J. Anim Sci. 2006. 84:2391-2398. doi:10.2527/jas.2005-281
© 2006 American Society of Animal Science
Meal size and feeding frequency influence serum leptin concentration in yearling horses
S. M. Steelman*,1,
E. M. Michael-Eller
,
P. G. Gibbs and
G. D. Potter
* Department of Medical Physiology, Texas A&M University Health Science Center, College Station, 77843; and
and
Department of Animal Science, Texas A&M University, College Station, 77843
 |
Abstract
|
|---|
Energy is an essential nutrient for all horses, and it is especially important in performance horses, pregnant and lactating mares, and young growing horses. A negative energy balance in horses such as these may result in unsatisfactory performance, decreased fertility, or slow growth. Therefore, ensuring adequate energy intake is an important aspect of the nutritional management of the equine. This study was undertaken to investigate the effects of feeding large, carbohydrate-rich, concentrate meals on the satiety-inducing hormone, leptin. Three groups of yearling horses were rotated through 3 feeding schedules in a replicated 3x3 Latin square design. Horses were fed 2, 3, or 4 times per day (2x, 3x, and 4xfeeding schedules, respectively), each for a period of 11 d, with the total amount of daily feed held constant. Horses were weighed and BCS was determined on the first day of each period. Blood samples were collected before the morning meal on d 1, 4, and 7 of each period. Additionally, blood was sampled for the last 24 h of the 2xand 4xdietary periods. Neither weight nor BCS changed during the study (P = 0.99 and P = 0.28, respectively). Both mean and peak plasma glucose were greatest in 2xhorses (P < 0.05), as were mean areas under the curve. Serum leptin concentration increased in 2xhorses (P < 0.05), but not in horses fed 3 or 4 times daily. Leptin was elevated in horses with greater BCS (P < 0.05) and increased steadily throughout the study (P < 0.05). Data from the 24-h collection indicated that 2xhorses had fluctuations in leptin production throughout the day (P < 0.05), whereas horses fed 4 times daily did not. Overall, this study indicates that feeding horses 2 large concentrate meals daily can increase mean serum leptin concentrations and may cause fluctuations in leptin production over a 24-h period. This departure from baseline leptin concentration has the potential to affect appetite, along with numerous other physiological processes.
Key Words: glucose • horse • leptin
|
INTRODUCTION
|
|---|
In today’s equine industry, many horses are fed concentrate feed, usually once or twice daily. This not only leads to an increased incidence of colic (Tinker et al., 1997
), but can also disrupt the horse’s homeostasis by increasing blood concentrations of glucose and hormones such as insulin and GH (Ropp et al., 2003). These changes in hormone concentrations have the potential to alter appetite in rodents (Menendez and Atrens, 1991; Wynne et al., 2005) along with other physiological processes, especially in the horse (DeKock et al., 2001; Sessions et al., 2004). Therefore, the effect of meal feeding on the release of hormones, especially those involved in appetite, needs to be determined.
One key hormone that regulates appetite is leptin (Campfield et al., 1995; Pelleymounter et al., 1995). Leptin is produced in the adipose tissue in response to glucose uptake and is an indicator of energy availability (reviewed in Muoio and Dohm, 2002). In many species, when serum leptin concentrations are high, appetite is decreased; however, when leptin concentrations fall, physiological processes such as reproduction and growth are put on hold to conserve energy. This relationship may hold true in the equine as well. Serum leptin concentrations increase with BCS (Buff et al., 2002) and both short-term and chronic feed restriction in mature mares result in a decline in serum leptin concentrations (Gentry et al., 2002a; McManus and Fitzgerald, 2000). The manipulation of leptin in the horse may provide a way to increase feed intake in growing horses, performance horses, and lactating mares.
