Dietary lecithin improves dressing percentage and decreases chewiness in the longissimus muscle in finisher gilts.

The influence of dietary lecithin at doses of 0, 4, 20 or 80 g/kg fed to finisher gilts for six weeks prior to slaughter on growth performance, carcass quality and pork quality was investigated. M. longissimus lumborum (loin) was removed from 36 pig carcasses at 24h post-mortem for Warner-Bratzler shear force, compression, collagen content and colour analyses. Dietary lecithin increased dressing percentage (P=0.009). Pork chewiness and collagen content were decreased by dietary lecithin (P<0.05, respectively), suggesting that improved chewiness may be due to decreased collagen content. However, dietary lecithin had no effect on shear force, cohesiveness or hardness (P>0.05, respectively). Dietary lecithin reduced loin muscle L* values and increased a* values (P<0.05, respectively) but no changes on b* values (P=0.56). The data showed that dietary lecithin improved dressing percentage and resulted in less chewy and less pale pork.

The interaction between ractopamine supplementation, porcine somatotropin and moisture infusion on pork quality.

UNLABELLED: Ninety six crossbred pigs were used in a 4×2×2 experiment to determine the influence of management strategy, moisture infusion and ageing on pork quality. The treatments were i) management strategy (MS) during the last 28days pre-slaughter ( CONTROL: conventional diet; Ractopamine (Rac): porcine somatotropin (pST); and combined (Rac+pST): Rac for 28days and pST for the final 14days), ii) moisture infusion (MI) (0% and 10%) and iii) ageing period (24h and 7days). L* was decreased by pST and Rac+pST, followed by Rac and then the CONTROL MS. Shear force was increased by Rac and Rac+pST but not by either pST or the CONTROL MS. MI decreased L* and shear force while ageing for 7days increased L* and yellowness, and decreased drip loss and WB shear force. MI or ageing for 7days improved sensory pork quality. The results from this experiment indicated that as expected MI and ageing can be used to improve pork quality.

Levels of copper and zinc in diets for growing and finishing pigs can be reduced without detrimental effects on production and mineral status.

One hundred and sixty pigs were used to evaluate dietary copper (Cu) and zinc (Zn) supplementation on performance, fecal mineral levels, body mineral status and carcass and meat quality. Diets differed in mineral form (MF) (Cu and Zn in the form of proteinate amino acid chelate (organic) or sulfate (inorganic)) and inclusion level (IL) (27 mg/kg of total Cu and 65 mg/kg of total Zn ('low') or 156 mg/kg of total Cu and 170 mg/kg of total Zn ('high')) according to a 2 × 2 factorial arrangement of treatments. Pigs were used from 25 to 107 kg body weight (BW) and fed their respective diets ad libitum. Blood and fecal samples were collected on days 14 and 77 of the experiment. Blood was analyzed for concentration of Cu and Zn, hemoglobin (Hb), Cu content of red blood cells (RBC Cu) and alkaline phosphatase (ALP) and feces for Cu and Zn concentration. Hot carcass weight (HCW) and backfat depth were measured at slaughter and indices of meat quality were assessed on a section of longissimus thoracis. Liver, kidney and bone samples were collected immediately after slaughter and liver and kidney were tested for Cu and Zn content, while bone was only tested for Zn. Over the entire experimental period (25 to 107 kg BW) no significant treatment differences in average daily gain (ADG) or average daily feed intake (ADFI) occurred; however, feed conversion ratio (FCR) was improved by the inclusion of proteinate amino acid chelate (P = 0.012). Copper and Zn concentrations in feces were in direct proportion to the IL in the diet. Blood mineral levels were within normal physiological ranges in all treatments and tissue Cu and Zn concentrations increased with dietary IL (P < 0.05). Results indicate that Cu and Zn fecal concentrations were reduced by approximately 6-fold for Cu and by 2.5-fold for Zn by feeding 27 mg/kg Cu and 65 mg/kg Zn, in either the proteinate amino acid chelate or the sulfate form, compared with a diet containing 156 mg/kg Cu and 170 mg/kg Zn. This decrease in total dietary Cu and Zn did not reduce performance or mineral status of pigs.

Agonist-induced serotonin 2A receptor desensitization in the rat frontal cortex and hypothalamus.

