J. Anim. Sci. 2003. 81:1581-1589
© 2003 American Society of Animal Science
The effect of dietary energy source on serum concentration of insulin-like growth factor-I, growth hormone, insulin, glucose, and fat metabolites in weanling horses1
J. K. Ropp1,2,
R. H. Raub1,3 and
J. E. Minton1,4
Department of Animal Sciences and Industry, Kansas State University, Manhattan 66506-0201
4 Correspondence:
253 Weber Hall (phone: 785-532-1238; fax: 785-532-7059; E-mail:
eminton{at}oznet.ksu.edu).
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Abstract
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Feeding diets high in soluble carbohydrates to growing horses has been implicated in the development of orthopedic diseases; as a result, substitution of dietary fat for soluble carbohydrates has received attention. Because IGF-I is integral to growth and cartilage development and because it is influenced by nutrition, we evaluated the effect of dietary fat substitution on metabolic endpoints and circulating GH and IGF-I in growing horses. Twelve Quarter Horse weanlings, four female and eight male, 151 to 226 d old, were blocked by sex and age and assigned to two treatment groups. Group one (CARB; n = six) was fed a concentrate containing 2.21% fat and 33.9% starch; group two (FAT; n = six) was fed a concentrate containing 10.3% fat and 24.0% starch. Both concentrates contained 3.0 Mcal/kg of DE and 16% CP. Brome hay also was fed. Diets were fed at 0800 and 1600 for 60 d. On d 0, 30, and 60, blood samples were obtained via a jugular catheter from 1 h before until 5 h after the morning feeding. Serum was analyzed for glucose, insulin, GH, IGF-I, NEFA, and total cholesterol (CHOL). Neither ADG (0.85 ± 0.04 and 0.84 ± 0.04 kg) nor concentrate DMI (4.04 ± 0.12 and 4.03 ± 0.12 kg/d) differed between treatments. There were consistent increases in glucose and insulin in response to feeding on d 0, 30, and 60 for both groups. On d 30, the glucose response to feeding was less (P = 0.07) over time in FAT vs. CARB; however, there were no significant treatment x time effects on d 0 or 60. On d 60, the insulin response to feeding was less (P < 0.05) over time in FAT compared with CARB; however, there was no treatment x time effect on d 0 or 30. Serum CHOL concentrations did not differ between groups on d 0. Horses in the FAT group had increased CHOL concentrations on d 30 and 60 compared with CARB (P < 0.01). Although treatment x time interactions were noted for GH on d 30 and 60 (P < 0.05), only transient and inconsistent differences in the secretory profiles between CARB and FAT treatments were evident at those sampling times. Serum NEFA and IGF-I did not differ between treatments on d 0, 30, or 60. These results suggest that dietary energy source, at least at the level used in this study, did not affect foal growth performance or serum IGF-I and NEFA concentrations. Fat substitution increased serum CHOL and variably affected serum GH, glucose, and insulin concentrations in response to feeding.
Key Words: Dietary Fat • Horses • Insulin-Like Growth Factor • Somatotropin
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Introduction
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In general, IGF-1 has both endocrine and autocrine influences on long bone growth cartilage development (Nilsson et al., 1990; Leach et al., 1994; Pavasant et al., 1996). IGF-I is thought to be the mediator of the majority of GH promotion of long bone growth cartilage development (Isaksson et al., 1991; Hanna et al., 1995; Loveridge et al., 1995). Additionally, insulin affects long bone growth cartilage development through IGF-1 mediation (Alarid et al., 1992).
