Influence of bovine growth hormone on growth rate, appetite, and food conversion of yearling coho salmon (Oncorhynchus kisutch) fed two diets of different composition

1977 ◽  
Vol 55 (1) ◽  
pp. 74-83 ◽  
Author(s):  
J. R. Markert ◽  
David A. Higgs ◽  
Helen M. Dye ◽  
D. W. MacQuarrie

Paired groups of yearling coho salmon at 10 °C and on a natural photoperiod were fed twice daily either Oregon moist pellets (OMP) or a diet with poultry offal (PO) as the main protein source. The fish were fed either 0.8% body weight per day (dry weight of food (g)/wet weight of fish (g)) or to satiation. Coho in one of the groups for each diet–ration combination received, by intramuscular injection, 10 μg (0.0092 IU) of bovine growth hormone (bGH) per gram body weight one time per week for 56 days. Those in the other group were not treated.Administration of bGH significantly enhanced growth and improved food and protein conversion. Ration level altered the effect of bGH on food and protein conversion as did diet formulation at satiation. The voluntary food intake of bGH-treated fish fed OMP was higher but not significantly different from that of the controls. Diet formulation differences did not significantly affect the growth rate of either bGH-treated or untreated coho at each ration level. Irrespective of the diet–ration combination, bGH administration lead to a significant decline in condition factor.At 56 days, bGH-treated fish had a significantly lower percentage of muscle protein and a significantly higher percentage of muscle water than untreated fish. At present, the use of bGH as a growth promoter for coho salmon is not economical.

1978 ◽  
Vol 56 (6) ◽  
pp. 1226-1231 ◽  
Author(s):  
David A. Higgs ◽  
Edward M. Donaldson ◽  
Jack R. McBride ◽  
Helen M. Dye

Groups of yearling coho salmon, held at 10 °C and on a 12-h photoperiod, were injected intramuscularly once weekly with 10 or 100 μg of a chinook salmon pituitary extract (oncPE)/g body weight, 0.1–10 μg (9.2 × 10−3 IU) of bovine growth hormone (bGH)/g body weight, solvent, or no treatment for 70 days.Both oncPE and bGH treatment stimulated growth in length and weight. The potency of oncPE per unit weight was about one-ninth that of bGH. The lowest effective bGH dosage was 3.2 μg/g body weight, while 10 μg/g body weight induced the maximum growth response. Coho given 100 μg of oncPE/g body weight had the highest growth rates. Condition factors of bGH-treated fish were depressed when the dosage exceeded 1.0 μg/g body weight.It is concluded that use of bGH is more economical than the available pituitary extracts or purified piscine growth hormones for coho salmon culture. Two alternatives to the use of native growth hormones in salmon culture are discussed.


1977 ◽  
Vol 55 (6) ◽  
pp. 1048-1056 ◽  
Author(s):  
David A. Higgs ◽  
Ulf H. M. Fagerlund ◽  
Jack R. McBride ◽  
Helen M. Dye ◽  
Edward M. Donaldson

Groups of yearling coho salmon held at 10 °C on a natural photoperiod, and fed excess ration daily, were administered either bovine growth hormone (bGH; 0.0092 IU/g body weight), L-thyroxine (T4; 1 μg/g), 17α-methyltestosterone (MT; 1 mg/kg diet), combinations of these hormones, or no hormone for 59 days. Fish received bGH and (or) T4 intramuscularly once weekly.Each individual hormone and hormone combination significantly enhanced growth. The sequence noted for growth rate of the groups was as follows: (bGH + MT + T4) > (bGH + MT) > (bGH + T4) > bGH > (T4 + MT) > MT > T4 > control groups. Three hormonal interactions were additive (T4 + MT; bGH + MT; bGH + MT + T4). The growth rate of fish treated with bGH + MT + T4 was over three times that of the controls.T4 or MT + T4 administration significantly increased condition factors, while MT, bGH, bGH + T4, bGH + MT, and bGH + MT + T4 decreased them.Significant elevations in percentages of muscle water (bGH) and lipid (T4; T4 + MT; bGH + MT) were found. Thyroid activity (follicle epithelial height) was significantly increased in MT and MT + bGH fish, but depressed in T4 fish. Hormone administration altered the histological structure of the endocrine pancreas (bGH and MT groups), ovary (bGH; MT groups), testis (MT groups), and interrenal tissue (bGH; MT).


1981 ◽  
Vol 61 (4) ◽  
pp. 977-981 ◽  
Author(s):  
S. LEESON ◽  
J. D. SUMMERS

Two trials were conducted with Nicholas strain turkeys. In trial 1, 300 male poults were reared to 49 days using either initial stages of 'large-turkey' feeding regime, or a situation allowing for diet self-selection of protein and energy. Within these programs, diets were supplemented with 10 ppm avoparcin, while a comparable number of controls received no growth promoter. Avoparcin improved growth rate (P < 0.01) irrespective of age, and improved feed utilization to 35 days of age. This effect was not confounded with the form in which diets were offered. In a second trial a 'broiler-turkey' feeding schedule was used, with birds slaughtered at 88 days. Diet treatments consisted of a control diet containing 33 ppm robenz and test diets containing either 33 ppm robenz + 10 ppm avoparcin or 10 ppm avoparcin alone. Avoparcin improved weight gain (P < 0.05) irrespective of coccidiostat inclusion. Feed utilization and carcass grades were not influenced by diet. The 7% improvement in body weight noted here with avoparcin was substantially greater than that previously observed with broiler chickens.


