Effects of growth hormone-releasing factor and feed intake on energy metabolism in growing beef steers: net hormone metabolism by portal-drained viscera and liver.

Effects of Growth Hormone-Releasing Factor and Feed Intake on Energy Metabolism in Growing Beef Steers: Net Hormone Metabolism by Portal-Drained Viscera and Liver 'r2r3

H. Lapierred, C. K. Reynoldss, T. H. Elsasser, P. Gaudreaue, P. Brazeaus, and H. F. Tyrrell'

ABSTRACT: Effects of growth hormone-releasing factor (GRF) and intake on arterial concentrations and net visceral metabolism of hormones were measured in six growing Hereford x Angus steers using a split-plot design with 4-wk injection periods within 8-wk intake periods. Steers were fed a 75% concentrate diet at two intakes and were injected S.C.twice daily with saline or GRF (10 pg/ kg of BW). Arterial concentrations of growth hormone (GH) were measured on d 1 and d 8 to 10 of injections. Eleven measurements, obtained at 30-min intervals, of arterial concentration and net flux of hormones across portal-drained viscera (PDVI and liver were obtained on d 8 to 10 of injections (six hourly measurements were used for insulin-like growth factor-I UGF-I1 and somatostatinl. The area under the GH curve and average and peak GH concentrations were increased (P
.lo) plasma flow through the splanchnic tissues (Table 21. Growth Hormone. Growth hormone response as measured by the total AUC following the injection was increased by GRF (P < .011 and was higher (P c .05) in steers fed at low than in those fed at high intake (Table 3). Similarly, the peak concentration reached after the injection was higher (P c .01) after GRF than after saline injection, but only tended (P < .lo) to be affected by intake. There was no significant (P > .lo) interaction of day x treatment for the peak, but there was a tendency (P < .lo) for GH-AUC after GRF injection to be higher on the last day of injection compared with the fiist day (control: 585 and 689; GRF: 1,879 and 2,467 ng.mjn-l.mL-l for the first and last days of injection, respectively). Generally, arterial GH concentrations reached peak levels within 40 min and returned to baseline levels within 210 min of GRF injection. The mean GH concentration of

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LAPIERRE ET AL.

Table 3. Effect of intake and growth hormone-releasing factor (GRP) on arterial growth hormone (GH) response in growing steersa Treatmentb

Treatment effect'

LO-SAL LOGRF HI-SAL HI-GRF

Item Peak, ng/mL AUC', ng.min-'.mL-'

7.0 907

3.1 367

28.7 2,874

15.8 1,471

WPEMS~ 178.1 1,250,708

SPEMS~ Intake 208.9 1,406,320

,098 ,041

GRF

Intake x GRF

.004 .002

.322 .235

concentration differences were not different (P > .lo) from 0 and were not affected (P > .lo) by treatments except for the HA difference, which was decreased (P < .05)at high compared with low intake (Table 2). Similarly, IGF-I net flux through TSP tissues was decreased (P < .051 and PDV net flux tended (P < .lo) to decrease at high compared

with low intake. Liver flux was not affected ( P > .lo) by treatments. Insulin. High intake increased (P < .05) and GRF tended to increase ( P < .lo) arterial insulin concentration. All insulin VA were different (P < .05) from 0. Portal-arterial difference was increased (P < .05) by both intake and GRF treatments.

Table 4. Effect of intake and growth hormone-releasing factor (GRF) on net flux (pg/h) of hormones across visceral tissues of growing steersa ~