Thus, the main objective of this study was to determine if feeding yearling horses multiple small carbohydrate meals daily would result in a lower serum leptin concentration than feeding 2 large meals daily. The effect of meal size and timing on the pattern of leptin secretion over a 24-h period as well as the effects of sex and BCS were also investigated.
|
MATERIALS AND METHODS
|
|---|
All experimental procedures were approved by the Texas A & M University Animal Care and Use Committee. This experiment utilized 9 Quarter Horse yearlings between the ages of 13 and 16 mo. Eight of the horses were housed in 15-x20-m drylot pens, whereas 1 horse was confined to a stall for the duration of the study due to a leg injury. Horses were divided into 3 groups, with each group randomly assigned 2 fillies and 1 gelding. All horses underwent a 10-d adaptation period to acclimate them to the pens and to eating increased amounts of feed. Horses were fed a 14% CP, pelleted concentrate (Producer’s CoOp, Bryan, TX) and coastal Bermuda grass hay in a 60:40 (wt/wt) ratio at a total intake of 2.5% of BW/d. During the adaptation period, horses were fed twice daily. Before the adaptation period, horses had been maintained on pasture and fed approximately 0.83 kg of 14% CP concentrate twice daily.
After the adaptation period, each group of horses was rotated through 3 feeding schedules in a replicated 3x3 Latin square design. The feeding schedules are summarized in Table 1. The horses were fed 2, 3, or 4 times per day (2x, 3x, and 4xfeeding schedules, respectively); amounts of hay and concentrate offered each day were held constant throughout the study at a total intake of 2.5% of BW/d. Concentrate was fed in individual stalls, whereas hay was group fed by pen. No fighting was observed during group feeding, and all horses had equal access to hay.
Each feeding schedule was fed for a period of 11 d. The following period was begun on the day after the end of the previous period, so that the duration of the entire experiment was 33 d. The study was conducted during the months of July and August. On the first day of each period, horses were weighed, BCS was determined, and blood samples were collected between 0600 and 0700, before the morning meal. Samples were also collected before the morning meal on d 4 and 7 of each period. Blood samples were collected by jugular venipuncture into Vacutainer tubes (Becton Dickinson, Franklin Lakes, NJ) and then stored at 4°C until serum was harvested.
All horses on the 2xand 4xschedules were intravenously catheterized between 1400 and 1700 on d 10. During this procedure, horses were held in stocks and restrained with an upper-lip twitch. It was necessary to sedate several of the horses with either xylazine or acepromazine or a combination of both. The 24-h blood collection began at 1800 on d 10. Blood was collected from horses every 2 h for 24 h, and the last collection occurred at 1800 on d 11. The 2xand 4xschedules were chosen for 24-h sampling because it was hypothesized that the differences in serum leptin concentrations would be most pronounced between horses fed 2 and 4 times daily. We also took into consideration the technical difficulties and animal discomfort associated with sampling that involved repeatedly placing intravenous catheters. Omitting the 3xschedule from the 24-h protocol provided the horses with a break between samplings. Blood was always taken from the horses in the same order, and all samples were taken within approximately 10 min. During these collections, the horses remained tethered to a rail, but were still fed according to the previously described schedules. Horses were tied in such a way that the concentrate could still be fed individually and hay could be group fed.
Blood samples were also collected before and after the 0700 meal on d 11 to determine the postprandial blood glucose response. These samples were taken via jugular venipuncture, and then the blood was transferred into tubes containing NaFl. The first collection was at 0630, horses were fed at 0700, and blood was taken again at 0730 and then every 30 min thereafter until 1300. Catheters were removed after the last blood collection at 1800 on d 11, and the horses were untied and allowed to move freely about their pens.
