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Biomedical subjects

J D Armstrong

Publications and source records attributed to J D Armstrong.

At least 37 records · Page 2Linked to original sources

Immunization against growth hormone releasing factor or chronic feed restriction initiated at 3.5 months of age reduces ovarian response to pulsatile administration of gonadotropin-releasing hormone at 6 months of age and delays onset of puberty in heifers.

A severe or moderate suppression of serum insulin-like growth factor I (IGF-I) was induced in heifers, beginning at 104 days of age, by active immunization against growth hormone-releasing factor (GRFi) or by chronic feed restriction (RES), respectively. We hypothesized that reduced serum IGF-I results in decreased serum estradiol-17 beta (E2), which in turn delays onset of puberty. The objectives of this experiment were to determine 1) whether GRFi and RES would alter follicular development and delay onset of puberty through similar mechanisms, and 2) whether GnRH would enhance follicular growth in control, GRFi, and RES heifers at 6 mo of age. Changes in IGF-I, somatotropin, LH, FSH, and E2 were evaluated. Serum IGF-I was greater in control than in RES heifers, and was greater in both these groups than in GRFi heifers by 169 days of age. Basal LH decreased in control and RES but not in GRFi heifers from 136 to 157 days of age. During the same period, a decrease in mean FSH was detected in control but not in GRFi and RES heifers. RES decreased mean serum E2 from 148 to 183 days of age. At 6 mo of age, pulsatile administration of GnRH (5 micrograms every 2 h for 42-46 h) increased serum LH and FSH similarly across treatments but had no effect on the number of follicles > or = 8 mm in GRFi and RES heifers relative to saline treatment. Serum E2 and IGF-I in follicular fluid from follicles > or = 8 mm were increased in all GnRH-treated heifers; however, concentrations of both hormones were lower in GRFi than in control or RES heifers. The main effect of treatments on serum IGF-I was reflected in follicles < or = 7 mm; follicular fluid IGF-I was greater in control than in RES heifers and was greater in both these groups than in GRFi heifers. Serum E2 was lower in RES than in control and GRFi heifers from 253 to 281 days of age. Because of an interaction, E2 was lower in GRFi-GnRH than in control-GnRH heifers but similar in GRFi-saline and control-saline heifers. By 393 days of age, 0% of RES and 32% of GRFi heifers had reached puberty compared to 71% of control heifers. These data support our hypothesis that decreased serum IGF-I results in decreased serum E2. GRFi appears to delay puberty in heifers because decreased serum IGF-I impairs the ovary's ability to synthesize preovulatory concentrations of E2, thereby delaying stimulation of an LH surge. In contrast, RES may delay puberty by delaying follicular development at two stages: a) decreased IGF-I in follicles < or = 7 mm may delay predominant follicular growth, and b) decreased LH may delay maturation of the preovulatory follicle.

Aging↗

Lung transplantation: indications, donor and recipient selection, and imaging of complications.

Lung transplantation has become a well-established treatment for end-stage pulmonary parenchymal and vascular disease. Careful selection of recipients and donors is important to decrease early graft failure, which is primarily due to rejection and bronchial dehiscence. Common complications include the reimplantation response, acute rejection, pleural effusion, lymphoproliferative disorders, bronchiolitis obliterans, infection, and airway stenosis or dehiscence. The reimplantation response is a form of noncardiogenic pulmonary edema that begins soon after surgery and resolves in days to weeks. Acute rejection occurs in most recipients; a dramatic response to steroid therapy is the most diagnostic clinical feature. Lymphoproliferative disorders are posttransplantation neoplasms that may disappear when immunosuppressive therapy is stopped and often manifest as a discrete lung mass. In bronchiolitis obliterans-a major long-term complication probably due to chronic rejection-computed tomography (CT) often shows bronchial dilatation and air trapping. Airway stenosis and dehiscence are easily diagnosed with bronchoscopy and CT. Infections remain the major cause of morbidity and mortality.

Adult↗

Ovarian expression of insulin-like growth factor-I (IGF-I), IGF binding proteins, and growth hormone (GH) receptor in heifers actively immunized against GH-releasing factors.

