Effect of dietary magnesium level on nephrocalcinosis and growth in rats

We studied the extent of kidney calcification by varying dietary levels of Mg, based on pathological examinations and calcium (Ca) and magnesium (Mg) balance tests. AIN-76 diets containing varying levels of Mg--0.3 (-M), 1.3 (1/20M), 2.4 (1/10M), 9.2 (1/5M), 19 (control), 38 (2M), 102 (5M), and 187 (10M) mmol/kg diet--were fed to 3-week-old male Fischer-344 rats for 14d. Although the magnitude of abnormality was highest in kidney of rats fed the -M diet, the damage was normalized as the dietary level of Mg increased, with increasing serum Mg concentration and urinary excretion of Mg. We found almost no deposition of Ca in rats fed the 10M diet. The mechanism by which the high dietary Mg induces these effects most likely involves a competition between Mg and Ca for reabsorption in proximal and/or distal tubules, since these diets increased the urinary excretion of Ca. However, these high Mg diets decreased food intake and body weight gain compared with the control diet, although these indices were not decreased in rats fed the 2M diet. The results suggest that a dietary magnesium level approximately twice the normal level effectively reduces kidney calcification while maintaining normal growth in rats.     

Characterization of dose-dependent metabolic responses to close arterial infusion of cimaterol in the hindlimb of steers

Dose-dependent effects of cimaterol (CIM) on hindlimb metabolism were determined in six steers (247 +/- 22 kg BW) using a close arterial infusion. The external iliac vessels of both hindlimbs were catheterized to accommodate measurement of blood flow, circulating concentrations, and net flux of NEFA, lactate, and alpha-amino nitrogen (AAN) during infusion of CIM at 0, .05, .1, .3, .7, 1 and 3 micrograms/ min. Close arterial infusion of CIM in the hindlimb of steers can be used to achieve a local concentration elevation that is required to differentiate local and systemic effects in vivo. Calculated plasma threshold CIM concentration required to initiate cardiovascular responses was 21 pg/mL, which resulted from an infusion rate of .3 microgram/min. Threshold concentrations of CIM for stimulation of NEFA and lactate net flux in the hindlimb were 38 and 34 pg/mL, respectively, and would be achieved with an infusion rate of .7 microgram/min. All measured responses except AAN net flux exhibited significant linear and quadratic dose effects, and responses in the treated hindlimb were always severalfold greater than in the contralateral control hindlimb. Maximal differences between treated and control hindlimb blood flow occurred with a CIM infusion rate of .7 microgram/min, but the highest infusion rate (3 micrograms/min) was required to maximize differences in NEFA and lactate flux. Therefore, to minimize cardiovascular and other systemic responses and optimize direct hindlimb responses, an infusion rate of .5 microgram of CIM/ min should cause significant stimulation of beta-adrenergic receptors only in the CIM-infused hindlimb of young, growing steers.     

Effects of laidlomycin propionate and monensin on glucose utilization and nutrient transport by Streptococcus bovis and Selenomonas ruminantium

The objective of this study was to compare the effects of laidlomycin propionate and monensin on cell growth, glucose fermentation, and glucose uptake in Streptococcus bovis strain JB1 and Selenomonas ruminantium strain HD4. Experiments were also conducted to compare the effects of both ionophores on sodium-dependent serine transport and cell yield in S. bovis. Batch cultures (500 mL) of each bacterium were grown on 3.6 g/L D-glucose in semidefined medium and treated with either 5 ppm monensin or 2 ppm laidlomycin propionate (n=2). Cell growth was monitored by measuring optical density at 600 nm (OD600). Glucose and L-lactate concentrations were measured using coupled enzyme assays. In S. bovis, both monensin and laidlomycin propionate decreased OD600, glucose utilization, and L-lactate production. Neither ionophore had any effect on glucose utilization by S. ruminantium. [14C]Glucose uptake between 5 and 30 min by both bacteria was not altered by either ionophore. Sodium-dependent [14C]serine uptake by S. bovis was inhibited by monensin but not laidlomycin propionate. When S. bovis was grown in glucose-limited continuous culture (dilution rate=.10 h(-1)) at extracellular pH 6.7, increasing concentrations of both ionophores decreased bacterial yield, and both ionophores were more potent at an extracellular pH of 5.7. However, monensin was a more potent inhibitor than laidlomycin propionate at pH 6.7 and 5.7. Collectively, these results suggest that the ionophore laidlomycin propionate inhibits the Gram-positive bacterium S. bovis in a manner similar to that of monensin, but, at the concentrations used in this study, laidlomycin propionate seems to be less potent than monensin in inhibiting serine uptake and cell yield.     