Blood tubes were centrifuged at 1,200xg for 25 min at 4°C, or until adequate separation had occurred. The resulting serum or plasma was stored at –20°C until analysis. Plasma glucose content was determined with a YSI 2300 Glucose/Lactate Analyzer (YSI, Inc., Yellow Springs, OH). Leptin was analyzed by RIA with a multi-species leptin RIA kit (Linco Research, St. Louis, MO) using established methods (McManus and Fitzgerald, 2000). According to the method of McManus and Fitzgerald (2000), our standard curve was created using solutions of 0.5, 1.0, 2.0, 5.0, 10.0, and 20.0 ng/mL of human leptin. This assay has previously been validated for use in horses (Buff et al., 2002). The intra- and interassay coefficients of variation for control serum samples were 6.7 and 15.7%, respectively. The limit of detection of the assay was 0.5 ng/mL. Results are reported in nanograms of human equivalents (HE) per milliliter.
Statistical analyses were performed using a statistical software package (Stata 7.0, StataCorp, College Station, TX). Areas under the plasma glucose concentration–time curves were calculated by using the trapezoidal rule. Plasma glucose concentrations were subjected to ANOVA. Variables within the model included time, feeding schedule, and the time by feeding schedule interaction. Analyses of variance were also performed on serum leptin concentrations to determine the influence of BCS, sex, feeding schedule, square, and period. When differences were found at P < 0.05, means were separated using a Fisher–Hayter pairwise comparison or Student’s t-test as appropriate. Additionally, some data were normalized to either a d 1 or a time zero value, which was representative of a baseline. This was done to better visualize changes in the concentration of leptin. Simple regression analysis was performed to determine the correlation between mean serum leptin concentrations and mean BCS. Regression analysis was also used to fit normalized serum leptin concentrations from the 24-h blood collections to either a linear or quadratic model.
|
RESULTS AND DISCUSSION
|
|---|
Feed Intake and Refusals
Horses on the 2x, 3x, and 4xfeeding schedules were offered an average of 2.58 ± 0.06 kg, 1.74 ± 0.04 kg, and 1.30 ± 0.08 kg concentrate per meal, respectively. Amounts of feed refused per meal were negligible. No difference in satiety was noted among horses on the 3 feeding schedules.
Weight and BCS
Although the horses used in this study were young, growing yearlings, BW did not increase appreciably (P = 0.99) during the experimental period (342 ± 10.1 kg during period 1 to 354 ± 10.1 kg during period 3). Furthermore, regression analysis of BW showed no correlation with period (r2 = 0.459, P = 0.71; data not shown). This may have been due to the short duration of the study or to variations in the horses’ hydration status or amount of digesta in the gut at the time of weighing. Average daily gain was 0.39 ± 0.14 kg. Body weight was not correlated with BCS (P = 0.19) or with sex. This was most likely due to the lack of variation in BW and BCS in this population of horses. Body condition score was influenced heavily by sex, with females having a greater mean BCS than males (P < 0.01; 5.14 vs. 4.61; data not shown). No effect of feeding schedule was observed (P = 0.90) on either BW or BCS (Table 2).
Postprandial Plasma Glucose
Baseline glucose concentrations did not differ among horses on feeding schedules (P = 0.83; Table 3). Post- prandial concentrations of plasma glucose varied over the 6 h that blood was drawn (P < 0.05; Figure 1). Plasma glucose concentration differed significantly among feeding schedules at only 2 time points: at 30 and 120 min postfeeding, glucose concentration was greatest (P < 0.05) in horses on the 2xschedule. Peak glucose was greater (P < 0.05) on the 2xcompared with the 4xschedule, but did not differ among horses on the 2xand 3xor 3xand 4xfeeding schedules (Table 3). Mean glucose varied with feeding schedule (P < 0.05): mean concentrations of glucose were greater in horses on the 2xschedule than those on the 3xor 4xschedules (P < 0.05), although there was no difference between the 3xand 4xschedules. The area under the curve on the 2xschedule was greater (P < 0.05) than that on the 3xand 4xschedules, but the 3xschedule did not differ from the 4x. These results in concert indicate that the larger amounts of concentrate fed per meal on the 2xschedule did in fact result in a larger plasma glucose response than the smaller amounts fed on the 3xand 4xschedules.