Active immunization against GRF at 6 months of age delays puberty in beef heifers. The objectives of the present study were to determine whether active immunization against GRF at an earlier age would affect normal onset of puberty and follicular growth and to determine whether these changes were related to alterations in ovarian insulin-like growth factor I (IGF-I) or IGF binding protein (IG-FBP) messenger RNA (mRNA) levels. Heifers were immunized against human serum albumin (HSAi; n = 15) or against GRF conjugated to HSA (GRFi; n = 18) at 3 months of age. A third group of heifers was not immunized (CON; n = 16). Immunization against GRF delayed puberty beyond 13 months of age in 75% of treated heifers. Unilateral ovariectomy at 191 days of age revealed that the delay in puberty was associated with a reduction in the number of large ( > or = 7 mm in diameter) follicles. Large follicles were present in only 22% of GRFi heifers compared to 77% of HSAi heifers. The number of small ( < or = 3 mm in diameter) and medium (4 to 6 mm in diameter) follicles was not affected by GRFi. The percentage of 1- to 3-mm follicles that were atretic was not different between HSAi (65%) and GRFi (62%) heifers. Unilateral ovariectomy had no effect on age at puberty. Immunization against GRF decreased (P < 0.01) concentrations of IGF-I in serum (23 +/- 2 ng/ml) compared to HSAi heifers (109 +/- 11 ng/ml). IGF-I levels in follicular fluid (FFL) of medium and small follicles were also decreased by GRFi from 82 +/- 3 ng/ml in HSAi heifers to 48 +/- 6 ng/ml (P < 0.01). Levels of IGFBP-3 (determined by ligand blot analysis) in serum and FFL of small follicles were decreased by GRFi (P < 0.01). In contrast, IGFBP-2 serum levels were increased from 422 +/- 32 ng/ml in HSAi heifers to 657 +/- 6 ng/ml in GRFi heifers (P < 0.05). Likewise, IGFBP-2 levels in FFL from small and medium follicles were increased from 785 +/- 44 ng/ml to 926 +/- 44 ng/ml (P < 0.05). Ligand blot analysis indicated that IGFBP levels were lower in FFL from large vs. small follicles. The band intensities of IGFBP-4 and -5 were drastically reduced ( > 80%) while the decreases in IGFBP-2 and -3 were less marked ( < 50%). The decreased levels of IGFBP-5 in FFL from large follicles was not associated with an increase in proteolytic fragments detectable by immunoblot analysis. While mRNA transcripts for IGF-I, GH receptor, and IGFBP-2, -3, -4, and -5 were readily detectable in ovarian tissue, GRFi had no effect on ovarian levels of mRNA for each of these proteins. This suggests that the decrease in follicular development associated with GRFi may be related to changes in circulating IGF-I and/or IGFBPs.

Animals↗

N-methyl-D,L-aspartate-induced growth hormone secretion in barrows: possible mechanisms of action.

Four experiments were conducted to determine mechanisms by which n-methyl-d,l-aspartate (NMA) increases serum concentrations of growth hormone (GH). Blood samples were collected from barrows every 15 min for 2 h (Exp. 1, 2, and 3) or 3 h (Exp. 4) immediately before and immediately after i.v. treatments. In Exp. 1, barrows (n = 4/treatment) received either .9% saline or 1.25, 2.5, or 5 mg of NMA/kg of BW. The change in circulating GH concentrations was greater (P < .05) for barrows receiving 2.5 mg (by 883%) or 5.0 mg of NMA/kg of BW (by 1,095%) than for those injected with saline. In Exp. 2, barrows (n = 4/treatment) received NMA (2.5 mg/kg of BW) or injections of 1.25 mg of the pure d or pure 1 isomers of NMA/kg of BW. Growth hormone concentrations increased by 177% (P < .025) after NMA treatment and by 245% (P < .01) after injection of the pure d isomer of NMA. The pure 1 isomer of NMA had no effect (P > .1) on GH concentrations. In Exp. 3, barrows received NMA (2.5 mg/kg of BW) 10 min after i.m. injection of saline (n = 7) or ketamine hydrochloride ( n = 8; 19.9 mg/kg of BW), an n-methyl-d-aspartate (NMDA) receptor antagonist. The NMA increased (P < .01) GH concentrations by 289% in saline-pretreated barrows but had no effect (P > .1) on barrows pretreated with ketamine hydrochloride. In Exp. 4, barrows (n = 4/treatment) received NMA 3 h after i.v. pretreatment with antisera to GH-releasing factor (GRF; 154 mL) or no pretreatment. Serum GH concentrations increased by 166% (P < .05) after injection of NMA in barrows receiving no pretreatment. The NMA had no effect (P > .1) on GH concentrations in barrows receiving antisera to GRF. Our results support the concept that NMDA stimulates GRF, and hence GH secretion, by activating an NMDA receptor.