Effect of amino acid supplementation on whole-body protein turnover in Holstein steers

We used the [15N]glycine single-dose urea end-product technique to measure whole-body protein turnover in six Holstein steers (250 +/- 18 kg). Steers were implanted with Revalor-S and continuously infused abomasally with water (4 L/d) or amino acids (AA; in 4 L/d water) in a crossover experiment (two 14-d periods). The AA infusion contained the following (g/d): lysine (5.3), methionine (3.3), threonine (3.2), tryptophan (1.0), histidine (2.1), and arginine (5.5). Steers were fed a diet containing 85% rolled corn, 10% prairie hay, and 1.1% urea (DM basis) at 2.16% of body weight. Nitrogen retention tended (P = .15) to increase with AA infusion, from 27.9 to 32.9 g N/d. Amino acid infusion numerically increased whole-body protein turnover from 168.6 to 183.2 g N/d, protein synthesis from 152.6 to 169.3 g N/ d, and protein degradation from 124.7 to 136.4 g N/d. Enhanced protein accretion may have resulted from a larger increase in protein synthesis than in degradation. The tendency for increased N retention is interpreted to suggest that the implanted, lightweight Holstein steers fed a corn-urea diet in our study were able to respond to AA supplementation, suggesting that at least one of the infused AA was limiting in the basal diet. Protein turnover data suggest that cattle, like other animals, may increase protein synthesis and protein degradation in response to supplementation with limiting AA. The [15N]glycine single-dose urea end-product technique for measuring whole-body protein turnover in cattle may be useful.     

Effects of a dietary mixture of meat and bone meal, feather meal, blood meal, and fish meal on nitrogen utilization in finishing Holstein steers

Our objective was to determine to what extent rate and efficiency of protein gain in finishing cattle can be enhanced by feeding an amino acid-balanced mixture of undegraded intake proteins. The Cornell Net Carbohydrate and Protein System (CNCPS) model was used to formulate a corn-based diet that would meet the rumen requirements for 410-kg large-framed steers with an estrogen implant and fed an ionophore. The CNCPS model was also used to formulate a highly undegradable intake protein (UIP) mixture from meat and bone meal, blood meal, fish meal, and hydrolyzed feather meal to provide the amino acids needed to supplement those derived from microbial protein to better meet amino acid requirements for growth. Four Holstein steers weighing 407 kg were offered a 90:10 concentrate-forage diet at hourly intervals at 95% of ad libitum intake. The steers were injected with 500 microg of estradiol-17beta at 12-h intervals to mimic the effects of an estrogenic implant. Treatments planned consisted of inclusion of the UIP mixture at 0, 2.5, 5, and 7.5% of the diet DM. Dry matter intake was fixed at 6.4 kg/d, and DM digestibility was not significantly affected by varying the amount of UIP addition. Apparent digestibility of N increased (P = .011) from 63.8 to 65.8, 70.7, and 71.5%, the amount of N absorbed increased (P = .001) from 73 to 84, 100, and 106 g/d, and N balance increased (P = .003) from 20 to 30, 33, and 39 g/d when UIP was fed at 0, 2.6, 5.2, and 7.8% of diet DM, respectively. The efficiency of N use increased 39.7%, and biological value increased 31.6% when the UIP mixture was added to the diet. Circulating concentrations of plasma urea N (PUN) were increased (P = .017) from 4.5 for the control diet to 5.7, 6.2, and 6.1 mg/dL when the UIP mixture was added at 2.6, 5.2, and 7.8%, respectively. Corresponding IGF-I concentrations were also increased from 491 to 558 and 624 ng/mL with 2.6 and 5.2% levels of UIP addition. Plasma glucose, NEFA, and insulin concentrations were not affected by feeding the UIP mix. The rate and efficiency of N use for growth improved with addition of an amino acid-balanced UIP mixture to the diet.     