View larger version (15K):
[in this window]
[in a new window]
|
Figure 1. Postprandial plasma glucose concentrations in yearling horses fed 2 (2x), 3 (3x), or 4 (4x) times daily. Measurements taken on d 11 of each period. Each point represents the mean ± SEM of 9 horses; arrow indicates time of feeding. Asterisks indicate difference (P < 0.05) between glucose concentrations of horses on the 2xfeeding schedule and horses on the 3xand 4xfeeding schedules at 0.5 and 2 h postfeeding.
|
|
Glucose concentration also varied with period, as shown in Table 4. Horses had a lower mean glucose concentration during period 1 (P < 0.05) than during the other 2 periods. Peak glucose concentration was greater in period 3 than in periods 1 or 2 (P < 0.05). Mean change from baseline to peak was greater during period 3 (35.27 mg/dL) than during either period 1 (17.53 mg/dL) or period 2 (16.84 mg/dL; P < 0.01). Interestingly, baseline concentrations of glucose were lower during period 3 (P < 0.05) than during period 2.
Leptin: Influence of Feeding Schedule
Serum leptin concentrations on the first day of each period served as baseline values (Table 5). These values differed among feeding schedules (P < 0.05) and would have been reflective of the previous feeding schedule rather than the current feeding schedule, so all data were normalized to leptin concentration on d 1 of each period. Additionally, the nonnormalized mean concentration of leptin did not differ among horses on different feeding schedules. Analysis of normalized data indicated an effect of feeding schedule, with the 2xschedule having a greater change in leptin than the 3xschedule, which changed more than the 4xschedule (P < 0.05). Additionally, the changes in leptin concentration from d 1 to d 7 were different than zero only on the 2xand 3xfeeding schedules (Table 5; P < 0.05). The change in leptin concentration on the 4xschedule was not different from zero. It is possible that further increases in leptin would have been apparent if the experimental periods had been longer.
View this table:
[in this window]
[in a new window]
|
Table 5. Effect of feeding schedule on serum leptin concentration in yearling horses fed 2 (2x), 3 (3x), or 4 (4x) times daily
|
|
These data lend support to the hypothesis that large carbohydrate meals can elevate serum leptin concentrations in the equine over a period of days, independent of total daily amount of feed consumed. Several short reports have indicated that serum leptin concentration rises postprandially in the equine (Cartmill et al., 2005; Crowley et al., 2005; Storer et al., 2005), perhaps stimulated by a rise in serum insulin concentration. However, this is the first evidence in any species that meal size alone influences the production of leptin. In a study of 5 obese women, Fogteloo et al. (2004) showed that increasing feeding frequency from 3 to 8 times daily did not affect mean leptin concentration over a 24-h period. However, the differences in species, age, sex, and nutritional status between subjects used in this study and by Fogteloo et al. (2004) may very well have contributed to the disparate results.
Leptin: Influence of BCS and Sex
Serum leptin concentrations were found to vary with BCS (P < 0.05), confirming the results of Buff et al. (2002). Figure 2 demonstrates the positive correlation between BCS and leptin concentration. Contrary to previous studies (Buff et al., 2002; Gentry et al., 2002b), sex did not significantly influence leptin concentration (P = 0.81). Mean leptin was 2.33 ± 0.12 ng of HE/mL in males and 2.17 ± 0.09 ng/mL in females, despite the fact that females had a much greater BCS than males, which could have caused a skewing of any sex effects. In other studies, the differences in leptin concentration between the 2 sexes may have been due to the presence of androgens and estrogens. Because all the horses in this study were fairly young, these variables may not have come into play, thus rendering the sex effect not significant. However, several studies have reported that sex hormones may not, in fact, be responsible for the sex differences seen in leptin concentration. Ovariectomy did not change serum leptin concentration in mares (Buff et al., 2005), and no differences have been seen between stallions and geldings fed a similar diet (Buff et al., 2002). It is also necessary to remember that many factors besides sex hormone concentrations differ between the young animals used in this study and the mature horses used in previously published work. For example, GH is greater in younger horses than in older ones (Stewart et al., 1993); it is also greater in stallions and geldings than in mares (Thompson et al., 1994). Because GH has been shown to increase serum leptin concentrations in other species (Lissett et al., 2001), this must be kept in mind when comparing this study to others.