~~

~~

~~~~~~~

Treatmentb Item

LO-SAL LO-GRF HI-SAL

Portal-drained viscera 52.4 Growth hormone InsULin 83.5 Glucagon 33.2 Somatostatin 7.1 IGF-I' 714.4 Liver Growth hormone -105.8 Insulin -33.4 Glucagon -19.8 Somatostatin -2.3 IGF-I -24 1.3 Total splanchnic tissues Growth hormone -132.8 Insulin 67.8 Glucagon 10.7 Somatostatin 9.2 IGF-I -503.4 Liver extraction ratio, % Growth hormone -8.5

Insulin Glucagon Somatostatin

-8.0 -13.1

-. 1

Treatment effect' HI-GRF

-66.1 102.5 23.5 8.8 945.1

12.4 104.9 40.9 13.1 -1.720.4

-181.1 187.5 49.0 -8.8 -88.4

-03.1 -22.8 -15.3 -3.3 281.5

-102.7 -23.1 -21.4

-286.7 -67.9 -16.5

-409.7

-129.7 79.3 8.4 0.3 005.3 -2.8 -5.4 -11.0 -1.3

WPEMS~

SPEMS~

7,883.0 40,882.2 092.2 928.9 191.5 86.7 15.4 80.2 1,168,267.2 2,203,207.7

n

Intake

GRF

Intake x GRF

20 20 20 20 20

.483 .001

.009

.107 .158 .913 .005 .240

.758 907 .142 .089 .444

.010

.258

-933.5

51,109.1 854.8 109.3 24.5 298,869.3

19,800.9 503.1 78.5 140.3 890,975.0

20 20 20 20 20

.311 .190 .773 .885 .190

.572 .172 .317 .206 950

.133 .082 .970 .229 .402

-73.7 123.1 20.7 3.1 -2,538.1

-414.4 137.5 31.2 -2.7 -1,351.2

52,893.8 1,021.5 108.2 84.8 1,705,815.4

32,031.6 2,715.5 45.7 218.4 3,461,099.0

23 23 23 23 23

.324 .020 .049 .133 .025

.070 .584 .210 .518 .200

.094 361 .093 .853 367

-12.2 -2.8

-10.3 -6.8 -5.9 2.2

105.4 12.1 13.2 4.0

54.7 22.1 22.4

20 20 20

25.0

20

.190 .460 .087 .803

.338 .759 .390 .338

375 .273 .838 .333

-10.6

-8.0

3.4

0.9

aLeast squares means with error mean squares from analysis of variance. hreatment: animals were fed at low [LO: 50 g/kg.751 or high MI: QO/kg.75) intake and received, during 3 wk, twice-daily S.C. injections of saline (SALI or GRF (10 p g k g per injection). Variables were measured after 8 to 10 d of injection. 'Probability corresponding to the hypothesis of no treatment effect. dWhole-plot error mean square with 3 (n = 201 or 4 (n = 23) df. 'Subplot error mean square with 5 (n = 201 or 7 (n 23) df. 'IGF-I: Insulin-like growth factor I. E

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*Least squares means with error mean squares from analysis of variance of the mean response observed on d 1 and d 8 to 10 of injections. ~ 1high CHI: 9O1kg'~) intake and received, during 3 wk, twice-daily S.C. hreatment: animals were fed at low (LO: 50 g / l ~ g . ~or injections of saline (SAL) or GRF (10 pg/kg per injection). CProbabfitycorrespondingto the hypothesis of no treatment effect. There WBS no significant day x treatment interaction (P > .lo) except for the AUC, where the interaction day x GRF tended Lp = .OB1 to be significant. dWhole-plot error mean square with 4 df. *Subplot error mean square with 8 df. fAUC: area under the curve.

HORMONE METABOLISM IN GRF-TREATED CA'ITLE

Discussion Plasma flow through PDV and liver tissues was not affected by GRF treatment. Similarly, GH treatment did not alter liver 4nd PDV blood flow in lactating dairy cows (Cohick et al., 19891. In dairy cows, GH treatment increased cardiac output and

mammary blood flow Davis et al., 1988) and tended to increase blood flow to leg muscle (McDowell et al., 1987).This redistribution of blood flow in GH-treated animals toward tissues requiring an extra supply of nutrients to respond to GH treatment may partly contribute to the proposed homeorhetic role of GH (Bauman and Currie, 1980). Increased intake increased plasma flow, as already reported Weynolds et al., 19911. Growth hormone arterial concentration and GH response to GRF were decreased in steers fed at high intake compared with low intake. In growing cattle, reduced feed, protein, or energy intake has already been repm-ted to increase GH concentration (Sersjen et al., 1983; Breier et al., 1986, 1988a; Houseknecht et al., 1988). However, in other reports, feed restriction had no effect on GH concentration Wrenkle and Topel, 1978; Serjsen et al., 1983; Peters, 1986) or decreased it (Rule et al., 1985; Elsasser et al., 1988). The reasons for these discrepancies are not clear, but the degree of restriction, the age of the animal, the type of diet, and the sampling protocol employed may interact to affect measured GH concentration. In cattle, the GH response to arginine (McAtee and Trenkle, 1971; Houseknecht et al., 1988) was higher in feedrestricted animals, whereas the GH response to thyrotropin-releasing factor was higher in feedrestricted prepubertal heifers but not in postpubertal heifers (Serjsen et al., 19831. In sheep, the mean GH postinjection concentration after GRF administration was higher in animals maintained in negative than in those maintained