1977 ◽  
Vol 55 (10) ◽  
pp. 1756-1758 ◽  
Author(s):  
Bryan Ludwig ◽  
David A. Higgs ◽  
Ulf H. M. Fagerlund ◽  
Jack R. McBride

As part of an ongoing survey to identify hormones capable of stimulating growth in Pacific salmon, groups of underyearling coho salmon were injected with bovine (Ultralente) insulin (0.32, 1.0, 3.2, or 10 IU/kg body weight) into the peritoneal cavity either once or twice weekly for 70 days.All doses of insulin, when injected twice weekly, increased the values for specific growth rates and decreased those for food–gain ratios relative to solvent-injected controls, but the differences were not statistically significant. All doses of insulin caused a marked increase in the granulation of the pancreatic B cells. Plasma glucose concentrations in starved coho injected with 10 IU insulin/kg body weight were significantly lower than in solvent-injected controls 4 h after injection.It is concluded that proper evaluation of the effectiveness of insulin as a growth promoter for salmon requires further studies preferably using insulin preparations specific to teleosts.


1976 ◽  
Vol 33 (7) ◽  
pp. 1585-1603 ◽  
Author(s):  
David A. Higgs ◽  
Edward M. Donaldson ◽  
Helen M. Dye ◽  
J. R. McBride

Groups of underyearling coho salmon (Oncorhynchus kisutch) were acclimated to 10 C well water and a photoperiod of 12 h L:12 h D. Excess ration (Oregon Moist Pellet) was presented daily. Doses of bovine growth hormone (5, 10, 20, 30, or 90 μg bGH/g body wt) and L-thyroxine (0.5, 5, or 30 μg T4/g) were administered over a period of 84 days (phase I) either by injection (via dorsal musculature or peritoneal cavity) or by hormone cholesterol implants into the muscle. Administration frequency of bGH and T4 was such (range 2 times/wk-1 time/3 wk) that fish theoretically received either 10 or 30 μg bGH/g per wk or 1 or 10 μg T4/g per wk. Control fish received either alkaline saline (pH 9.5) or a cholesterol pellet. After cessation of treatment the fish were observed for an additional 84 days (phase II). During phase I, growth rates (weight) for bGH fish (2.0–2.4% per day) and for T4 fish (0.97–1.1% per day) were significantly higher than those of control fish (0.42–0.59% per day). Among bGH fish, dorsal musculature injection (2 times/wk) was significantly more effective than intraperitoneal injection (1 time/2 wk).Increases in weight above control for bGH fish at 84 days ranged from 220 to 369%. Those for T4 fish extended from 47 to 78%. In phase II, control fish growth rates were higher (0.61–0.67% per day) than those for bGH fish (0.47–0.57% per day) and T4 fish (0.32–0.44% per day). Administration of bGH and T4 (high dose) caused a progressive decline in condition factor of fish from the control range. This trend was stopped and reversed in phase II.At 84 days, generally no significant differences were detected among groups for percentages of muscle water. However, some groups had significantly higher (bGH) and others lower (T4) percentages of muscle protein relative to those of control fish. Also, significant increases (T4) and decreases (bGH) in muscle lipid percentages were found. Hormone treatment altered the histological structure of the ovary, thyroid, exocrine (T4) and endocrine (bGH) pancreas, and somatotrop cells (T4) of the pituitary. A poor growth response was noted for two groups of coho administered bGH after acclimation to sea water.


1993 ◽  
Vol 264 (6) ◽  
pp. E986-E992 ◽  
Author(s):  
J. C. Byatt ◽  
N. R. Staten ◽  
W. J. Salsgiver ◽  
J. G. Kostelc ◽  
R. J. Collier

Recombinant bovine prolactin (rbPRL) or bovine growth hormone (rbGH) was administered to mature female rats (10/treatment group) by daily subcutaneous injection for 10 days. Doses ranged from 7 to 5,000 micrograms/day (0.03-24 mg/kg body wt). Both rbPRL and rbGH increased body weight gain and food intake, but these parameters were increased at lower doses of rbPRL (7-63 micrograms/day) than rbGH (> 190 micrograms/day). Weight gain and food intake were maximally stimulated by 190 micrograms/day rbPRL, whereas maximal increased weight gain was obtained with the highest dose of rbGH (5,000 micrograms/day). Total carcass protein was increased by both hormones; however, protein as a percentage of body weight was unchanged. Similarly, neither rbPRL nor rbGH changed the percentage of carcass moisture. Percentage of body fat was increased by rbPRL but was decreased by rbGH. Weight of the gastrointestinal tract and kidneys was increased by both hormones, but increases were in proportion to body weight gain. These data confirm that ungulate prolactin is a hyperphagic agent in the female rat. In addition, they suggest that, while prolactin stimulates growth in mature female rats, this growth is probably not via a somatogenic mechanism.