View larger version (8K):
[in this window]
[in a new window]
|
Figure 2. Correlations between mean leptin concentration [ng of human equivalents (HE)/mL] and mean BCS (r2 = 0.88, P = 0.02). Each point represents the mean ± SEM of 9 yearling horses.
|
|
Leptin: Influence of Period
Mean leptin concentration for all horses increased over all 3 periods (P < 0.05), as shown in Table 4
. The increase in leptin is most likely attributable to the rise in BCS: a larger fat mass has a greater capacity to produce leptin. Although BCS did not increase significantly during the course of the study, the pattern of change is uniform and it may have been enough to change leptin concentration. Furthermore, the greater plasma glucose concentrations experienced by the horses during period 3 may have also contributed to the elevation in leptin from period 2 to period 3.
Other Factors
Several variables differed among the groups, most notably the administration of medications. Horses not receiving sedation may have been more stressed during catheterization, resulting in a release of cortisol. This could have increased production of leptin because glucocorticoids have been shown to stimulate leptin production in the horse (Gentry et al., 2002a). Alternatively, many of the horses were sedated for the catheterization procedure, and the effect of sedatives on leptin production is unknown. However, data from those individuals receiving sedation does not indicate that this had any effect on leptin concentration (data not shown). Because many equine studies involve stressful situations such as catheterization, as well as the administration of sedatives, the effects of both cortisol and sedatives on leptin production needs to be taken into consideration in future research.
Previous studies have also shown variations in serum leptin concentrations with season. For example, leptin concentrations are greater in the winter than in the summer in both young and mature mares (McManus and Fitzgerald, 2003), although the opposite was found in undernourished mares (Buff et al., 2005). However, due to the short duration of this study, it is unlikely that our results reflect seasonal changes in leptin concentration.
Circadian Rhythm of Leptin
Analysis of data taken over a 24-h period showed many of the same results as the data taken on d 1, 4, and 7. The 24-h leptin concentrations were heavily influenced by period (P < 0.05; Table 6). Although we found a strong correlation between BCS and leptin in samples taken on d 1, 4, and 7, we were unable to demonstrate a relationship between mean 24-h serum leptin concentration and BCS (Figure 3). This suggests that BCS may only be correlated with prefeeding serum leptin concentrations. Unlike leptin concentration data from samples obtained once per day, the 24-h data indicated a strong effect of sex (P < 0.01). Average leptin concentration in males was 2.48 ng of HE/mL and only 2.17 ng of HE/mL in females. This is surprising given the difference in BCS between the sexes, but corroborates previous results (Buff et al., 2002).
View this table:
[in this window]
[in a new window]
|
Table 6. Effect of period on mean serum leptin concentration over 24 h in yearling horses fed either twice (2x) or 4 times (4x) daily
|
|
View larger version (7K):
[in this window]
[in a new window]
|
Figure 3. Correlation between mean leptin concentration [ng of human equivalents (HE)/mL] in samples taken during a 24-h period and mean BCS (r2 = 0.05; P = 0.61).
|
|
One of the most prominent features of this portion of the study was the highly individualized pattern of leptin secretion over the 24-h period. Some horses responded very differently to the 2xand 4xschedules, whereas some did not differ at all. Likewise, some horses showed variations in serum leptin concentration with time, whereas some did not. This is illustrated in Figures 4A and 4B. The 2 horses represented in Figure 4 were both fillies of approximately the same BCS, yet they show 2 very different patterns of leptin release over the 24-h period.