Lasalocid effects on ruminal degradation of protein and postruminal supply of amino acids in Holstein steers

Five ruminally and duodenally cannulated Holstein steers (305 kg) were used in a switchback experiment with three periods to evaluate two experimental treatments: a basal diet with or without 45 ppm of lasalocid. The basal diet contained approximately 43% rolled corn, 45% alfalfa hay, and 10% soybean meal (DM basis). Lasalocid did not affect feed intake or ruminal digestion of OM and NDF. Ruminal digestion of ADF tended to increase with supplemental lasalocid. Total tract digestion of OM, NDF, ADF, and N and intestinal flow of amino acids were not affected by lasalocid. Also, the ratio of microbial to nonmicrobial N fractions at the duodenum remained unchanged. Ruminal pH and concentrations of NH3, VFA, peptides, and amino acids were not affected by lasalocid. Ruminal protease activity decreased with supplemental lasalocid, but this decrease was not reflected in other variables, such as ruminal concentrations of peptides and amino acids. Ruminal deaminase activity remained unchanged. Thus, we concluded that dietary lasalocid did not alter ruminal protein degradation or postruminal flow of amino acids.     

Influence of dietary sulfur level on growth performance and digestive function in feedlot cattle

Using ammonium sulfate, three levels of dietary S (.15, .20, and .25%, DM basis) were evaluated in a finishing trial with 108 yearling crossbred heifers (384 kg). The basal diet contained (DM basis) 4% alfalfa hay, 6% sudangrass hay, 74% steam-flaked corn, 4% yellow grease, 6% cane molasses, and 6% protein-mineral supplement. Increasing dietary S decreased ADG (quadratic effect, P < .10), DMI (linear effect, P < .10), feed efficiency (quadratic effect, P < .10), diet NE (quadratic effect, P < .10), and longissimus muscle area (linear effect, P < .05). Six Holstein steers (218 kg) with cannulas in the rumen and proximal duodenum were used to evaluate treatment effects on characteristics of digestion. Treatment effects on ruminal and total tract digestion of OM and N were small (P > .10). However, ruminal digestion of ADF and starch was slightly lower (quadratic effect, P < .10), and postruminal digestion of ADF and starch was correspondingly greater (quadratic effect, P < .05) with supplemental S. Dietary S level did not influence (P > .10) ruminal synthesis of microbial N. Increasing dietary S did not influence (P > .10) ruminal pH or lactic acid. Increasing S decreased molar proportions of acetate (quadratic effect, P < .10) and increased molar proportions of propionate (linear effect, P < .10). We conclude that S in excess of .20% of dietary DM may have detrimental effects on growth performance and dietary NE. Excessive dietary S may also compromise carcass merit by decreasing longissimus muscle area.     

Metabolic responses to dietary supplements of bran

During a metabolic ward study, the addition of dietary fiber in the form of wheat bran biscuits to the diet of five volunteer subjects resulted in an increase in the stool wet weight and fecal solids. The excretion of fecal solids was highly correlated with the intake of unavailable carbohydrates, and fecal losses of water were similarly correlated with fecal excretion of these constituents. The major component of the increase in fecal solids was due to the noncellulosic polysaccharide fraction of dietary fiber. There was an increased fecal excretion of nitrogen fat and energy by most subjects when the supplement was eaten. However, the increased loss of energy in the feces was only 40-80 kcal/day, and therefore a large supplemental intake of dietary fiber had only minor effects on energy metabolism. Supplemental fiber is thus unlikely to induce a useful loss of calories in the management of obesity. The addition of dietary fiber caused an increased excretion of most inorganic constituents, particularly sodium and phosphorus; increased excretion of iron and magnesium was also found in two subjects.     