1970 ◽  
Vol 27 (2) ◽  
pp. 347-358 ◽  
Author(s):  
Donald R. Buhler ◽  
W. E. Shanks

Median Survival Time was directly proportional to body weight in young coho salmon of the same age that were fed a diet containing technical DDT. Supplementation by additional feeding with DDT-free diet prolonged the lifespan of these fish but the Median Survival Time remained a direct function of body weight.The primary effect of body size on lethality was to control the rate of DDT intake by the fish. The smallest fish consumed the greatest amounts of diet and, consequently, these fish received the highest milligram per kilogram doses of DDT.In addition, however, the smaller salmon succumbed to a lower milligram per kilogram cumulative lethal dose than did the larger fish, perhaps because the smallest fish contained a lower percentage of lipid and thus failed to provide for adequate storage detoxification of the DDT.


1964 ◽  
Vol 42 (3) ◽  
pp. 299-301 ◽  
Author(s):  
Anna Sirek ◽  
Karl Schoeffling ◽  
Monica Webster ◽  
Otakar V. Sirek

A highly purified growth hormone preparation (Wilhelmi) was tested for its hypoglycemic activity in four fasting, hypophysectomized–depancreatized dogs (Houssay dogs) maintained without exogenous insulin for 2–4 weeks. A single intravenous injection of growth hormone, 5 mg per kg body weight, had no effect on blood sugar over a period of 6 hours. It was concluded that highly purified growth hormone has no hypoglycemic effect in the absence of biologically active insulin.


1991 ◽  
Vol 66 (3) ◽  
pp. 505-521 ◽  
Author(s):  
Inge Dørup ◽  
Allan Flyvbjerg ◽  
Maria E. Everts ◽  
Torben Clausen

Nutritional deficiencies of magnesium or zinc lead to a progressive and often marked growth retardation. We have evaluated the effect of Mg and Zn deficiency on growth, serum insulin-like growth factor-1 (s-IGF-1), growth hormone (s-GH) and insulin (s-insulin) in young rats. In 3-week-old rats maintained on Mg-deficient fodder for 12 d the weight gain was reduced by about 34%, compared with pair-fed controls. This was accompanied by a 44% reduction in s-IGF-1, while s-insulin showed no decrease. After 3 weeks on Mg-deficient fodder, growth had ceased while serum Mg (s-Mg) and s-IGF-1 were reduced by 76 and 60% respectively. Following repletion with Mg, s-Mg was completely normalized in 1 week, and s-IGF-1 reached control level after 2 weeks. Growth rate increased, but the rats had failed to catch up fully in weight after 3.5 weeks. Absolute and relative pair-feeding were compared during a Mg repletion experiment. Absolute pair-fed animals were given the same absolute amount of fodder as the Mg-deficient rats had consumed the day before. Relative pair-fed animals were given the same amount of fodder, on a body-weight basis, consumed in the Mg-deficient group the day before. In a repletion experiment the two methods did not differ significantly from each other with respect to body-weight, muscle weight, tibia length and s-IGF-1, although there was a tendency towards higher levels in the relative pair-fed group. The peak in s-GH after growth hormone-releasing factor 40 (GRF 40) was 336 (se 63) μg/l in 5-week-old rats that had been Mg depleted for 14 d, whereas age-matched control animals showed a peak of 363 (se 54) μg/l (not significant).In 3-week-old rats maintained on Zn-deficient fodder for 14 d weight gain was reduced by 83% compared with pair-fed controls. Serum Zn (s-Zn) and s-IGF-1 were reduced by 80 and 69% respectively, while s-insulin was reduced by 66%. The Zn-deficient animals showed a more pronounced growth inhibition than that seen during Mg deficiency and after 17 d on Zn-deficient fodder s-IGF-1 was reduced by 83%. Following repletion with Zn, s-Zn was normalized and s-IGF-1 had increased by 194% (P <0.05) after 3 d. s-IGF-1, however, was not normalized until after 2.5 weeks of repletion. Growth rate increased but the catch-up in weight was not complete during 6 weeks. The maximum increase in s-GH after GRF 40 was 774 (se 61) μg/l in control animals ν. 657 (se 90) μg/l in 6-week-old rats that had been Zn-depleted for 12 d (not significant). In conclusion, both Mg and Zn deficiency lead to growth inhibition that is accompanied by reduced circulating s-IGF-1, but unchanged s-GH response. Zn deficiency, but not Mg deficiency, caused a reduction in s-insulin. The reduction in s-IGF-1 could not be attributed to reduced energy intake, but seems to be a specific effect of nutritional deficiency of Mg or Zn. It is suggested that the growth retardation seen during these deficiency states may be mediated through reduced s-IGF-1 production.


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