This study examined the time course and possible mechanisms of agonist-induced desensitization of 5-hydroxytryptamine serotonin 2A receptors in the rat frontal cortex and hypothalamic paraventricular nucleus after 1, 4, and 7 days of treatment with (-)-1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane HCl [(-)-DOI] (1 mg/kg i.p.), a selective 5-HT(2A/2C) receptor agonist. In the frontal cortex, 5-HT-mediated phospholipase C (PLC) enzyme activity decreased by 24 to 30% after 4 to 7 days of (-)-DOI treatment without any significant changes in the guanosine 5'-3-O-(thio)triphosphate-mediated PLC enzyme activity. Additionally, treatment with (-)-DOI did not significantly change the levels of G(alpha11), regulator of G protein signaling (RGS)4, or RGS7 proteins in the frontal cortex, whereas G(alphaq) protein levels in the frontal cortex decreased (47%) only after 7 daily (-)-DOI injections. The functional status of 5-HT(2A) receptors in the hypothalamic paraventricular nucleus was examined using 5-HT(2A) receptor-mediated increases in plasma hormone levels. Plasma adrenocorticotrophic hormone (ACTH) and oxytocin measurements showed that 5-HT(2A) receptor desensitization began after only 1 day of (-)-DOI treatment, and the desensitization continued to increase after 4 and 7 days of treatment (ACTH response decreased 64.2-67.7%; oxytocin response decreased 82.3-90.1%). There were no significant alterations in levels of G(alphaq) or G(alpha11) lamic paraventricular proteins in the hypothanucleus. In conclusion, these results suggest that chronically administered (-)-DOI induces desensitization of 5-HT(2A) receptors in vivo, via a reduction in the ability of 5-HT(2A) receptors to activate G proteins without consistently altering levels of G(alpha) proteins or RGS proteins.

Destruction of serotonergic nerve terminals prevents fluoxetine-induced desensitization of hypothalamic 5-HT(1A) receptors.

RATIONALE: Selective serotonin (5-HT, 5-hydroxytryptamine) reuptake inhibitors (SSRIs) such as fluoxetine produce a gradual desensitization of hypothalamic post-synaptic 5-HT(1A) receptor systems. It is assumed that the effects of SSRIs on post-synaptic 5-HT(1A) receptors are mediated by 5-HT reuptake inhibition, leading to an increase of 5-HT in the synapse. However, there is no direct evidence to support this hypothesis. OBJECTIVES: The present study determined whether 5-HT(1A) receptor desensitization was mediated by fluoxetine's effects on serotonergic nerve terminals. METHODS: Serotonergic nerve terminals were destroyed by intracerebroventricular (i.c.v.) injection of the serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) combined with injection of the norepinephrine/dopamine reuptake inhibitor nomifensine. 5,7-DHT-induced loss of serotonergic terminals was confirmed by a 95% reduction in the density of [(3)H]paroxetine-labeled 5-HT transporters in the hypothalamus and a 97% reduction in the levels of 5-HT and 5-hydroxyindoleacetic acid in the cortex. Two weeks after the 5,7-DHT injections, rats were injected daily with fluoxetine (5 mg/kg or 10 mg/kg, i.p.) or saline for 14 days. RESULTS: Injections of 10 mg/kg fluoxetine produced a significant decrease in body weight gain. Destruction of serotonergic nerve terminals reduced body weight and potentiated the ability of fluoxetine to further inhibit body weight gain. Increases in plasma levels of adrenal corticotrophic hormone (ACTH, corticotropin), corticosterone, and oxytocin after injection of the 5-HT(1A) agonist 8-hydroxy-2-dipropylaminotetralin [(+/-)8-OH-DPAT] were used as peripheral markers of 5-HT(1A) receptor function in the hypothalamus. In vehicle-pretreated rats, fluoxetine produced a dose-dependent reduction in the (+/-)8-OH-DPAT-induced increase in plasma ACTH and oxytocin levels. Destruction of serotonergic nerve terminals blocked the ability of fluoxetine to produce a desensitization in the ACTH, corticosterone, and oxytocin responses to (+/-)8-OH-DPAT. CONCLUSIONS: The ability of fluoxetine to induce a desensitization of hypothalamic post-synaptic 5-HT(1A) receptor systems is dependent on the integrity of serotonergic nerve terminals in the hypothalamus, while its effect on body weight is not mediated by serotonergic nerve terminals in the hypothalamus.

The effect of genotype, sex and management strategy on the eating quality of pork.

Two hundred and sixteen (Large White×Landrace×Duroc) crossbred pigs were used to determine the influence of genotype, sex, and management strategies on pork quality. The experiment was a 2×3×3 factorial design with the main treatments being genotype (A - 50% and B - <25% Duroc bloodline), sex (females, surgical barrows and immunological barrows) and management strategy (control - C, dietary conjugated linoleic acid supplementation - CLA, and porcine somatotropin administration - pST). Genotype A pigs had less backfat (P2 site), higher intramuscular fat percentage, higher muscle ultimate pH (pH(u)) and surface exudate, and the pork was tougher and less acceptable compared with Genotype B pigs. Female pigs had lower muscle pH(u), higher surface exudate and tougher pork compared with both surgical and immunological barrows. Pigs fed the control diet had lower muscle pH(u) and higher surface exudate compared with pigs fed the CLA supplemented diet or administered pST. Pigs fed the control diet had higher consumer likeness scores for flavour, tenderness, juiciness and overall acceptability compared with pigs fed the CLA supplemented diet or administered pST. The results from this experiment indicate that pork eating quality is reliant on a complex interaction between genotype and sex. The results also indicate that management strategies such as pST administration and CLA supplementation, while being effective in reducing backfat, have the potential to have a negative impact on pork quality.

Sexual dimorphism in the response to N-methyl-D-aspartate receptor antagonists and morphine on behavior and c-Fos induction in the rat brain.