Influence of dietary capsaicin and onion on the metabolic abnormalities associated with streptozotocin induced diabetes mellitus

This case report describes a 3-year-old American Quarter Horse with acquired immunodeficiency. Clinical signs included chronic diarrhea due to Salmonella typhimurium and bacterial pneumonia. Characterization of the immunodeficiency involved in vivo phytohemagglutinin (PHA) intradermal testing, in vitro lymphocyte proliferation in response to concanavalin A, immunofluorescence flow cytometry data on blood lymphocytes, serum protein electrophoresis and immunoglobulin (Ig) quantification. A diagnosis of B lymphocyte deficiency with resulting deficiencies in serum IgG, IgA and IgM and a concurrent decrease in T cell function was made based on these tests. Postmortem examination revealed no evidence of lymphosarcoma. This case represents a variation of young adult-onset B cell deficiency not previously described in the literature.     

Genome-linked toxic responses to dietary iron overload

Genome-related differences to Fe overload between and within rodent species were evaluated in the present study. Male B6C3F1 mice, yellow and black C5YSF1 mice, and Fischer 344 (F344) rats were fed AIN-76A diets containing 35 (control), 1,500, 3,500, 5,000, or 10,000 micrograms carbonyl Fe/g for 12 wk. No effects on body weight gain were observed in the B6C3F1 and black C5YSF1 mice, whereas at all doses of Fe above the control, weight gain was reduced in yellow C5YSF1 mice and F344 rats. At the 10,000 micrograms Fe/g dose, 9 of 12 rats died, but there was no mortality among the mice. In all animals, there was a dose-related increase in liver nonheme Fe, and the Fe was stored in hepatocytes predominantly in the periportal region. There was significant hypertrophy of the hepatocytes in both B6C3F1 mice and F344 rats fed the 10,000 micrograms Fe/g diet. PCNA assays showed significant stimulatory effects of the high dose of Fe on hepatocyte proliferation in the F344 rats and the C5YSF1 mice but not in the B6C3F1 mice. In the rat, there was pancreatic atrophy with loss of both endocrine and exocrine tissue. Morphometric evaluation of pancreas showed fewer beta cells in B6C3F1 and yellow C5YSF1 mice but not in the black C5YSF1 mice. There were fewer islets in the yellow C5YSF1 mice, and total and mean islet areas were smaller than in the control mice. Rats in the 10,000 micrograms Fe/g dose group had markedly exacerbated dose-dependent nephropathy and changes in glomerular and tubular epithelium associated with Fe accumulation. The rats also showed degeneration of the germinal epithelium of the testis, formation of multinucleated giant cells, and lack of mature sperm.     

Metabolic responses of postmenopausal women to supplemental dietary boron and aluminum during usual and low magnesium intake: boron, calcium, and magnesium absorption and retention and blood mineral concentrations

