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Biomedical subjects

R M Campbell

Publications and source records attributed to R M Campbell.

At least 37 records · Page 2Linked to original sources
PubMed1996

Cardiovascular effects of cocaine in neonates exposed prenatally.

This blinded cross-sectional study was to determine whether chronic cocaine exposure in utero produces abnormalities in left ventricular function (shortening fraction), heart rate, rhythm, and conduction in term neonates. Three groups of neonates were evaluated by two-dimensional echo Doppler and 24 hour Holter monitor, with studies initiated in the first 24 hours of life. Group A (n = 32) neonates had a positive history of chronic maternal cocaine use in pregnancy (MCU+) and a positive neonatal urine cocaine test (NUC+). Group B (n = 23) neonates were MCU+ but NUC-. Group C (n = 32) neonates were MCU- and NUC-. Measured parameters were compared statistically by analysis of variance. p < 0.05 was regarded as significant. Echocardiography showed no significant difference between groups A, B, and C for left ventricular shortening fraction. Holter monitor likewise revealed no significant difference between groups in minimal, maximal, and average heart rate, or in the incidence of supraventricular and ventricular arrhythmias greater than 20 beats/h in the 24-hour period. None of the patients had atrioventricular or bundle branch block. It is possible that the developmental state of the newborn heart makes it less responsive to the adverse effects of cocaine.

Analysis of Variance↗
PubMed1996

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↗
PubMed1996

A study of the incorrect use of ventilator disconnection alarms.

Pressure-sensitive ventilator disconnection alarms may fail to function correctly when used with discharging compliance ventilators such as the Manley Blease. The increase in gas flow on disconnection generates raised pressure owing to the resistance provided by components of the breathing system. Thirty-four anaesthetists, who were unaware of the nature of the survey, were observed to see if previous recommendations for the correct adjustment of the ventilator alarm were being followed. It was found that 77% of alarms were incorrectly adjusted and would not have alarmed in the event of a true disconnection occurring.

Anesthesia, General↗
PubMed1996

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↗
PubMed1996

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↗
PubMed1995

Rational design, synthesis, and biological evaluation of novel growth hormone releasing factor analogues.

Since its initial discovery in 1982, growth hormone-releasing factor (GRF) has been the subject of intense investigation. This interest was prompted by the potential application of GRF for stimulating growth in dwarf humans and for performance enhancement in livestock. Substantial research has been focused upon the development of potent, long-acting analogs as therapeutics. Herein is described a summary of the cumulative efforts of various laboratories endeavoring in this quest. The rationale utilized in GRF analog development is discussed: 1) determination of bioactive core, 2) evaluation of secondary structure, and 3) elucidation of degradation pathways (chemical and enzymatic). Using this information, several series of linear (unnatural and natural sequence) and cyclic GRF analogs were designed, synthesized, and evaluated. Stimulated by the constraints of commercial production, innovative, alternative methods of synthesis were explored: solid-phase, solution-phase, enzymatic, and recombinant. To date, the most promising candidate for drug development is [His1, Val2, Gln8, Ala15, Leu27]-hGRF(1-32)-OH. This natural sequence analog, consisting of rodent and human sequences, incorporates the bioactive core, preferred secondary structure, resistance to chemical and enzymatic degradation; with the added benefit of amenability to large-scale recombinant synthesis.

Amino Acid Sequence↗
PubMed1995

Tilt table evaluation for control pediatric patients: comparison with symptomatic patients.

This study was designed to evaluate pediatric control patients during head-up tilt in comparison with symptomatic neurocardiogenic syncope patient head-up tilt responses. Twenty-three pediatric control (c) patients (13 females, 10 males; 11.9 +/- 3.1 years) were tested with head-up tilt (HUT) and compared with 66 symptomatic (s) patients. Baseline drug-free HUT (cHUT-1), a second drug-free HUT (cHUT-2), and a final HUT with isoproterenol infusion (cHUT-3) were each performed at 80 degrees tilt angle for 30 min or until positive. For comparison, 66 symptomatic patients (41 females, 25 males; 13.6 +/- 2.5 years) underwent drug-free HUT (sHUT-1); negative responders during sHUT-1 underwent follow-up HUT with isoproterenol (sHUT-2). HUT data were compared for both groups at both 30 and 20 min tilt duration. Twelve control patients (52%) had a symptomatic response during cHUT-1 at 18 +/- 8 min. During cHUT-2, 5 of 23 patients were positive at 13 +/- 5 min; each had previously tested positive during cHUT-1. Two patients, each positive in cHUT-1 and cHUT-2, refused cHUT-3. The only patient testing positive during cHUT-3 was test positive in cHUT-1 but negative for cHUT-2. In comparison, 43 of 66 (65%) symptomatic patients tested positive during drug-free sHUT-1 at 11 +/- 6 min. Subsequently, 20 of the 23 negative patients underwent HUT with isoproterenol (sHUT-2), with 8 of 20 testing positive. Thus, 51 of 66 symptomatic patients (77%) were called "true positives."(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Complex asparagine-linked oligosaccharides in Mgat1-null embryos.