It has been suggested that there are sex differences in the neural response to drugs of abuse. Previous studies have shown that, upon administration of morphine, the immediate early gene c-Fos is induced in the striatum, nucleus accumbens and cortex of the rat brain. This induction of c-Fos is reduced by administration of the N-methyl-D-aspartate receptor antagonist dizocilpine maleate. However, in studies using immunocytochemistry, we found that the pattern of this expression differed markedly between the sexes. In male rats treated with morphine (10 mg/kg, s.c.) and killed 2 h later, there was an induction of c-Fos in the dorsomedial caudate-putamen, the nucleus accumbens and in the intralaminar nuclei of the thalamus. Administration of dizocilpine maleate (0.2 mg/kg, i.p.; 30 min before morphine) partially blocked the response in the caudate-putamen, but not in the thalamus. In females, morphine induced c-Fos in the caudate-putamen, but with more inter-animal variability than in males. In the midline intralaminar thalamic nuclei, female rats showed less induction than males. In male rats, dizocilpine maleate alone caused negligible induction of c-Fos, whereas in female rats, it caused a large induction in the rhomboid, reuniens and central medial nuclei of the thalamus, and in the cortex. Whereas dizocilpine maleate partially blocked the morphine-induced c-Fos expression in the caudate-putamen of males, it completely blocked this response in females. With dizocilpine maleate alone, there was little or no effect on behavior in male rats, whereas in female rats, it caused head bobbing, thrashing, hyperactivity and uncoordinated movements. These behavioral sex differences were not seen on treatment of rats with the competitive N-methyl-D-aspartate receptor antagonist 2R,4R,5S-2-amino-4,5-(1,2-cyclohexyl)-7-phosphoheptanoic acid (NPC-17742; 10 mg/kg, i.p.) and this drug did not induce c-Fos expression in either sex. In the caudate-putamen, morphine-induced c-Fos expression was significantly reduced by NPC-17742 (30 min before morphine) in males and completely blocked in females. These results suggest that the responses to both morphine and N-methyl-D-aspartate receptor antagonists differ between the sexes and emphasize that glutamate is involved in morphine-induced immediate early gene expression in the brain. These studies thus have important implications for gender differences in drug addiction.

Comparison of different dietary magnesium supplements on pork quality.

Forty-eight crossbred (Large White×Landrace) boars were used to compare the effect of dietary magnesium aspartate (MgAsp), magnesium sulphate (MgSO(4)) and magnesium chloride (MgCl(2)) on muscle glycogenolysis and pork quality. The pigs were fed finisher feed supplemented with either MgAsp, MgSO(4) and MgCl(2) for 5 days prior to slaughter. At the abattoir, all pigs received 15 electric shocks from an electric goad 5min prior to slaughter. Pigs fed the diet supplemented with MgSO(4) had the highest plasma Mg concentrations at slaughter in comparison with pigs fed the MgAsp and MgCl(2) supplemented diets. There were no differences in plasma adrenaline and noradrenaline concentrations at slaughter between the different diets. Pigs fed the Mg diets had higher muscle glycogen concentrations in the Longissimus thoracis (LT) muscle at 5min and at 40min (except MgCl(2)) post-slaughter compared to pigs fed the control diet. Also pigs fed the Mg diets had lower muscle lactic acid concentrations in the LT at 5min post-slaughter and lower drip loss at 24hr post-slaughter compared to pigs fed the control diet. These results indicate that cheaper magnesium sources, MgSO(4) and MgCl(2), are as efficacious as MgAsp in reducing drip loss and improving pork quality.

The effect of dietary magnesium aspartate supplementation on pork quality.

Large White x Landrace boars (n = 48) were used to determine the effect of dietary magnesium aspartate supplementation (MgAsp) on subsequent stress and meat quality indicators. Dietary MgAsp supplementation increased plasma magnesium levels compared with pigs fed the control diet. Pigs fed the MgAsp-supplemented diet had lower norepinephrine concentrations at slaughter than pigs fed the control diet. Pigs fed the MgAsp-supplemented and the control diet had similar glycogen concentrations in the longissimus thoracis (LT) and biceps femoris (BF) muscle, whereas pigs fed the MgAsp-supplemented diet had lower lactic acid in the LT and BF muscle compared to pigs fed the control diet. Negative handling of pigs before slaughter reduced muscle glycogen in the LT and the BF muscle and increased the lactic acid levels in the LT and BF muscle compared to when pigs were minimally handled at the abattoir. Comparison of meat quality traits indicates that MgAsp supplementation to pigs raised the muscle pH in the LT muscle at 40 min and 24 h after slaughter. Pigs that were fed the MgAsp-supplemented diet had lower percentage of drip loss, lower surface lightness L, and had no PSE carcasses compared to pigs fed the control diet. Also, pigs that were fed the control diet and negatively handled at the abattoir before slaughter had the highest percentage of drip loss and incidence of PSE compared to other treatment groups. The results indicate that dietary MgAsp supplementation to pigs can significantly improve ultimate meat quality and reduce the incidence of PSE meat.