The regulation by neuropeptide Y of alpha2-adrenoceptors in the nucleus tractus solitarii was evaluated in the adult normotensive Wistar Kyoto rat and the adult spontaneously hypertensive rat. The microinjection of a submaximal dose of l-noradrenaline (800 pmol in 50 nl) alone into the nucleus tractus solitarii produced a significant reduction in the mean arterial blood pressure in either strain. The threshold dose (1 pmol in 50 nl) of neuropeptide Y(1-36) for the vasodepressor response in the Wistar Kyoto rat was five times higher than that (0.2 pmol in 50 nl) in the spontaneously hypertensive rat. Furthermore, neuropeptide Y(1-36) at 0.2 pmol in 50 nl could significantly counteract the vasodepressor response to l-noradrenaline (800 pmol in 50 nl) in the spontaneously hypertensive rat, but not in the Wistar Kyoto rat, in which 1 pmol in 50 nl of neuropeptide Y(1-36) must be employed to counteract the vasodepressor response to l-noradrenaline (800 pmol in 50 nl), although the vasodepressor responses are of a similar magnitude. The in situ hybridization and quantitative receptor autoradiographical experiments showed that the alpha2A-adrenoceptor messenger RNA levels and the B(max) value of the alpha2-adrenoceptor agonist [3H]p-aminoclonidine binding sites measured in the nucleus tractus solitarii of the spontaneously hypertensive rat were substantially lower than those in the Wistar Kyoto rat. The quantitative receptor autoradiographical results were consistent with the cardiovascular results and showed that in the spontaneously hypertensive rat, neuropeptide Y(1-36) at 1 nM led to a significant increase in the K(d) value of [3H]p-aminoclonidine binding sites. In the Wistar Kyoto rat, neuropeptide Y(1-36) produced this effect only at 10 nM. The present study provides evidence for an increase of the potency of neuropeptide Y(1-36) to antagonistically modulate alpha2-adrenoceptors in the nucleus tractus solitarii of the spontaneously hypertensive rat. This enhanced antagonistic action may partly be related to a reduction in the number of alpha2A-adrenoceptors in the nucleus tractus solitarii of the spontaneously hypertensive rat, since a decrease has been observed in the alpha2A-adrenoceptor messenger RNA levels and the alpha2-adrenoceptor binding sites in the spontaneously hypertensive rat. This increased potency of neuropeptide Y(1-36) to antagonize alpha2-adrenoceptor function in the nucleus tractus solitarii of the spontaneously hypertensive rat may contribute to the development of high blood pressure in this hypertensive strain.     

Mechanism of coronary microvascular responses to metabolic stimulation

Previous studies from our laboratory have shown that coronary microvascular dilation to increased myocardial oxygen consumption (MVO2) is greater in vessels < 100 microns. The mechanism responsible for this response is uncertain. OBJECTIVES: We tested the hypothesis that microvascular dilation to increased MVO2 is mediated by nitric oxide (NO). Since NO release may occur in response to increased shear, we also tested the hypothesis that metabolic byproducts released in response to increase in MVO2 will stimulate opening of the ATP-sensitive potassium channel. METHODS: Changes in epicardial coronary microvascular diameters were measured in 9 dogs given NG-nitro-L-arginine (LNNA; 100 microM, topically), 7 dogs given glibenclamide (10 microM, topically) and 12 control (C) dogs during increases in metabolic demand using dobutamine (DOB, 10 micrograms/kg/min, i.v.) with rapid atrial pacing (PAC, 300 bpm). Diameters of arterioles were measured using intravital microscopy coupled to stroboscopic epi-illumination. RESULTS: During the protocol, MVO2 increased to a similar degree in both experimental groups (LNNA and glibenclamide). Baseline hemodynamics and coronary microvascular diameters were similar between the two experimental groups and their respective control groups. In the presence of LNNA, coronary arteriolar (< 100 microns) dilation (% change from baseline) was impaired during the protocol (DOB: vehicle 18 +/- 5, LNNA 2 +/- 2 [P < 0.05]; DOB + RAP: vehicle 40 +/- 11, LNNA 6 +/- 2% [P < 0.05]). In contrast, glibenclamide did not impair coronary microvascular responses to increased MVO2 despite increases in MVO2. CONCLUSION: This study indicates that coronary microvascular dilation in response to increased metabolic stimulation using dobutamine in conjunction with rapid pacing is mediated through a nitric-oxide-dependent mechanism and not ATP-sensitive potassium channels. These results may have important implications in pathological disease states where nitric oxide mechanisms are impaired, such as diabetes and hypertension.     

Parallel metabolic and feeding responses to lateral hypothalamic stimulation

Energy metabolism and food intake effect each other. Many studies demonstrated that the lateral hypothalamus (LH) participates in the control of both feeding behavior and energy metabolism. We assessed the effect of a bipolar near threshold feeding eliciting electrical stimulation of the LH first on the feeding response and then on the background metabolism (metabolism free from the part due to locomotion) and respiratory quotient (RQ), on Wistar male rats, during either the light or the dark phase of the nycthemeron. LH stimulation resulted in a delayed and rather long increase in background metabolism that was more dramatic during the light phase. This metabolic response paralleled the delayed feeding response (more than 10 min) we obtained during behavioral tests. The increase in energy production was sustained by release of energy substrates from the endogenous stores, and this showed a circadian dependence. Mainly carbohydrates (rise in RQ) were used during the light phase stimulation whereas lipids (decrease in RQ) were released in the dark phase.     