To investigate the developmental role of complex N-linked oligosaccharides, we previously inactivated the mouse Mgat1 gene which encodes UDP-N-acetylglucosamine: alpha-3-D-mannoside beta-1,2-N-acetylglucosaminyltransferase I (GlcNAc-TI). Mgat1-null embryos developed morphogenic abnormalities by embryonic day (E) 9.5 and failed to survive beyond E10.5. Prior to E8.5, mutant and wild-type embryos were phenotypically indistinguishable, raising the unexpected possibility that earlier embryonic development may not require complex N-glycans. We have now used in situ RNA hybridization to assess the temporal and spatial pattern of Mgat1 expression in normal embryos, and lectin histochemistry to determine whether Mgat1-null embryos lack complex N-glycans at pre-E9.5 developmental stages. In situ RNA analysis indicated that Mgat1 transcripts normally increase dramatically between E7.0 and E9.5, 1-2 days prior to the death of mutant embryos. However, apparently normal levels of complex N-glycans were observed in E3.5 pre-implantation Mgat1-null embryos prior to declining to undetectable levels by E7.5. Complex N-glycans were not observed in E7.5-E9.5 Mgat1-null embryos with the notable exception of vesicular structures within cells of the visceral extra-embryonic endoderm, perhaps reflecting the ability of these cells to take up and transport maternally derived glycoproteins. Mgat1-null embryos appear to complete pre-implantation development in the presence of maternally derived complex N-glycans, and may die at later stages, post E7.5, when a requirement for embryonically derived complex N-glycans arises.

Animals↗
PubMed1995

GlcNAc-transferase V and core 2 GlcNAc-transferase expression in the developing mouse embryo.

UDP-GlcNAc:Manalpha1-6Manbeta-R beta1-6-N-acetylglucosaminyltransferase V (GlcNAc-TV) and UDP-GlcNAc:Galbeta1-3GalNAc-R beta1-6-N-acetylglucosaminyltransferase (core 2 GlcNAc-T) are Golgi enzymes that catalyse the biosynthesis of beta1-6GlcNAc-branched intermediates in the N- and O-linked biosynthesis pathways, respectively. The activities of these enzymes change during haematopoiesis, embryo-carcinoma cell differentiation and following malignant transformation, but little is known about their expression in normal adult tissues and during embryogenesis. We have examined the expression of GlcNAc-TV and core 2 GlcNAc-T in sections of post-implantation mouse embryos by in situ RNA hybridization. The two enzymes showed distinct temporal and spatial patterns of expression. Core 2 GlcNAc-T mRNA was widely expressed at embryonic day (E) 7, and became restricted to a subset of mucin- and cartilage-producing tissues at E11.5 through to E17.5. GlcNAc-TV transcripts were absent at E7, became expressed throughout E9.5 embryos, and then progressively restricted to regions of the developing central nervous system and to specialized epithelia of skin, intestine, kidney, endocrine tissues and respiratory tract. In the adult gonads, GlcNAc-TV transcripts were excluded from germ cells, but were detected in the follicular and testicular cells. Leukoagglutinin (L-PHA)-reactive oligosaccharides co-localized with GlcNAc-TV transcripts in skin, kidney and intestine, but brain showed unexpectedly low overall staining punctuated by bright staining of the vascular endothelium. A common feature of cells in basal epithelia and in the cortical neural epithelium is the capacity to migrate, a cellular function which may require GlcNAc-TV-dependent glycoconjugates.

Animals↗
PubMed1995

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↗
PubMed1994

Interaction between dietary intake and ovariectomy on concentrations of insulin-like growth factor-I, GH and LH in plasma of heifers.