View larger version (12K):
[in this window]
[in a new window]
|
Figure 4. Serum leptin concentration [ng of human equivalents (HE)/mL] over a 24-h period in 2 yearling fillies fed 2 (2x) or 4 (4x) times daily. A) shows data from horse 3A, and B) shows data from horse 2C.
|
|
Mean leptin concentration over the 24-h period was 2.24 ± 0.08 ng of HE/mL on the 2xschedule and 2.32 ± 0.07 ng of HE/mL on the 4xschedule (Table 6). Because of the differences in baseline concentrations of leptin between horses, data were normalized to the first data point, which was taken at 1800 on d 10. Three hours after feeding, the normalized leptin concentration was lower on the 2xschedule than on the 4xschedule (P < 0.05; Figure 5). At this point, leptin concentration on the 2xschedule was also lower (P < 0.05) than at 0600, 0800, 1000, 1200, and 1400. Because horses were fed at 1900 and 0700, these data seem to indicate that leptin concentration fell after the evening meal, only to rise again before the morning feeding, and then remain elevated postprandially. Because horses were tethered for the entire 24-h period, it is possible that the stress of restraint caused a prolonged release of cortisol, and that this affected the pattern of leptin secretion. Synthetic glucocorticoids have been shown to elevate serum leptin concentration in equines (Gentry et al., 2002a; Cartmill et al., 2003); thus, elevated cortisol levels may account for the sustained rise in leptin seen from 0200 to 1600. A postprandial decrease in leptin (from 1900 to 2200) has been noted previously in cattle (Delavaud et al., 2002), although small post-prandial peaks have been found in sheep 2 to 8 h after a meal (Marie et al., 2001). Two studies have found that, in mature horses, leptin concentrations are greater in the evening than in the morning (Buff et al., 2005; Cartmill et al., 2005). Furthermore, horses that are not grain-fed do not display a diurnal variation in leptin (Cartmill et al., 2005; Buff et al., 2005). The fact that horses on the 4xschedule did not experience the same fluctuations in leptin as those on the 2xschedule suggests that feeding 4 small meals daily results in a pattern of leptin secretion that more closely mimics that of grazing horses. Analysis of leptin concentration in 2xhorses shows a significant effect of time (P < 0.05), whereas leptin concentration did not vary with time in horses fed 4 times daily (Figure 5). Regression analysis of the normalized data from the 2xfeeding schedule indicates that leptin concentrations vary significantly with time in a quadratic model (P < 0.05). Regression analysis of data from the 4xschedule showed no variance with time in either a linear or quadratic model. This indicates that, when horses are fed 2 large concentrate meals daily, there are definite changes in leptin secretion over a 24-h period. On the other hand, when horses are fed multiple small meals daily, serum leptin does not change with time. However, a study done by Piccione et al. (2004) found an innate circadian rhythm of leptin in horses, wherein leptin peaked during dark hours and fell during the day. This pattern was not abolished by feed deprivation. The reason for the discordance in results is unknown, but may be due to experimental procedure or the age of the horses used in this study, as mentioned previously. As stated earlier, horses may require several days for their serum leptin concentrations to reach a new steady-state level after an acute stimulus: if Piccione et al. (2004) only measured leptin concentration after 24 h of fasting, the effects may not have been visible at that time point. Furthermore, our results are in accordance with a study done by Marie et al. (2001), which found no innate circadian rhythm of leptin in sheep. This suggests that the imposition of meal feeding upon horses affects more than simply gut function; it may also disrupt the release of hormones and change the homeostasis of the animal.
View larger version (16K):
[in this window]
[in a new window]
|
Figure 5. Mean serum leptin concentrations [ng of human equivalents (HE)/mL] over a 24-h period in yearling horses fed 2 (2x) or 4 (4x) times daily. All values were normalized to first concentration at 1800. Solid arrows indicate feeding times on the 2xschedule, whereas open arrows indicate feeding times on the 4xschedule. Each point represents the mean ± SEM of 9 horses; asterisk indicates a difference in means (P < 0.05).
|
|
1 Corresponding author: smbruce{at}neo.tamu.edu
Received for publication May 26, 2005.
