cells and Madison 109 lung carcinoma cells, with equal efficiency. Treatment with PLA was performed daily for 5 consecutive days with a dose of 100 mg/kg intraperitoneally in C57/BL mice, which previously had been inoculated with MBL-2 tumor cells. Treatment was initiated on the first day after tumor inoculation. Oral treatment with PLA (200 mg/kg) dissolved in the drinking water was also performed for 7 days. In addition, some groups received PLA treatment 1 or 2 days before tumor implantation but not afterwards, to elucidate the in vivo efficacy of M phi activation. Intraperitoneal therapy with PLA after tumor inoculation resulted in a highly significant increase in lifespan (46%); intraperitoneal pretreatment caused a significant increase (15%); orally administered PLA was without effect. Thus intraperitoneal treatment with PLA was found to have protective and therapeutic effects against the MBL-2 ascites tumor in vivo. These effects are most likely caused by macrophage activation.

Animals↗
PubMed1983

Increased membrane-associated nucleoside diphosphate kinase activity as a possible basis for enhanced guanine nucleotide-dependent adenylate cyclase activity induced by picolinic acid treatment of simian virus 40-transformed normal rat kidney cells.

A biochemical analysis of an increase in guanine nucleotide-dependent adenylate cyclase activity induced by treatment of cultured SV40-transformed normal rat kidney cells with picolinic acid is described. In purified membranes from drug-treated cells with an ATP regenerating system in assay, GTP- and GTP plus hormone-stimulated adenylate cyclase activities were increased, whereas basal and NaF-stimulated cyclase activities, and steady state rate with guanosine 5'-(beta, gamma-imino)triphosphate were essentially unaltered by drug treatment. In assay systems devoid of ATP regenerating system, the drug-induced increase in cyclase activity was seen with GDP as well as with GTP, it being larger with GDP than with GTP in terms of activity ratio, whereas such an increase was not observed with their analogs, guanosine 5'-O-(2-thiodiphosphate) or guanosine 5'-(beta, gamma-imino)triphosphate. Guanosine 5'-(beta, gamma-imino)triphosphate-stimulated from drug-treated membranes became less sensitive to the inhibition by GDP as shown by a rightward shift in inhibition curve, but this shift could not be reproduced with guanosine 5'-O-(2-thiodiphosphate). From these results, it was concluded that altered guanine nucleotide metabolism in membranes was involved. Neither the amount of guanine nucleotide-binding protein nor its related functions including GTPase activity were changed by drug treatment. However, we observed in the drug-treated cell membranes, an increase in activity of nucleoside diphosphate kinase, an additional factor which has been proposed to play a role in regulating adenylate cyclase by replenishing GTP near the guanine nucleotide binding site (Kimura, N., and Shimada, N. (1983) J. Biol. Chem. 258, 2278-2283). The altered features of adenylate cyclase with the natural guanine nucleotides induced by drug treatment were explained as a result of this enhanced nucleoside diphosphate kinase activity associated with the membranes.

Adenylyl Cyclases↗
PubMed1982

Antitumor activity of picolinic acid in CBA/J mice.

The growth of a solid tumor induced by im implantation of Ehrlich ascites tumor cells in inbred CBA/J mice was retarded by treatment with an iron chelator, picolinic acid (PLA). Survival of the mice was also significantly increased after PLA treatment. However, the iron chelator deferoxamine had no such effects; tumor growth was slightly enhanced, and survival was decreased.

Animals↗