in positive energy balance (Hart et al., 1985). However, in one report, response to i.v. GRF was not affected by the plane of nutrition in growing cattle CElsasser et al., 1989). Greater GH response to different stimuli in feedrestricted animals may indicate a greater propensity of the pituitary to release GH when animals are in a deficient nutritional status. Circulating metabolites affected by feed restriction such as glucose and nonesterified fatty acids (NEFAI were proposed to affect GH secretion. However, lowering NEFA concentration and increasing glucose concentration slightly (a contrary effect of feed restriction) increased GRF action on GH concentration in sheep (Sartin et al., 1988). Also, a feedback control through circulating IGF-I concentration can alter GH secretion. In vitro, IGF-I acted to decrease GH secretion at both the hypothalamus and the pituitary level (Berelowitz et al., 1981). However, feed restriction failed to decrease IGF-I concentration in our study. An increase in pituitary responsiveness to secretagogues may not be the only cause of increased GH concentration in feed-restricted animals. Postsecretory metabolism of GH may also affect GH


Treatments did not affect 0 > .lo) HA difference, and there was a GRF x intake interaction (P < .051 on HP difference because GRF decreased HP difference at low intake but increased it at high intake (Table 2). Net PDV release was increased (P < .05)by intake but was not affected (P > .lo) by GRF. Intake and GRF tended (P < .lo) to interact on liver net flux. Total splanchnic flux waa increased (P < .05)by intake but was not affected (P r .lo) by GRF CI'able 4). The liver extraction ratio was not affected (P > .lo) by treatments. The percentage of insulin released into the portal vein and removed by the liver averaged 34,21, 14, and 41% for LO-SAL, LO-GRF, HI-SAL,, and HI-GRF, respectively. Intake and GRF tended (P < .lo) to interact on this trait. GIucugon. Glucagon arterial concentration was increased (P < .05)by intake but was not affected ( P > .lo) by GRF (Table 2). Glucagon VA were different CP < .01) from 0. The VA measured were not affected (P > ,101 by treatments [Table 2). Net PDV flux was increased CP < .05) by intake; liver flux was not affected (P > .lo) by treatments. Net TSP flux was affected CP < .05) by intake but the interaction GRF x intake tended to be significant CP < .lo) because GRF decreased TSP flux at low intake but increased it at high intake (Table 41. The liver extraction ratio tended (P < .lo) to decrease with increased intake (Table 4). Glucagon removed by the liver as a percentage of the glucagon released into the portal vein was decreased (P < .05)on high intake and averaged 66,63, 54, and 31% LO-SAL, LO-GRF, HI-SAL, and HI-GRF, respectively. Sornufostutin. Arterial concentration of somatostatin was not affected (P > .lo) by treatments (Table 21. The PA and HA VA were significantly different (P < .05) from 0, but HP VA was not (P> .lo). The PA difference was decreased CP < .05) by GRF but there was a tendency (P e .lo) for a GRF x intake interaction because GRF decreased the VA more at high than at low intake. The HP difference was not affected (P > .lo) by treatments and, finally, the HA difference was higher (P < .05) on low than on high intake (Table 21. For net flux measurements, GRF tended to decrease (P < .lo) PDV net flux only at high intake, whereas treatments had no effect on liver and TSP net flux [Table 4).

747

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LAPIERRE ET AL.

old has to be reached before feed restriction begins to affect blood concentration. Direct GH administration increased IGF-I concentration in growing cattle, following acute (Breier et al., 1988a; Elsasser et al., 1989) or chronic treatment (Sandles and Peel, 1987). Similarly, GRF treatment increased IGF-I concentration Blouzek et al., 1988; Abribat et al., 1990). The effect of a single GH injection on IGF-I concentration was dependent on nutritional status. In animals under severe feed restriction, GH administration did not elicit any increase in IGF-I concentrations (Breier et al., 1988a; Elsasser et al., 1989). However, in other animals in which feed restriction was less drastic, the magnitude of the response to exogenous GH was similar regardless of the plane of nutrition (Elsasser et al., 1989). This is in agreement with our observations: GRF treatment increased IGF-I concentration to a similar extent at both intakes. The relevance of blood IGF-I as a driving force for growth and metabolism rather than a reflection of growth and metabolism enhanced by