The increasing incidence of developmental orthopedic diseases (DOD) in horses has been partially attributed to the practice of feeding for maximal growth with diets high in soluble carbohydrates (Glad and Belling, 1986; Savage et al., 1993). It is well documented that IGF-I, GH, and insulin are affected by nutrition (Ketelslegers et al., 1995; Scanlon et al., 1996). It is speculated that DOD problems may be associated with high concentrations of glucose after feeding, resulting in suppression of the central regulation of GH secretion and subsequent disruption of the GH/IGF-I axis (Glade, 1986; Scanlon et al., 1996). The use of fat in place of soluble carbohydrates as a dietary energy source, and its associated benefits to long bone cartilage development, has been explored (Rich et al., 1981; Scott et al., 1987; Davison et al., 1991). These studies demonstrate that fat supplementation appears to be suitable to support growth, and it does not appear to have negative effects on bone development.
The objective of this study was to examine the effect of dietary energy source on the somatotropic axis in weanling horses. Related ancillary data were collected as positive markers of dietary treatment effects. Specifically, glucose, insulin, and NEFA were measured since they were predicted to change postprandially. In addition, total cholesterol (CHOL) was measured because it was predicted to be increased by dietary fat supplementation.
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Materials and Methods
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Experimental Design
Twelve Quarter horse weanlings, 4 female and 8 male, ranging in ages from 151 to 226 d, were blocked by age and sex and assigned to two treatments: a soluble carbohydrate-based concentrate (CARB, n = 6) or a 10% fat-supplemented soluble carbohydrate-based concentrate (FAT, n = 6) (Table 1
). The diets were formulated to supply 100% of nutrient requirements (NRC, 1989). Horses were gradually converted to the treatment diets over a 4-d period. Then, horses were weighed weekly at 1400 and fed a 70% concentrate, 30% hay diet to achieve a desired ADG of 0.9 kg/d. Horses in both treatments were commingled in 32-m2 pens, and had unlimited access to water and trace mineral salt blocks. Concentrates were fed individually, and hay was group-fed based on average pen weight. The concentrate for individual horses and the total hay ration for each pen of horses was divided into two daily feedings given at 0800 and 1600 and was fed for 60 d starting on d 1 of the experiment.
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Table 1. Nutrient composition of the soluble carbohydrate (CARB) and 10% fat-supplemented (FAT) concentrates and brome hay fed to weanling horsesa
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Blood Sampling
On d -1, 29, and 59 of the experiment, the horses were housed individually in 5.5-m2 stalls, and an indwelling 14-gauge jugular catheter was inserted. To maintain patency, the catheters were flushed with a sterile 3.5% sodium citrate solution every 4 h after installation and after withdrawal of each blood sample during the sampling period. On d 0 (before beginning dietary adaptation to the concentrates), 30, and 60, blood sampling began at 0700 and continued until 1300, for a total of 6 h. Morning feedings occurred at 0800. Blood samples of approximately 10 mL were collected every 12 min into 16 x 100-mm borosilicate glass tubes. Following each 6-h bleed session, all the sample tubes were refrigerated overnight at 4°C. The following day, samples were centrifuged at 2,400 rpm and 4°C for 20 min. The serum was then harvested, placed in 12 x 75-mm polypropylene tubes, and frozen at -20°C.
Feed Sample Analyses
The concentrates and hay were sent to a commercial laboratory for analysis of DM, CP, ADF, NDF, nonstructural carbohydrates (NSC), ether extract (EE), calcium, and phosphorous. An estimate of DE was determined from the following formula (Pagan, 1997) (Table 1
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Serum Sample Analyses
Concentrations of glucose and insulin were measured in every other sample, beginning with the -1-h sample, to create a pre- and postprandial profile on d 0, 30, and 60 of the study. Concentrations of NEFA were measured in the 0- and 3-h samples at d 0, 30, and 60. Concentrations of CHOL and IGF-I were measured in the 0- and 3-h samples, and the values for these two times were subsequently averaged to obtain a single value for each horse at d 0, 30, and 60. Concentrations of GH were measured in all samples on every sampling day to create complete pre- and postprandial profiles for every experimental animal.
Concentrations of glucose (Sigma Diagnostics, St. Louis, MO), NEFA (Wako Chemicals, Dallas, TX; modified as described in Eisemann, et al., 1988), and CHOL (Sigma Diagnostics) were determined using commercial colorimetric kits.