Animals↗

Perforation of the great vessels during central venous line placement.

BACKGROUND: Placement of central venous lines for the administration of a variety of therapies has become common practice. The most severe complication of this procedure is perforation of a large vessel, with bleeding, infusion of fluids into an extravascular site, and death. It is not clear from currently available data how often this occurs, what risk factors are associated, and how this complication can be avoided. METHODS: We reviewed the records of all patients who were identified as having perforation of a major vessel during central venous line placement occurring between 1986 and 1993 at the University Hospital, the major teaching facility of the University of Colorado Health Sciences Center, Denver. Data collected included the age and sex of the patient, diagnosis, type of catheter and site of placement, operator means and time to the diagnosis of perforation, and outcome. RESULTS: Eleven such complications were identified and 10 of them are reviewed in detail. The overall incidence was less than 1%. Most complications occurred when the right subclavian vein approach was attempted, and they were thought to result from guidewire kinking during advancement of a vessel dilator. All medical specialties and levels of training were involved. Four of 10 patients died of immediate or subsequent complications of the perforation. CONCLUSIONS: Perforation of a great vessel is an uncommon, but often fatal, complication of central venous line placement. It occurs most often, when using the right subclavian vein approach, from guidewire kinking. Physicians performing this procedure should have formal training in central venous catheterization and be aware of this complication, its presumed cause, diagnosis, and treatment.

Adult↗

Myosin heavy chain expression within the tapered ends of skeletal muscle fibers.

BACKGROUND: The pectoralis muscle of the chicken contains fast-twitch glycolytic fibers, which during development undergo a transformation in their myosin heavy chain (MyHC) content from embryonic to a neonatal to an adult isoform (Bandman et al., 1990). Little, however, is known of MyHC expression within the ends of these or other muscle fibers. Here we test the hypothesis that the tapered ends of mature skeletal muscle fibers contain a less mature MyHC isoform than that typically found throughout their lengths. METHODS: We apply an ammoniacal silver histological stain for endomysium and monoclonal antibodies against neonatal and adult MyHCs of chicken pectoralis to transverse serial sections of pectoralis from five mature chickens. The "lesser fiber diameters" of populations of fibers from each bird are also measured. RESULTS: Most (approximately 81.8%) of the small (< 12 microns) and none of the larger (> 20 microns) diameter fibers contain the neonatal MyHC. Following these smaller fibers through serial sections, we show that they are the tapered ends of the larger fibers. Whereas neonatal MyHC is restricted to the tapered fiber ends, adult MyHC is present throughout the entire lengths of all fibers. We also demonstrate acetylcholinesterase (AChE) activity at some of these fiber ends. CONCLUSIONS: We postulate that longitudinal growth of myofibrils in adult muscle is characterized by the sequential expression of MyHC isoforms similar to that observed in rapidly growing muscle and that the presence of the neurotransmitter hydrolase AChE at the tapered fiber ends may be related to the retention of neonatal MyHC.

Acetylcholinesterase↗

Excision repair and gene orientation modulate the strand specificity of UV mutagenesis in a plasmid-borne yeast tRNA gene.

Ultraviolet (UV) mutagenesis in a plasmid-borne Saccharomyces cerevisiae tRNA gene (SUP4-o) occurs preferentially at sites where the pyrimidine in the base pair is part of a dipyrimidine sequence on the transcribed strand. In this study, we examined whether excision repair, or strand identity with respect to DNA replication, influences this strand bias. The specificity of UV mutagenesis was determined for a wild type (RAD) strain and an isogenic excision repair-deficient (rad1) derivative, each carrying SUP4-o on the vector YCpMP2, or another vector (YCpJA1) that differed only in the orientation of SUP4-o with respect to a unique origin of replication. Most (> or = 90%) of the SUP4-o mutations induced by UV in these strains were single base pair substitutions, predominantly (> 87%) transitions. The rad1 defect and inversion of SUP4-o in the RAD strain eliminated the strand preference, whereas inversion of SUP4-o in the rad1 strain caused it to reappear. Both conditions also altered the distribution of frequently mutated sites and the relative fraction of transitions at TT sequences. These results suggest that excision repair and gene orientation can be important determinants for the strand and site specificities of UV mutagenesis in SUP4-o on YCpMP2 and YCpJA1. We consider several possible explanations for our observations, including potential roles for transcription by RNA polymerase II, sequence context effects on the efficiency of excision repair, and inherent differences in strand mutability or translesion synthesis by the leading and lagging strand DNA replication complexes.