other factors or even by locally produced IGF-I remains to be determined. In this regard, the proposed role of the liver as a source of IGF-I for an endocrine function is uncertain. In fact, many tissues contain IGF-I (D'Ercole et al., 1984) and messenger RNA encoding for IGF-I (Roberts et al., 1986). However, the liver is a major source of IGF-I (Steele and Elsasser, 1989) and there is a close correlation between liver GH receptors and IGF-I concentration in plasma lSreier et al., 1988131. In our study, the HP difference for IGF-I was not different from 0 and was often negative, and there was no treatment effect on IGF-I flux through the liver. In dairy cows, the HP difference for IGF-I was not different from 0 and varied from positive to negative (Reynolds et al., 1989). Cohick et al. (1989) also reported no effect of GH treatment on the pattern of IGF-I response in hepatic and portal veins in dairy cows. But, even if all the IGF-I increase had come from the liver, liver blood flow is so large that the difference in VA would have been below the detection limit of the IGF-I assay. In another study, GH treatment during the 1st mo of life of dairy calves increased hepatic vein IGF-I concentration severalfold. However, variations in IGF-I concentrations in the portal vein and artery were not clearly reported and the increase was noted as early as 90 min after the beginning of the treatment (Coxam et al., 1988). The IGF-I VA were not different from 0,so the effect of intake on IGF-I flux through TSP tissues should be interpreted with care. This effect mainly came from a tendency of PDV tissues to remove more IGF-I when animals were fed at high intake. In dairy cows, PA difference switched from posi-


concentration in peripheral circulation. In bulls, a 23-h fast increased the half-life and decreased the metabolic clearance rate of GH compared with a 4-h fast [Trenkle, 1976). However, feed restriction of growing steers failed to alter the kinetics of GH (Trenkle and Topel, 1978). The lack of significance of VA for GH across PDV, already reported in steers [Reynolds et al., 1986) and in cows (Reynolds et al., 19891, resulted in a PDV flux that fluctuated from positive to negative. This variation in PDV flux of GH has been observed in steers (Harmon and Avery, 1987) and in cows (Reynolds et al., 1989) and provides no clear explanation of the fate of GH in PDV tissues. Receptors for GH have been reported to be localized on many cells of the digestive tract in the rat (Lobie et al., 1990). In contrast, negative significant values for HP difference and liver flux indicate a net uptake of GH by the liver. In cows, HP differences were also negative, but not significant, and the liver extraction ratio was smaller than the extraction ratio observed in this experimentation (Reynolds et al., 1989). The uptake of GH by the liver is in agreement with the presence of GH receptors on the liver, reported in many species, including bovines (Breier et al., 198813). In growing steers, feed restriction decreased the binding of GH to liver membranes (Breier et al., 1988b1, but at a level of intake (1% DM per kilogram of BWI that decreased blood IGF-I concentration (Breier et al., 1988a). In our study, intake did not affect IGF-I concentration and similarly had no effect on GH uptake by the liver. Treatment with GH increased liver binding in pigs (Chung and Etherton, 19861 and in sheep Bosner et al., 1980). In the present study, treatment did not affect GH uptake by the liver. However, the tendency of TSP tissues to remove more GH in GRF-treated steers fed at high intake might indicate a greater use of GH by TSP tissues in those animals. Arterial IGF-I concentration was not d e c t e d by intake. A n increase in GH concentration without any concomitant change in IGF-I concentration has been reported in steers fed a medium plane of nutrition compared to a high plane of nutrition (1.8%vs 3% DM of BW per day), even if a further decrease of intake to 1%DM of BW per day finally decreased IGF-I concentration (Breier et al., 1986). However Elsasser et al. (1989) observed no effects of intake on GH but reported a decrease in IGF-I when intake was restricted in steers using intakes similar to those in the present experiment. Severe feed or energy restriction decreased IGF-I concentrations (Elsasser et al., 1988; Houseknecht et al., 1988; Abribat et al., 19901. Overall, these data indicate that nutritional status is a major factor affecting IGF-I concentration, but a certain thresh-

HORMONE

METABOLISM

GRF-TREATED CATTLE

749