Concentrations of insulin were measured with a commercially available RIA kit (Coat-a-Count, Diagnostic Products Corp., Los Angeles, CA) that was validated previously for use in bovine serum (Rushe et al., 1993). Quantitative recovery of human insulin (the standard for the assay) and dilutional parallelism of equine serum with the standard curve for the assay was also demonstrated. The slope of the regression of insulin concentration measured in the assay, on concentration expected in equine serum to which human insulin had been added, had a 95% confidence interval that included 1.00. When volumes between 25 and 200 µL of serum were corrected for dilution, the concentrations measured in the assay were similar across all volumes. The slope of the regression of concentration measured on volume assayed had a 95% confidence interval that included zero. The sensitivity of the assay (95% confidence interval about buffer control tubes) averaged 0.04 ng/mL in four assays. The intraassay CV averaged 8.81% and the interassay CV averaged 9.40%.
Insulin-like growth factor-1 was measured using a commercially available immunoradiometric assay (Diagnostic Systems Laboratories, Inc., Webster, TX). This assay utilized acid-ethanol extraction of serum and therefore measured total serum IGF-I. The assay did not detect related compounds (IGF-II, insulin, pro-insulin, or GH; information supplied by the manufacturer). Human IGF-I, which shares 100% homology with equine IGF-I (Otte et al., 1995), was used as the standard in the assay. IGF-I could be recovered quantitatively in the assay when added to equine serum. The slope of the regression of concentration measured in the assay on concentration expected following addition of IGF-I to equine serum had a 95% confidence interval that included 1.00. Extraction of differing volumes of equine serum produced similar volume-corrected concentrations. The slope of the regression of concentrations measured on volume of serum extracted had a 95% confidence interval that included zero. The sensitivity of the assay (95% confidence interval about buffer control tubes) was 0.51 ng/mL for the single assay in which all samples were quantified. The intraassay CV was 3.58%.
Concentrations of GH in serum were measured utilizing a competitive, time-resolved immunofluorescent assay (IMFA) that was developed in our laboratory. A preparation of equine GH (eGH) (L4490B) that had been conjugated to keyhole limpet hemocyanin (Pierce Chemical Co., Rockford, IL; catalog No. 77107) was injected into rabbits to develop the polyclonal antibody used in the assay. Primary and booster injections of antigen were given in TiterMax adjuvant (CytRx Corp., Los Angeles, CA; catalog R-1). Highly purified eGH (AFP7112) was used as the standard, and this preparation also was biotinylated (Pierce Chemical Co.; catalog No. 21335) for use as the assay tracer. Plates for the assay were purchased precoated with a polyclonal antibody against the Fc region of rabbit IgG (PerkinElmer Life Sciences, Inc., Boston, MA; catalog No. C1221-105). For the assay, 25 µL of sample or standard (in assay buffer; PerkinElmer Life Sciences, Inc.; catalog No. 1244-111) were pipetted in duplicate, followed immediately by the addition of 100 µL of a 1:10,000 dilution of rabbit anti-eGH antibody. The plate was placed on a shaker for 4 h at room temperature. Then, 100 µL of biotinylated eGH was added and the plate was shaken for an additional 30 min at room temperature. The plate then was washed thoroughly, and 200 µL of Eu-streptavidin (PerkinElmer Life Sciences, Inc.; catalog No. 1244-360) was added to each well. The plate was then incubated for 30 min at room temperature with shaking. Next, the plate was again washed thoroughly and 200 µL of an acidic chelating detergent solution for detection of Eu (PerkinElmer Life Sciences, Inc; catalog No. 1244-105) was added to the each well. The plate was again incubated with shaking at room temperature for 5 min. Then, the fluorescence was read in an automated plate reader equipped for time-resolved fluorescence detection (Wallac Victor2; PerkinElmer Life Sciences, Inc; catalog No. 1420-012).