Base Sequence↗

Subdivision of the Drosophila mushroom bodies by enhancer-trap expression patterns.

Phylogenetically conserved brain centers known as mushroom bodies are implicated in insect associative learning and in several other aspects of insect behavior. Kenyon cells, the intrinsic neurons of mushroom bodies, have been generally considered to be disposed as homogenous arrays. Such a simple picture imposes constraints on interpreting the diverse behavioral and computational properties that mushroom bodies are supposed to perform. Using a P[GAL4] enhancer-trap approach, we have revealed axonal processes corresponding to intrinsic cells of the Drosophila mushroom bodies. Rather than being homogenous, we find the Drosophila mushroom bodies to be compound neuropils in which parallel subcomponents exhibit discrete patterns of gene expression. Different patterns correspond to hitherto unobserved differences in Kenyon cell trajectory and placement. On the basis of this unexpected complexity, we propose a model for mushroom body function in which parallel channels of information flow, perhaps with different computational properties, subserve different behavioral roles.

Animals↗

Functional dissection of the Drosophila mushroom bodies by selective feminization of genetically defined subcompartments.

Relatively little is known about the neural circuitry underlying sex-specific behaviors. We have expressed the feminizing gene transformer in genetically defined subregions of the brain of male Drosophila, and in particular within different domains of the mushroom bodies. Mushroom bodies are phylogenetically conserved insect brain centers implicated in associative learning and various other aspects of behavior. Expression of transformer in lines that mark certain subsets of mushroom body intrinsic neurons, and in a line that marks a component of the antennal lobe, causes males to exhibit nondiscriminatory sexual behavior: they court mature males in addition to females. Expression of transformer in other mushroom body domains, and in control lines, has no such effect. Our data support the view that genetically defined subsets of mushroom body intrinsic neurons perform different functional roles.

Animals↗

Recombinant bovine somatotropin increases milk yield and calf gain in diverse breeds of beef cattle: associated changes in hormones and indices of metabolism.

In Exp. 1, Angus (A, n = 30), Charolais (C, n = 37), and Simmental (S, n = 30) multiparous cows received (s.c.) recombinantly derived bovine somatotropin (bST; sometribove, 500 mg) or vehicle (VEH) at 2-wk intervals from 124 to 228 d postpartum (DPP). Calves were weaned at 228 DPP. Bovine somatotropin increased (P < .01) milk yield and percentage of milk fat similarly in A, C, and S cows. Calf weaning weight was greater (P < .05) in cows treated with bST than in those given VEH. Administration of bST decreased deposition of fat and increased concentrations of IGF-I, insulin, glucose, and nonesterified fatty acids. In Exp. 2, we compared effects of bST initiated before or after the breeding season. Charolais (n = 33) and S (n = 40) cows were administered (at 2-wk intervals) VEH or bST beginning at 28 DPP (B-bST) or bST beginning at 105 DPP (A-bST). Calves were weaned at 243 DPP. Administration of bST before or after the breeding season increased milk yield on DPP 136 and 194; however, yields were greater in A-bST than in B-bST cows. Milk yields were similar in all cows at 236 DPP, corresponding to decreased forage availability. Calf body weight was greater (P < .05) in A-bST than VEH; B-bST calves were similar to VEH. Fat depth was greater in VEH than in bST-treated cows in C but not in S cows. Serum IGF-I was greater in A- and B-bST than in VEH cows. Mean days from calving to serum progesterone > 1 ng/mL and pregnancy rates were similar in VEH, A-, and B-bST cows. Administration of bST increased cow milk yield and subsequent calf weaning weight when initiated after 100 d postpartum. As anticipated, bST increased IGF-I, insulin, glucose, and nonesterified fatty acids. Administration of bST before and during the breeding season did not affect reproductive performance.