The objective of this study was to determine if alterations in dietary intake and(or) ovariectomy influence plasma concentrations of IGF-I, GH and LH in heifers. Cyclic heifers (n = 23) were individually fed for 10 wk either 1) 1.8% of body weight in dry matter per day (GAIN; n = 7) 2) 1.1% of body weight in dry matter per day (MAINT; n = 8); or 3) 0.7% of body weight in dry matter per day (LOSE; n = 8). After 10 wk of dietary treatment, heifers were ovariectomized 36 to 40 h following the second injection of prostaglandin F2alpha analog (2 injections 11 d apart). Heifers weighed 444 +/- 13, 387 +/- 8, and 349 +/- 9 kg in the GAIN, MAINT and LOSE groups, respectively, at the time of ovariectomy; the average daily weight gains during the 10-wk period were 0.96, 0.17 and -0.31 kg, respectively (P < 0.001), for the 3 groups. Blood plasma was collected for 6 h at 15-min intervals 1 d before and 2 wk after ovariectomy. The MAINT group of heifers had greater IGF-I concentrations than either the LOSE or GAIN groups; IGF-I decreased (P < 0.05) by 23 and 35% after ovariectomy in the MAINT and GAIN groups, respectively, but did not change (P > 0.10) in the LOSE groups. Dietary restriction tended to increase (P < 0.10) GH pulse frequency and mean GH. Ovariectomy had no effect (P > 0.10) on mean GH or GH pulse frequency but increased (P < 0.05) GH pulse amplitude in the GAIN groups. Dietary treatment had no effect (P > 0.10) on mean LH, or LH pulse amplitude and frequency. However, across dietary treatments, ovariectomy increased mean LH and LH pulse frequency but did not affect (P > 0.10) LH pulse amplitude. In summary, dietary restriction increased GH secretion while ovariectomy increased LH secretion. There appears to be a dichotomy of response between GH and IGF-I in the way heifers respond to dietary treatment and(or) ovariectomy.

Journal Article↗
PubMed1994

Enhanced stability and potency of novel growth hormone-releasing factor (GRF) analogues derived from rodent and human GRF sequences.

Native human GRF(1-44)-NH2(hGRF44) is subject to biological inactivation by both enzymatic and chemical routes. In plasma, hGRF44 is rapidly degraded via dipeptidylpeptidase IV (DPP-IV) cleavage between residues Ala2 and Asp3. The hGRF44 is also subject to chemical rearrangement (Asn8-->Asp8, beta-Asp8 via aminosuccinimide formation) and oxidation [Met27-->Met(O)27] in aqueous environments, greatly reducing its bioactivity. It is therefore advantageous to develop long-acting GRF analogues using specific amino acid replacements at the amino-terminus (to prevent enzymatic degradation): residue 8 (to reduce isomerization) and residue 27 (to prevent oxidation). Inclusion of Ala15 substitution (for Gly15), previously demonstrated to enhance receptor binding affinity, would be predicted to improve GRF analogue potency. Substitution of [His1,Val2]-(from the mouse GRF sequence) for [Tyr1,Ala2]-(human sequence) in [Ala15,Leu27]hGRF(1-32)-OH analogues completely inhibited (24-h incubation) DPP-IV cleavage and greatly increased plasma stability in vitro. Additional substitution of Thr8 (mouse GRF sequence), Ser8 (rat GRF sequence), or Gln8 (not naturally occurring) for Asn8 (human GRF sequence) resulted in analogues with enhanced aqueous stability in vitro (i.e., decreased rate of isomerization). These three highly stable and enzymatically resistant hGRF(1-32)-OH analogues, containing His1, Val2, Thr/Gln8, Ala15, and Leu27 replacements, were then bioassayed for growth hormone (GH)-releasing activity in vitro (rat pituitary cell culture) and in vivo (SC injection into pigs). Enhanced bioactivity was observed with all three hGRF(1-32)-OH analogues. In vitro, these analogues were approximately threefold more potent than hGRF44, whereas in vivo they were eleven- to thirteenfold more potent.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1994

Influence of adenosine or adrenergic agonists on growth hormone stimulated lipolysis by chicken adipose tissue in vitro.

In vitro lipolysis by chicken adipose explants was stimulated by growth hormone (GH) or glucagon. Adenosine or the adenosine agonist, N6-phenylisopropyladenosine (PIA), inhibited GH stimulated lipolysis, the effect of adenosine not being observed in the presence or adenosine deaminase. Glucagon induced lipolysis was also reduced by PIA. It is suggested that adenosine may act by Gi linked to either adenylate cyclase (for glucagon) or the signal transduction mechanism for GH. Lipolysis was not stimulated by GH in the presence of phenylephrine (alpha 1 adrenergic agonist), isoproterenol (beta adrenergic agonist), adrenaline or glucagon. Although the presence of p-amino clonidine (alpha 2 adrenergic agonist) depressed basal lipolysis, a response to GH was still present. Either glucagon or beta-adrenergic agonists (isoproterenol, adrenaline) stimulated lipolysis. In both cases, GH attenuated the lipolytic response to these hormones, which act via a cyclic adenosine monophosphate signal transduction mechanism.

Adenosine↗
PubMed1994

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↗
PubMed1994

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↗