Accepted for publication April 26, 2006.
|
LITERATURE CITED
|
|---|
Buff, P. R., A. C. Dodds, C. D. Morrison, N. C. Whitley, E. L. McFadin, J. A. Daniel, J. Djiane, and D. H. Kiesler. 2002. Leptin in horses: Tissue localization and relationship between peripheral concentrations of leptin and body condition. J. Anim. Sci. 80:2942–2948.[Abstract/Free Full Text]
Buff, P. R., C. D. Morrison, V. K. Ganjam, and D. H. Keisler. 2005. Effects of short-term feed deprivation and melatonin implants on circadian patterns of leptin in the horse. J. Anim. Sci. 83:1023–1032.[Abstract/Free Full Text]
Campfield, L. A., F. J. Smith, Y. Guisez, R. Devos, and P. Burn. 1995. Recombinant mouse OB protein: Evidence for a peripheral signal linking adiposity and central neural networks. Science 269:546–549.[Abstract/Free Full Text]
Cartmill, J. A., D. L. Thompson Jr., L. R. Gentry, H. E. Pruett, and C. A. Johnson. 2003. Effects of dexamethasone, glucose infusion, adrenocorticotropin, and propylthiouracil on plasma leptin concentrations in horses. Domest. Anim. Endocrinol. 24:1–14.[CrossRef][Medline]
Cartmill, J. A., D. L. Thompson Jr., W. A. Storer, J. C. Crowley, N. K. Huff, and C. A. Waller. 2005. Effect of dexamethasone, feeding time, and insulin infusion on leptin concentrations in stallions. J. Anim. Sci. 83:1875–1881.[Abstract/Free Full Text]
Crowley, J. C., D. L. Thompson, Jr., W. A. Storer, and J. A. Cartmill. 2005. The role of insulin in the rise in plasma leptin concentrations after a meal in stallions. Page 146 in Proc. Equine Sci. Soc., Tuscon, AZ. Equine Sci. Soc., Savoy, IL.
De Kock, S. S., J. P. Rodgers, B. C. Swanepoel, and A. J. Guthrie. 2001. Administration of bovine, porcine and equine growth hormone to the horse: Effect on insulin-like growth factor-I and selected IGF binding proteins. J. Endocrinol. 171:163–171.[Abstract]
Delavaud, C., A. Ferlay, Y. Faulconnier, F. Bocquier, G. Kann, and Y. Chilliard. 2002. Plasma leptin concentrations in adult cattle: Effects of breed, adiposity, feeding level, and meal intake. J. Anim. Sci. 80:1317–1328.[Abstract/Free Full Text]
Fogteloo, A. J., H. Pijl, F. Roelfsema, M. Frolich, and A. E. Meinders. 2004. Impact of meal timing and frequency on the twenty-four-hour leptin rhythm. Horm. Res. 62:71–78.[CrossRef][Medline]
Gentry, L. R., D. L. Thompson, G. T. Gentry, K. A. Davis, and R. A. Godke. 2002a. High versus low body condition in mares: Interactions with responses to somatotropin, GnRH analog, and dexamethasone. J. Anim. Sci. 80:3277–3285.[Abstract/Free Full Text]
Gentry, L. R., D. L. Thompson, G. T. Gentry, K. A. Davis, R. A. Godke, and J. A. Cartmill. 2002b. The relationship between body condition, leptin, and reproductive and hormonal characteristics of mares during the seasonal anovulatory period. J. Anim. Sci. 80:2695–2703.[Abstract/Free Full Text]
Lissett, C. A., P. E. Clayton, and S. M. Shalet. 2001. The acute leptin response to GH. J. Clin. Endocrinol. Metab. 86:4412–4415.[Abstract/Free Full Text]
Marie, M., P. A. Findlay, L. Thomas, and C. L. Adam. 2001. Daily patterns of plasma leptin in sheep: Effects of photoperiod and food intake. J. Endocrinol. 170:277–286.[Abstract]