Animals↗

Subclinical mastitis and milk production in primiparous Simmental cows.

The prevalence of subclinical mastitis in beef cows was investigated and its relationship with milk production and 205-d adjusted calf weaning weights (ADJWW) determined. Primiparous Simmental cows (n = 25) were milked six times at approximately 30-d intervals. Before each milking, milk samples were aseptically collected from each quarter for bacteriological analyses. After recording milk weights, samples were obtained for determination of somatic cell counts (SCC), butterfat (BF), and protein (PRO). Somatic cell counts were transformed to Dairy Herd Improvement Association linear scores for statistical analyses. Cows were retrospectively assigned to one of two groups based on their SCC linear score being either less than (LOSCC) or more than (HISCC) 4.5, which corresponded to a SCC of 292 x 10(3) cells/mL. Milk samples from 32% (8/25) of the cows and 18% (18/100) of the quarters were culture-positive for bacteria (Staphylococcus aureus, Streptococcus dysgalactiae, Streptococcus species, Actinomyces pyogenes, and[or] coagulase-negative Staphylococcus) at one or more times. Milk production was higher in LOSCC than in HISCC cows (6.3 +/- .2 vs 5.4 +/- .3 kg/24 h; P = .004). Mean SCC linear score tended to be negatively correlated with mean milk production over the entire study (r = -.36; P = .08). Adjusted weaning weights were similar between calves suckling LOSCC and HISCC cows (243 +/- 5 vs 236 +/- 10 kg; P = .57). In summary, milk SCC concentrations in primiparous Simmental cows were highly variable. Higher SCC concentrations were associated with lower milk production in cows.

Animals↗

Endocrine and ovarian responses to exogenous estradiol-17 beta in 6-month-old heifers previously immunized against growth hormone-releasing factor.

We hypothesized that estradiol-17 beta (E2) was capable of stimulating an LH surge in 6-mo-old heifers immunized against growth hormone-releasing factor (GRFi). To test this hypothesis Angus x Simmental heifers were immunized against GRF (n = 11) or human serum albumin (HSAi) (n = 6) at 113 d of age. Heifers were injected i.m. with 500 micrograms of E2 at 172 d of age. To characterize the LH response, samples were collected at frequent intervals for 1 h before and 32 h after E2. To assess ovarian responses, real-time ultrasonography was performed from d 9 to 20, and serum progesterone was evaluated from d 6 to 25 after E2, then weekly for 13 wk. Exogenous E2 stimulated (P < .001) LH surges, preceded by negative E2 feedback that decreased serum LH, in all GRFi and HSAi heifers. During the negative feedback period, serum LH was greater (P < .001), and the change in LH from before to after E2 was lower (P < .05), in GRFi than in HSAi heifers. Puberty occurred in 7/17 heifers within 66 d after receiving E2. We conclude that GRFi does not impair the release of an E2-induced LH surge, but it does decrease hypothalamo-hypophyseal sensitivity to the inhibitory effect of E2.

Animals↗

Roles for the yeast RAD18 and RAD52 DNA repair genes in UV mutagenesis.

Experimental evidence indicates that although the Saccharomyces cerevisiae RAD18 and RAD52 genes are not required for nucleotide excision repair, they function in the processing of UV-induced DNA damage in yeast. Conflicting statements regarding the UV mutability of strains deleted for RAD18 prompted us to re-examine the influence of RAD18, and RAD52, on UV mutagenesis. To do so, we characterized mutations induced by UV in SUP4-o, a yeast suppressor tRNA gene. SUP4-o was maintained on a plasmid in isogenic strains that either carried one of two different rad18 deletions (rad18 delta) or had RAD52 disrupted. Both rad18 deletions decreased the frequency of UV-induced SUP4-o mutations to levels close to those for spontaneous mutagenesis in the rad18 delta backgrounds, and prevented a net increase in mutant yield. A detailed analysis of mutations isolated after UV irradiation of one of the rad18 delta strains uncovered little evidence of the specificity features typical for UV mutagenesis in the isogenic repair-proficient (RAD) parent (e.g., predominance of G.C-->A.T transitions). Evidently, UV induction of SUP4-o mutations is highly dependent on the RAD18 gene. Compared to the RAD strain, disruption of RAD52 reduced the frequency and yield of UV mutagenesis by about two-thirds. Closer inspection revealed that 80% of this reduction was due to a decrease in the frequency of G.C-->A.T transitions. In addition, there were differences in the distributions and site specificities of single base-pair substitutions. Thus, RAD52 also participates in UV mutagenesis of a plasmid-borne gene in yeast, but to a lesser extent than RAD18.