To validate the assay for equine serum, eGH was added to a serum pool containing 12.17 ng/mL GH, such that expected concentrations were 37.17, 62.17, 112.17, and 212.17 ng/mL. Concentrations of GH measured in the IMFA were 34.88, 58.72, 118.09, and 186.59 ng/mL, respectively. Thus, the average concentration measured in the assay was 95.35% of the expected concentration in the pools. The volume of standard and unknown samples estimated in the assay was 25 µL. Analyses of a pool of equine serum at 25 µL produced an estimated concentration of 24.55 ng/mL. To evaluate the presence of serum matrix effects, this serum was diluted 1.66- and twofold and assayed for GH. Concentrations measured in the IMFA were 25.38 and 25.34 ng/mL, respectively, when corrected for dilution. Thus, the concentration measured in the assay averaged 103.3% of the concentration expected in the diluted samples. The rabbit anti-eGH antibody was tested for cross-reactivity with equine LH (AFP5130A), equine thyroid-stimulating hormone (AFP5144B), and equine prolactin (AFP7730B). Cross-reactivity of equine prolactin was 2.13%, whereas both equine LH and equine TSH cross-reacted less than 0.02%. The standard curve routinely ranged from 1.56 to 100 ng/mL, and the lowest concentration in the standard curve was regarded as the lower limit of detection for the assay. The intraplate CV averaged 8.97%, and the interplate CV averaged 10.42% across the 37 plates required to complete the analyses for samples in the study.
Statistical Procedures
All data were analyzed using the GLM procedure of SAS (SAS Inst., Inc., Cary, NC). Glucose, insulin, CHOL, NEFA, GH, and IGF-I were analyzed using a split plot ANOVA. Terms in the model included effects of treatment, time, treatment x time, and animal within treatment. Treatment effects in the whole plot were tested using the animal within treatment variance as the error term. The subplot effects of time and treatment were tested using the residual error. Treatment effects within sampling times were compared only when there was a significant F-test (P < 0.05) for the treatment x time interaction effect in the ANOVA. Least squares ANOVA were used to analyze animal growth and feed intake data. Least significant difference tests were used to compare least squares means between treatments.
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Results and Discussion
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Weight Gain and Feed Intake
Although the 10% fat concentrate crumbled slightly, there were no feed refusals by either treatment group. The daily concentrate DMI (4.04 ± 0.12 and 4.03 ± 0.12 kg/d) and DE intake (11.70 ± 0.34 and 12.10 ± 0.34 Mcal/d) did not differ between the CARB and FAT treatments, respectively. Similarly, weight gain was not affected by treatment (Table 2). This represents a rapid rate of growth for weanling horses and is generally reflective of industry practice (Breuer et al., 1996).
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Table 2. Body weights and gain (mean ± SEM) of weanling horses fed a conventional (CARB) or fat-supplemented (FAT) concentrate
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The similar DMI and ADG between treatment groups in our study are in agreement with the results of Scott et al. (1987), who found no difference in feed efficiency between a conventional concentrate and a 10% added fat concentrate fed to yearling horses. Several other studies have shown that feeding adult horses a diet containing a 10% added fat concentrate does not affect energy (Kane et al. 1979; Jones et al., 1992) or protein (Snyder et al., 1981; Worth et al., 1987) digestibility of the concentrate. However, in another study, weanlings fed a 10% added fat concentrate had reduced DMI compared to weanlings fed a conventional concentrate of 70 d (Davison et al., 1991). In that study, the weanlings fed the 10% fat concentrate tended to have greater ADG and greater feed efficiency. Although not reported to be significant, there were differences in DE and CP in the 10% fat concentrate and conventional concentrate, respectively, that may have contributed to the growth differences reported in that study (Davison et al., 1991). Saastamoinen et al. (1994) found that foals (2 to 7 mo old) fed a 10.5% fat-supplemented diet consumed less energy and DM than foals fed a 5% fat-supplemented diet. As a result, foals on the 10.5% fat-supplemented diet had improved feed efficiency per kilogram of gain. Results from the current study, coupled with those of previous studies, suggest that up to 10% fat can be substituted for soluble carbohydrates in the concentrate portion of horse diets without any detrimental effect on growth performance.