Influence of pregnancy on dietary selection

Three interrelated symptom ' complexes' are implicated in dietary changes during pregnancy: nausea and vomiting of pregnancy (NVP), dietary aversions, and dietary cravings. These are discussed with particular emphasis on NVP and the fate of the fetus.     

Electrophysiological responses to coarticulatory and word level miscues.

The influence of coarticulation cues on spoken word recognition is not yet well understood. This acoustic/phonetic variation may be processed early and recognized as sensory noise to be stripped away, or it may influence processing at a later prelexical stage. The present study used event-related potentials (ERPs) in a picture/spoken word matching paradigm to examine the temporal dynamics of stimuli systematically violating expectations at three levels: entire word (lexical), initial phoneme (phonemic), or in coarticulation cues contained in the initial phoneme (subphonemic). We found that both coarticulatory and phonemic mismatches resulted in increased negativity in the N280, interpreted as indexing prelexical processing of subphonemic information. Further analyses revealed that the point of uniqueness differentially modulated subsequent early or late negativity depending on whether the first or second segment matched expectations, respectively. Finally, it was found that word-level but not coarticulatory mismatches modulated the later-going N400 component, indicating that subphonemic information does not influence word-level selection provided no lexical change has occurred. The results indicate that acoustic/phonetic variation resulting from coarticulation is preserved in and influences spoken word recognition as it becomes available, particularly during prelexical processing. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Influence of fluid replacement on serum magnesium concentration and proper magnesium supplementation during general anesthesia

We have established a convenient synthesis process for the synthesis of[18F]haloperidol using a single-step 18F-for-Cl exchange reaction and a new elution system for the preparative high performance liquid chromatography (HPLC) using C18 bonded vinylalcohol copolymer gel (ODP) and a basic eluent. We successfully applied the product to cat-PET study and got clear images of the striatum, showing the usefulness of this synthesis.     

Opioid-mediated responses of dietary protein on reticular motility and plasma insulin

This study explores the effects of infusion of nerve growth factor (NGF) on behavioral outcome and cell death in the septal region using the clinically relevant model of fluid-percussion brain injury in the rat. Animals were subjected to fluid-percussion brain injury and 24 hours later a miniosmotic pump was implanted to infuse NGF (12 animals) or vehicle (12 animals) directly into the region of maximum injury for 2 weeks. Four weeks postinjury the animals were tested for cognitive function using a Morris Water Maze paradigm. Neurological motor function was evaluated over a 4-week postinjury period. The rats receiving NGF infusions had significantly higher memory scores than vehicle-treated animals. Examination of the cholinergic neurons in the medial septal region using choline acetyltransferase immunohistochemistry demonstrated significant cell loss after injury. Infusion of NGF significantly attenuated loss of these cholinergic neurons. A second group of animals was subjected to fluid-percussion brain injury alone (23 rats) or injury followed by NGF infusion (18 rats). These animals were killed between 24 hours and 2 weeks postinjury and the septal region was examined for the presence of apoptotic cells using the terminal deoxynucleotidyl transferase-mediated biotinylated-deoxyuridinetriphosphate nick-end labeling technique. Apoptotic cells were identified as early as 24 hours postinjury; their numbers peaked at 4 and 7 days, and then declined by 14 days. The NGF-treated animals had some apoptotic cells; however, even at 7 days there were significantly fewer of these cells. No significant motor differences were observed between the NGF- and vehicle-treated groups. These data indicate that NGF administration beginning 24 hours after fluid-percussion brain injury has a beneficial effect on cognition and results in sparing of cholinergic septal neurons. These improvements persist after cessation of NGF administration. The beneficial effects of NGF may be related to its ability to attenuate traumatically induced apoptotic cell death.