Base Sequence↗

Effect of somatotropin and/or equine chorionic gonadotropin on serum and follicular insulin-like growth factor I and insulin-like growth factor binding proteins in cattle.

We investigated the effect of administration of somatotropin (ST) and/or eCG on insulin-like growth factor I (IGF-I) and IGF-binding proteins (IGFBP) in serum and follicular fluid (FFL) of cattle actively immunized against growth hormone-releasing factor (GRF). Cyclic beef cattle, previously immunized against GRF-(1-29)-Gly-Gly-Cys-NH2 conjugated to human serum albumin (synthesized and provided by Hoffmann-LaRoche, Inc., Nutley, NJ; GRFi, n = 31) or to human serum albumin alone (HSAi, n = 26), received (i.m.): 1) 25 mg recombinantly derived methionyl somatotropin (rbST, n = 14; sometribove provided by Monsanto Co., St. Louis, MO); 2) 1100 IU eCG (n = 10); 3) rbST and eCG (rbST-eCG, n = 15); or 4) vehicle (VEH, n = 17) at 0 and 24 h after receiving prostaglandin F2 alpha (PGF2 alpha). Serum samples were collected at 0 and 40 h after PGF2 alpha, and the ovary bearing the largest follicle (DOM) was removed 44.0 +/- 0.5 h after PGF2 alpha; FFL was harvested from DOM and the subordinate follicle (SUB). Before treatment (0 h), GRFi cows had lower serum ST (0.6 +/- 0.2 vs. 2.2 +/- 0.2 ng/ml; p < 0.01) and IGF-I (26 +/- 4 vs. 72 +/- 4 ng/ml; p < 0.01), but greater IGFBP-2 (594 +/- 48 vs. 384 +/- 52 ng/ml; p < 0.01) than HSAi cows. Serum and FFL concentrations of IGF-I or IGFBP-2 were not different between rbST- and rbST-eCG-treated cows or between VEH- and eCG-treated cows at Hour 40 after the initial treatment injection; therefore, data were combined and designated as rbST and VEH, respectively. Serum IGF-I was increased to a greater extent (percentage increase above 0 h) by rbST treatment in GRFi (362 +/- 24) than in HSAi (176 +/- 16) cows (immunization by treatment, p < 0.01). Across GRFi and HSAi, rbST lowered serum IGFBP-2 (342 +/- 31 vs. 541 +/- 27 ng/ml, rbST vs. VEH; p < 0.01). Diameters of DOM or SUB were not affected by immunization or treatment. Concentrations of IGF-I and IGFBP-3 (determined by ligand blot analysis) in FFL from both DOM and SUB were lower (p < 0.05) in GRFi than in HSAi cows. In contrast, IGFBP-2 in FFL was elevated in SUB, but not DOM, in GRFi compared to HSAi cows.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗

Concentrations of hormones and metabolites, estimates of metabolism, performance, and reproductive performance of sows actively immunized against growth hormone-releasing factor.

Cyclic females actively immunized against growth hormone-releasing factor (GRF; n = 5) or human serum albumin (HSAi; n = 4) were used to determine the effects of reduced serum somatotropin (ST) and IGF-I on metabolism and production in gestating and lactating sows. Sows farrowed, pigs were weaned at 28 d of lactation, and sows were observed for estrus after weaning. Blood samples were collected at 15-min intervals for 5 to 6 h on d 110 of gestation and d 21 of lactation. Mean ST (nanograms/milliliter) was less (P < .05) in GRFi than in HSAi sows at d 21 of lactation, but it was similar at d 110 of gestation. Serum concentrations of IGF-I were less (P < .05) in GRFi than in HSAi sows at d 21 of lactation but not at d 110 of gestation. Serum thyroxine was greater (P < .05) in GRFi than in HSAi sows during gestation and lactation. Sows actively immunized against GRF weighed less (P < .01) and had more backfat (P < .01) at d 110 of gestation than HSAi sows; in vitro glucose oxidation and lipogenic rate of adipose tissue were greater (P < .05 for treatment x day interaction) in GRFi than in HSAi sows at d 110 of gestation. Across treatment, mammary gland oxidation of glucose and glucose clearance rates increased (P < .05), whereas adipose tissue utilization of glucose decreased (P < .05) during lactation. During lactation, GRFi sows mobilized more (P < .05) backfat than did controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

Effect of daily replacement therapy with recombinant bovine somatotropin on somatotropin, insulin-like growth factor I, and onset of puberty in beef heifers immunized against growth hormone-releasing factor.