casein infused abomasally increased arterial glucagon concentration (Guerino et al., 19891, but an 8-d fast did not affect glucagon concentration (Rule et al., 1985). In dairy cows, a lo-d feed restriction did not change glucagon concentration (Cohick et al., 19861, but a more prolonged period of food restriction reduced glucagon concentration (Vicini et al., 1988). Treatments had no significant effect on the glucagon VA measured. Greater intake increased net PDV glucagon flux without altering the total quantity of glucagon removed by the liver. This resulted in a higher TSP flu,which could account for the increased arterial concentration observed. The glucagon flux across PDV tissues reported here is higher than the value of 16 pg/h reported by Reynolds et al. (1986) and in a range similar to that observed by Guerino et al. (19891. The tendency of the liver extraction ratio to decrease between the low and the high intake is quite similar to the decrease that Guerino et al. (1989) observed from 13% in control animals to 8% after casein infusion. The ratio at low intake is also similar to the ratio observed in dairy cows in early lactation, 13% (Reynolds et ai., 19891. The percentage of PDV glucagon flux removed by liver was also decreased a t high intake and the percentage observed at low intake was also similar to the ratio in cows in early lactation, 67% (Reynolds et al., 19891. In other studies, GH treatment did not affect glucagon concentration or kinetics (DeBoer and Kennelly, 1989; Sechen et al., 1989). In our study, GRF did not change glucagon concentration or flux, except that steers fed at high intake tended to have a higher glucagon flux through TSP tissues when they were injected with GRF. However, this did not affect the arterial concentration. As previously discussed by Reynolds et al. (19891, peripheral concentrations of insulin and glucagon are as much dependent on liver metabolism as their release into the portal vein. Arterial concentration of somatostatin was not affected by treatments; similarly, casein m i o n did not affect somatostatin concentration (Guerino et al., 1989). Flux across PDV tissues was in the range of flux reported in growing steers (Reynolds et al., 1986; Guerino et al., 1989) except for steers fed at high intake and receiving GRF, for which PDV flux was negative. The reason why there was a net PDV uptake of somatostatin for this treatment, instead of a release, is not clear. As reported by Guerino et al. (1989) and Reynolds et al. (19891, HP difference for somatostatin was not significant, indicating that metabolism of somatostatin by the liver was not major or was too subtle to be measured. In conclusion, our results indicate that greater feed intake increases arterial concentration of


tive to negative between 4 and 8 wk of lactation, but again, PA difference was not significantly different from 0 Reynolds et al., 1989). Insulin arterial concentration waa decreased by low intake. Food restriction is known to decrease insulin concentration (Serjsen et al., 1983; Hart et al., 1985; Rule et al.,19851. However, feeding steers at two-thirds of ad libitum intake did not affect insulin concentration (Trenkle and Topel, 1978). In our experiment, GRF tended to increase arterial insulin concentration, as did chronic GH treatment (Eisemann et al., 1986; Peters, 1986). Chronic treatment of bull calves with GRF for 10 d did not affect insulin concentration (Plouzek et al., 19881, but the dose used (.067 g/kg of BW i.v. every 4 h) was lower than the dose used in our study. The higher arterial concentration of insulin in steers fed at high intake reflects a higher insulin release by PDV and TSP tissues. Thus, a higher intake level finally results in more insulin available to peripheral tissues. The GRF treatment also increased PA difference, but the difference was not big enough to result in a signifkant increase in PDV flux. In lactating ewes, GH treatment also nonsignificantly increased insulin flux through PDV tissues, but liver flux was not measured aeenanuruksa et al., 1980). Eisemann (19891 reported no effect of GH administration on insulin flux through PDV and liver of growing steers, whereas Cohick et al. (1989) observed after 7 d but not 10 d of treatment a decrease of liver insulin uptake. Overall, these data suggest that the increased insulin concentration observed with GH treatment does not primarily result from an increased production by the pancreas. The decreased sensitivity to insulin observed in GHtreated growing animals (Hart et al., 1984; Gopinath and Etherton, 1989) might play a role in increasing circulating insulin concentrations if decreased