Serum Glucose
Generally, increasing and maximal concentrations of serum glucose were seen 1 to 3 h postprandially on d 0, 30, and 60 (Figure 1). This is similar to the time of glucose peaks seen in previous equine experiments (Glade and Belling, 1986; Stull and Rodiek, 1988). There were no treatment x time differences in serum glucose concentrations on d 0 (Figure 1). This was expected since CARB- and FAT-fed horses were on the same pretreatment diet. A treatment x time interaction (P = 0.07) tended to emerge on d 30, with serum glucose concentration being greater in CARB- vs. FAT-fed horses 1 (time = 2.0 h) to 5 h postprandially (time = 6.0 h). On d 60, however, there was no significant effect of treatment or treatment x time on serum glucose concentration.
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Figure 1. Serum glucose from 1 h before feeding to 5 h after feeding in weanling horses fed a conventional (CARB) or fat-supplemented concentrate (FAT). Each point represents the mean ± SEM of six horses per treatment. Concentrate was fed at 0 h. On d 30, asterisks denote increased glucose in CARB- vs. FAT-fed horses (P < 0.05).
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The d-30 glucose results are consistent with human studies that show a greater concentration and shorter duration in blood glucose elevation postprandially in people fed a low- vs. high-fat diet containing the same amount of dietary glucose (Griffiths et al., 1994). This was attributed to dietary fat sparing glucose, as well as slowing down gastric emptying time, thereby decreasing and prolonging glucose release into the circulation. Stull and Rodiek (1988), using isoenergetic diets, showed that horses fed a concentrate containing 12.3% fat had a reduced postprandial peak in plasma glucose concentration compared with horses fed concentrates containing 3.5% fat. This result also was attributed to fat since it is a potent stimulator of gastric-inhibiting peptide from the small intestine, which slows gastric emptying time.
The 60-d glucose results are consistent with other experiments involving horses. These studies show no significant treatment effects on glucose concentrations or clearance by feeding fat at 10% of the concentrate portion of the diet (Rich et al., 1981; Julen et al., 1995; Kline et al., 1997; Ott, 1997). A possible explanation for the discrepancy seen in the present experiment between the d-30 and d-60 glucose results may be a dietary adaptation by CARB-fed horses to a higher soluble carbohydrate diet between d 30 and d 60 (discussed below in relation to insulin). The CARB-fed horses had a maximal serum glucose concentration of 165.3 ± 5.4 mg/dL on d 30 and 132.4 ± 4.4 mg/dL on d 60. The d-30 maximal concentration is greater than concentrations measured in a glucose-tolerance experiment performed by Alexander (1955; approximately 150 mg/dL) and a diet-response experiment reported by Stull and Rodiek (1988; approximately 140 mg/dL). However, the d-60 maximal concentration is below or close to these previously reported values, suggesting a possible physiological adjustment by CARB-fed yearlings between d 30 and d 60 to the high-soluble carbohydrate diet to prevent hyperglycemic tendencies.
Serum Insulin
Serum insulin concentrations increased 1 to 2 h after feeding (P < 0.05) during all three collection periods (Figure 2). Insulin peaks occurred within 2 to 3 h postprandially, which is in agreement with previous experiments (Glade and Belling, 1986; Stull and Rodiek, 1988). There was no significant treatment x time interaction on serum insulin concentrations on d 0 (Figure 2, top panel). The apparent divergence in average insulin concentrations between 3.6 to 6 h on this day is due to an unexplained increase in insulin during that interval in one horse in the FAT group. Because no treatment x time interaction was observed, this horse’s data were retained in the analysis. For comparison, however, the data for this treatment are also plotted with this animal removed.