Two experiments examined whether replacement therapy with recombinantly derived bovine somatotropin (rbST) would induce puberty in heifers that had been actively immunized at 6 mo of age against growth hormone-releasing factor (GRF). Heifers received daily i.m. injections of 25 mg of rbST (Exp. 1, n = 6; Exp. 2, n = 4) or vehicle (VEH; Exp. 1, n = 6; Exp. 2, n = 4) for 56 d. Serum concentrations of somatotropin (ST, nanograms/milliter) were low in all heifers before first injection in Exp. 1 (1.56 +/- .04) and 2 (.95 +/- .03). During treatment, serum ST was greater (P < .01) in rbST than in VEH heifers (75.4 +/- 4.8 vs 2.8 +/- .1 ng/mL, respectively) in both experiments and remained increased through d 57 (32.2 +/- 6.4 vs .90 +/- .01 ng/mL). IN Exp. 1 and 2, concentrations of serum IGF-I were similar in rbST and VEH heifers before treatment, increased (P < .01) 12 h after first rbST, and remained increased (P < .01) through d 57 in rbST heifers. Concentrations of serum insulin (INS) and plasma glucose (GLU) were similar (P > .10) in rbST and VEH heifers before first injection (Exp. 1 and 2). Serum INS (micro-units/milliliter) was greater (P < .01) in rbST (61.7 +/- 3.7 and 36.0 +/- 2.4) than in VEH (12.4 +/- 1.6 and 8.1 +/- 1.0) heifers on d 1 or 2 only, in Exp. 1 and 2, respectively. In Exp. 1, GLU was increased (P < .05) by rbST on d 2 through 57, but only on d 1 in Exp. 2. Proportion of heifers pubertal by d 21 tended to be greater (P < .07) in rbST (3 of 6) than in VEH (0 of 5) heifers in Exp. 1, but not in Exp. 2 (1 of 4 vs 1 of 4, respectively). All heifers in Exp. 1 and 50% of the heifers in Exp. 2 attained puberty by d 56. Daily rbST increased ST, IGF-I, INS, and GLU but did not hasten onset of puberty in heifers immunized against GRF.

Animals↗

Effect of feed restriction on serum somatotropin, insulin-like growth factor-I-(IGF-I) and IGF binding proteins in cyclic heifers actively immunized against growth hormone releasing factor.

Feed restriction often increases serum somatotropin (ST) and decreases insulin-like growth factor-I (IGF-I) in ruminants; however, the mechanisms responsible for this change in ST and IGF-I are not well defined. We investigated the effects of feed restriction on serum ST, IGF-I, IGF binding proteins (IGFBP), insulin and nonesterified fatty acids (NEFA) in cyclic Angus and Charolais heifers (n = 15) previously immunized against growth hormone releasing factor (GRFi) or human serum albumin (HSAi). Cows were fed a concentrate diet ad libitum (AL) or were restricted to 2 kg cotton seed hulls (R) for 4 d. Each heifer received each dietary treatment in a single reversal design. As anticipated, GRFi decreased ST, IGF-I and insulin (P < .05). In addition, GRFi decreased serum IGFBP-3 (P < .01), but increased IGFBP-2 (P < .01). Feed restriction resulted in an increase in serum ST in HSAi, but not in GRFi heifers. Regardless of immunization treatment, feed restriction decreased serum IGF-I and insulin, and increased NEFA (P < .01). In conclusion, the increase in serum ST levels observed during feed restriction was blocked by active immunization against GRF. However, feed restriction resulted in decreased serum IGF-I in GRFi heifers in spite of initial low levels of IGF-I (due to GRFi). Although GRFi decreased levels of IGFBP-3 and increased levels of IGFBP-2, feed restriction for 4 d did not alter serum IGFBP.

Animals↗