sensitivity results in a decreased utilization of insulin by peripheral tissues. This needs further .investigation, because GH treatment did not change insulin kinetics in pigs (WrayCahen et al., 19871 or cows (DeBoer and Kennelly, 1989). Insulin fluxes reported in this study for nonrestricted animals are in the range of fluxes measured in growing steers (Reynolds et al., 1986; Harmon and Avery, 1987). Liver extraction ratio was similar to the 8% reported in sheep (Brockman and Bergman, 19751, which is lower than the 13% reported in dairy cows (Reynolds et al.,1989). Net removal of insulin by the liver accounted for 28% of net PDV production. This ratio is lower than that reported in sheep (50%; Brockman and Bergman, 1975) and than that reported in dairy cows (59 to 83%; Lomax et al., 1979; Reynolds et al., 19891. Arterial concentration of glucagon was greater at high than at low intake. In growing steers,

IN

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LAPIERRE ET AL.

insulin and glucagon mainly through an increased net PDV release. Liver metabolism also plays a major role in their metabolism, on a net basis removing, respectively, an average of 28 and 54% of insulin and glucagon released by PDV. Treatment with GRF increased GH, insulin,and IGF-I concentrations but splanchnic metabolism was not primarily responsible for those increments.

As shown previously, twice-daily injection of growth hormone-releasing factor is an effective method for growth hormone elevation in cattle. In the present study, effects of intake on hormones of the somatrophic axis and their response to growth hormone-releasing factor were not as dramatic as in previous studies in which intakes at or below maintenance were compared to intakes at least twice maintenance. This emphasizes that, above maintenance, effects of reduced intake on endocrinology may differ from effects of more severe nutrient restriction. Insulin and glucagon data emphasize that changes in peripheral concentrations of hormones are not solely due to changes in their secretion rate.

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Implications

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Effects of growth hormone-releasing factor and feed intake on energy metabolism in growing beef steers: net nutrient metabolism by portal-drained viscera and liver.

Effects of growth hormone-releasing factor and feed intake on energy metabolism in growing beef steers: whole-body energy and nitrogen metabolism.

Effect of dietary net energy concentrations on growth performance and net energy intake of growing gilts.

Net absorption of macrominerals by portal-drained viscera of lactating Holstein Cows and beef steers.

Effect of excess dietary protein on feed intake and nitrogen metabolism in steers.

[The conversion of feed energy by growing pigs. 1. Energy and nitrogen metabolism in the early stage of growth].

Effects of diet forage-to-concentrate ratio and intake on energy metabolism in growing beef heifers: whole body energy and nitrogen balance and visceral heat production.

Effect of human growth hormone-releasing factor on bone and mineral metabolism in growing pigs.

Association of residual feed intake with growth and slaughtering performance, blood metabolism, and body composition in growing lambs.

Profile of the Spleen Transcriptome in Beef Steers with Variation in Gain and Feed Intake.

Effect of prepartal hormone administration on feed intake and mineral metabolism of cows.

Effects of growth hormone on body composition and metabolism.

Effects of a growth hormone-releasing factor analogue and an estradiol-trenbolone acetate implant on somatotropin, insulin-like growth factor I, and metabolite profiles in growing Hereford steers.

Effect of diet composition and feed intake level on diet digestibility and ruminal metabolism in growing lambs.

Growth hormone and drug metabolism. Acute effects on microsomal mixed-function oxidase activities in rat liver.

Effects of decreased dietary roughage concentration on energy metabolism and nutrient balance in finishing beef cattle.

Effects of growth hormone on tissue metabolism in broiler chicks.

Cluster and meta-analyses of genetic parameters for feed intake traits in growing beef cattle.

Growth hormone and protein metabolism.

6 Mice.

Thyroid - hormone effects on steroid - hormone metabolism.

Thyroid hormone signaling in energy homeostasis and energy metabolism.

Protein and energy metabolism with biosynthetic human growth hormone in patients on full intravenous nutritional support.

Effects of R51163 on intake and metabolism in moose.