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Figure 2. Serum insulin from 1 h before feeding to 5 h after feeding in weanling horses fed a conventional (CARB) or fat-supplemented concentrate (FAT). Each point represents the mean ± SEM of six horses per treatment. Concentrate was fed at 0 h. On d 60, asterisks denote increased insulin in CARB- vs. FAT-fed horses (P < 0.05).
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On d 30 there were no significant differences between treatment groups over time. There was a treatment x time interaction (P < 0.05) seen on d 60, with maximal concentrations for CARB of 1.75 ± 0.15 ng/mL at 4.8 h, and for FAT of 0.99 ± 0.15 ng/mL at 3.6 h. All measurements at 4 h and later on d 60 were greater (P < 0.05) for CARB than FAT. Stull and Rodiek (1988) showed that feeding a soluble carbohydrate-based concentrate produced a more marked insulin response than feeding a fat-supplemented concentrate. This also was observed by Davison et al. (1991) and Saastamoinen et al. (1994). The results of these studies generally agree with the d-30 and -60 insulin results of the present experiment.
The possibility of dietary adaptation by the CARB group to a high-soluble carbohydrate diet between d 30 and 60 is further supported by the greater postprandial increase in insulin seen on d 60 compared to d 30 in CARB. The lower postprandial concentrations of glucose on d 60 compared to d 30 in CARB may be a result of increased postprandial concentrations of insulin on d 60 compared to d 30 in order to prevent hyperglycemic tendencies.
Serum Total Cholesterol
On d 0 there were no treatment, time, or treatment x time effects on serum total cholesterol (CHOL) concentrations. On d 30 and 60, however, there were greater (P < 0.01) overall serum CHOL concentrations for horses in the FAT treatment (Figure 3). These results were expected and agree with other equine experiments that show a consistent positive association between serum CHOL concentration and dietary fat consumption (Hambleton et al., 1980; Rich et al, 1981; Apter et al., 1995). An experiment conducted by Hightshoe et al. (1991) showed that feeding beef cows ruminally protected fat also increased their serum CHOL concentrations in comparison with other conventional diets. The consistent elevations in CHOL in FAT-fed yearlings at d 30 and 60 can be regarded as positive biomarkers of the effectiveness of the dietary treatment.
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Figure 3. Serum cholesterol in weanling horses fed a conventional (CARB) or fat-supplemented concentrate (FAT). Each bar represents the mean ± SEM of six horses per treatment. On d 30 and 60, superscripts indicate increased cholesterol in FAT vs. CARB treatments (P < 0.01).
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Serum Nonesterified Fatty Acid
The analyses of d-0, -30, and -60 serum samples showed no significant treatment or treatment x time effects on NEFA concentrations. On d 30 and 60, however, there was a time effect (P < 0.01), with the 3-h concentration being significantly reduced compared to the 0-h concentration for both treatment groups (Table 3). Similarly, NEFA concentrations also tended to decrease (P = 0.13) postprandially on d 0. Concentrations of NEFA tend to decrease postprandially as metabolism shifts from a catabolic state to an anabolic state (Guyton and Hall, 1994). Therefore, this postprandial decrease was expected.
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Table 3. Nonesterified fatty acid concentrations (g/dL) in weanling horses fed a conventional (CARB) or fat-supplemented concentrate (FAT) at d 0, 30, and 60 of treatment in serum collected at 0 and 3 h relative to concentrate feedinga
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Serum Growth Hormone and Insulin-Like Growth Factor-I
Circulating GH was similar between dietary treatments on d 0 (Figure 4), but a treatment x time interaction was noted for both d 30 and 60 (P < 0.01). On d 30, GH was greater in the FAT treatment in samples taken immediately after feeding, but GH increased in CARB-fed horses between 1.4 and 1.8 h postfeeding. On d 60, GH was increased between 2.8 to 3.8 h postfeeding in horses fed the FAT diet. Both on d 30 and 60, these transient differences in GH between the CARB and FAT treatments could be accounted for by rather large secretory episodes in one or two individual animals. Thus, although periodic dietary treatment effects were noted, these effects were transient and inconsistent, and did not suggest major GH secretory differences between CARB and FAT treatments.