McManus, C. J., and B. P. Fitzgerald. 2000. Effects of a single day of feed restriction on changes in serum leptin, gonadotrophins, prolactin, and metabolites in aged and young mares. Domest. Anim. Endocrinol. 19:1–13.[CrossRef][Medline]
McManus, C. J., and B. P. Fitzgerald. 2003. Effect of daily clenbuterol and exogenous melatonin treatment on body fat, serum leptin and the expression of seasonal anestrus in the mare. Anim. Reprod. Sci. 76:217–230.[CrossRef][Medline]
Menendez, J. A., and D. M. Atrens. 1991. Insulin and the paraventricular hypothalamus: Modulation of energy balance. Brain Res. 555:193–201.[CrossRef][Medline]
Muoio, D. M., and G. L. Dohm. 2002. Peripheral metabolic actions of leptin. Best Pract. Res. Clin. Endocrinol. Metab. 16:653–666.[CrossRef][Medline]
Pelleymounter, M. A., M. J. Cullen, M. B. Baker, R. Hecht, and D. Winters. 1995. Effects of the obese gene product on body weight regulation in ob/ob mice. Science 269:540–543.[Abstract/Free Full Text]
Piccione, G., C. Bertolucci, A. Foa, and G. Caola. 2004. Influence of fasting and exercise on the daily rhythm of serum leptin in the horse. Chronobiol. Int. 21:405–417.[CrossRef][Medline]
Ropp, J. K., R. H. Raub, and J. E. Minton. 2003. The effect of dietary energy source on serum concentration of insulin-like growth factor-I growth hormone, insulin, glucose, and fat metabolites in weanling horses. J. Anim. Sci. 81:1581–1589.[Abstract/Free Full Text]
Sessions, D. R., S. E. Reedy, M. M. Vick, B. A. Murphy, and B. P. Fitzgerald. 2004. Development of a model for inducing transient insulin resistance in the mare: Preliminary implications regarding the estrous cycle. J. Anim. Sci. 82:2321–2328.[Abstract/Free Full Text]
Stewart, F., J. A. Goode, and W. R. Allen. 1993. Growth hormone secretion in the horse: Unusual pattern at birth and pulsatile secretion through to maturity. J. Endocrinol. 138:81–89.[Abstract/Free Full Text]
Storer, W., D. Thompson, C. Waller, and J. Cartmill. 2005. Endocrine profiles in hyperleptinemic and normal mares in response to common feeding practices. Page 144 in Proc. Equine Sci. Soc., Tuscon, AZ. Equine Sci. Soc., Savoy, IL.
Thompson, D. L., Jr., C. L. DePew, A. Ortiz, L. S. Sticker, and M. S. Rahmanian. 1994. Growth hormone and prolactin concentrations in plasma of horses: Sex differences and the effects of acute exercise and administration of growth hormone-releasing hormone. J. Anim. Sci. 72:2911–2918.[Abstract]
Tinker, M. K., N. A. White, P. Lessard, C. D. Thatcher, K. D. Pelzer, B. Davis, and D. K. Carmel. 1997. Prospective study of equine colic risk factors. Equine Vet. J. 29:454–458.[Medline]
Wynne, K., S. Stanley, B. McGowan, and S. Bloom. 2005. Appetite control. J. Endocrinol. 184:291–318.[Abstract/Free Full Text]
This article has been cited by other articles:
|
|
|
|
 
W. A. Storer, D. L. Thompson Jr., C. A. Waller, and J. A. Cartmill
Hormonal patterns in normal and hyperleptinemic mares in response to three common feeding-housing regimens
J Anim Sci,
November 1, 2007;
85(11):
2873 - 2881.
[Abstract]
[Full Text]
[PDF]
|
|
|
Top
Abstract
INTRODUCTION