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Figure 4. Serum GH from 1 h before feeding to 5 h after feeding in weanling horses fed a conventional concentrate (CARB) or a fat-supplemented concentrate (FAT). Each point represents the mean ± SEM of six horses per treatment. Concentrate was fed at 0 h. On d 30 and 60, asterisks denote differences in GH in CARB- vs. FAT-fed horses (P < 0.05).
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Specifically regarding the question of meal feeding and GH secretion in the horse, the published data are conflicting. Some reports suggest that meal feeding can alter GH secretion after prolonged feed restriction, but not after normal meal consumption (Christensen et al., 1997), whereas another report did not detect changes in GH that could be associated with feeding (DePew et al., 1994). In regard to the GH results of the current experiment, consistent increases in GH were not observed following concentrate feeding. However, it should also be noted that horses in the current experiment had access to the hay portion of their diet at times other than just at the time of concentrate feeding. So, strictly speaking, these horses were not meal-fed.
There were no significant treatment x time, time, or treatment effects on serum IGF-I concentrations on d 0, 30, or 60 (Figure 5). Thus, feeding a concentrate containing 10% fat did not affect serum IGF-I concentration in weanlings when compared with a more conventional concentrate. Dietary treatment produced moderate effects on glucose and somewhat more prolonged effects on insulin; however, the lack of consistent treatment effects on GH and IGF-I suggests that these changes were not reflected in the endocrine somatotropic axis. Thus, these results suggest that feeding diets high in fat as an alternative energy source for young, rapidly growing horses will not result in altered serum IGF-I. If dietary lipids offer advantages in terms of rendering horses less susceptible to DOD, it does not appear to be reflected in systemic GH and, in turn, peripheral IGF-I. However, it should be pointed out that local production of IGF-I in bone (McCarthy and Centrella, 2001) and muscle (Florini et al., 1996; Le Roith et al., 2001) could be affected by dietary energy source, but not reflected in systemic IGF-I concentrations, which are mainly from hepatic sources (Sjogren et al., 1999).
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Figure 5. Serum insulin like growth factor-I (IGF-I) in weanling horses fed either a conventional (CARB) or fat-supplemented concentrate (FAT). Each bar represents the mean ± SEM of six horses per treatment.
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Implications
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Previous research indicated that feeding soluble carbohydrates might manipulate the growth hormone and insulin-like growth factor-I axis. This might be a causal factor in developmental orthopedic diseases in horses predisposed to such detrimental growth complications. Our data indicate that feeding a 10% fat-supplemented concentrate does not affect serum concentrations of insulin-like growth factor-I compared with a conventional soluble carbohydrate concentrate, nor does it affect feed efficiency or average daily gain. The results of the current study provide additional data supporting the concept that fat may replace a portion of the energy source in concentrates fed to young, rapidly growing horses. However, because insulin-like growth factor-I did not differ between fat-supplemented and conventional carbohydrate-supplemented foals, substitution of fat for soluble carbohydrate may not necessarily alleviate orthopedic diseases associated with rapid growth in susceptible horses.
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Footnotes
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1 Contribution No. 03-49-J from the Kansas Agric. Exp. Stn. The authors gratefully acknowledge receipt of reagents for the development of the GH assay from H. Papkoff and J. F. Roser, UC-Davis, and A. F. Parlow, National Hormone and Peptide Program, Harbor-UCLA Medical Center. 
2 Present address: Department of Animal and Veterinary Sciences, University of Idaho, Moscow 83844-2330.
3 Present address: Purina Mills, LLC, Horse Business Group, St. Louis, MO 63144.
Received for publication August 12, 2002.
Accepted for publication February 6, 2003.
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Abstract
Introduction
