scholarly journals Comparison of Sulfate Metabolism in Costal Cartilage of Normal and 'Little' Mice

1983 ◽  
Vol 36 (3) ◽  
pp. 263 ◽  
Author(s):  
NeiI M McKern
Keyword(s):  
Growth Hormone ◽  
Growth Rate ◽  
Body Weight ◽  
Costal Cartilage ◽  
Cartilage Degradation ◽  
Skeletal Growth ◽  
Sulfate Uptake ◽  
Sulfate Metabolism ◽  
C 50

C57BL/6J and mutant 'little' (lit/lit) mice c. 50 days of age were injected with doses of [35S]sulfate proportional to their body weight. Despite the diminished growth rate of lit/lit mice compared with normal mice at this age, uptake of radioactivity per unit mass of cartilage was similar for both mouse types, confirming previous data. Additional experiments with these mice established that the similarity of sulfate uptake could not be accounted for by differences in the location of bound sulfate or (for females) by differences in cartilage cellularity. Investigation of sulfate loss by costal cartilage in vivo indicated that cartilage degradation occurred at a greater rate in lit/lit mice than in normally growing mice. These latter data suggest that growth hormone, which is lacking in lit/lit mice, may in part regulate skeletal growth (at least for female mice) by inhibiting degradation of cartilage.

scholarly journals Sulfate Uptake and Somatomedin Levels in the 'Little' (lit/lit) Mouse

1981 ◽  
Vol 34 (2) ◽  
pp. 221 ◽  
Author(s):  
NeiI M McKern ◽  
Donald B Cheek ◽  
WGordon Crewther
Keyword(s):  
Growth Hormone ◽  
Costal Cartilage ◽  
Fresh Medium ◽  
Bovine Growth Hormone ◽  
Consistent Difference ◽  
Sulfate Uptake ◽  
Low Levels ◽  
In Vivo Uptake

The mutant 'little' (lit/lit) mouse is deficient in growth hormone and has correspondingly low levels of serum somatomedin. Injection of these mice with human or bovine growth hormone significantly r(l.ises serum somatomedin levels within 6 h. In vivo uptake of radioactive sulfate by costal cartilage in lit/lit mice is similar to that of normal mice, which is unexpected in view of the low levels of circulating somatomedin. If costal cartilages from normal and lit/lit mice are preincubated in medium 199 in vitro before transfer to fresh medium containing radioactive sulfate and serum, there is no consistent difference in uptake of sulfate, demonstrating similar endogenous cartilage activity. In contrast, omission of the preincubation step reveals a lower uptake of sulfate in vitro by cartilage from lit/lit mice as compared with normal mice. Cartilage removed from lit/lit mice 24 h after injection with growth hormone, however, takes up greater amounts of sulfate than cartilage from untreated normal mice.

scholarly journals In Vivo Radioprotective Activity of Cell-Permeable Bifunctional Antioxidant Enzyme GST-TAT-SOD against Whole-Body Ionizing Irradiation in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Jianru Pan ◽  
Huocong He ◽  
Ying Su ◽  
Guangjin Zheng ◽  
Junxin Wu ◽  
...  
Keyword(s):  
Growth Rate ◽  
Antioxidant Activity ◽  
Body Weight ◽  
Whole Body ◽  
White Pulp ◽  
Radioprotective Activity ◽  
Significant Difference ◽  
Wbc Count

GST-TAT-SOD was the fusion of superoxide dismutase (SOD), cell-permeable peptide TAT, and glutathione-S-transferase (GST). It was proved to be a potential selective radioprotector in vitro in our previous work. This study evaluated the in vivo radioprotective activity of GST-TAT-SOD against whole-body irradiation. We demonstrated that intraperitoneal injection of 0.5 ml GST-TAT-SOD (2 kU/ml) 2 h before the 6 Gy whole-body irradiation in mice almost completely prevented the splenic damage. It could significantly enhance the splenic antioxidant activity which kept the number of splenic white pulp and consequently resisted the shrinkage of the spleen. Moreover, the thymus index, hepatic antioxidant activity, and white blood cell (WBC) count of peripheral blood in irradiated mice pretreated with GST-TAT-SOD also remarkably increased. Although the treated and untreated irradiated mice showed no significant difference in the growth rate of animal body weight at 7 days postirradiation, the highest growth rate of body weight was observed in the GST-TAT-SOD-pretreated group. Furthermore, GST-TAT-SOD pretreatment increased resistance against 8 Gy whole-body irradiation and enhanced 30 d survival. The overall effect of GST-TAT-SOD seemed to be a bit more powerful than that of amifostine. In conclusion, GST-TAT-SOD would be a safe and potentially promising radioprotector.

EFFECTS OF GROWTH HORMONE, PROLACTIN AND THYROXINE ON BODY WEIGHT, SOMATOMEDIN-LIKE ACTIVITY AND IN-VIVO SULPHATION OF CARTILAGE IN HYPOPITUITARY DWARF MICE

1980 ◽  
Vol 85 (1) ◽  
pp. 35-47 ◽  
Author(s):  
A. T. HOLDER ◽  
M. WALLIS ◽  
P. BIGGS ◽  
M. A. PREECE
Keyword(s):  
Growth Hormone ◽  
Costal Cartilage ◽  
Tail Length ◽  
Bovine Growth Hormone ◽  
Dwarf Mouse ◽  
Dwarf Mice ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
In Vivo Uptake

SUMMARY Hypopituitary dwarf mice were found to have reduced levels of serum somatomedin-like activity compared with normal mice of the Snell strain. Treatment with bovine growth hormone for 3 and 7 days resulted in growth without significantly increased levels of serum somatomedin-like activity, as detected by in-vitro uptake of 35SO42− into normal rat cartilage; only after treatment for 14 days was somatomedin activity significantly raised. However, treatment for 2 days with bovine growth hormone, bovine prolactin or thyroxine resulted in a dose-dependent increase in in-vivo uptake of 35SO42− into dwarf mouse costal cartilage; growth hormone and thyroxine did not act synergistically. Ten days of treatment with growth hormone promoted a dose-dependent increase in both growth (increased weight gain and tail length) and in-vivo uptake of 35SO42−. Increase in tail length was correlated with uptake of 35SO42−. Thus, in-vivo uptake of 35SO42− into dwarf mouse costal cartilage provides a sensitive method for detecting a dose-related effect of growth hormone.

EFFECT OF BOVINE GROWTH HORMONE AND A PARTIALLY PURE PREPARATION OF SOMATOMEDIN ON VARIOUS GROWTH PARAMETERS IN HYPOPITUITARY DWARF MICE

1981 ◽  
Vol 89 (2) ◽  
pp. 275-282 ◽  
Author(s):  
A. T. HOLDER ◽  
E. M. SPENCER ◽  
M. A. PREECE
Keyword(s):  
Body Weight ◽  
Growth Parameters ◽  
Costal Cartilage ◽  
Regression Line ◽  
Tail Length ◽  
Once Daily ◽  
Organ Weights ◽  
Dwarf Mice ◽  
Weight Velocity

The growth-promoting effects of a partially purified preparation of somatomedin (12·7 units/mg) were compared with those of various doses of bovine GH (5, 20 and 80 μg/day) when injected into hypopituitary dwarf mice. Growth parameters studied were body-weight and tail-length velocities (calculated as the slope of a regression line fitted to daily measurements against time), uptake of 35SO2−4 into costal cartilage in vivo and organ weights (heart, liver and kidney). In the first experiment somatomedin (6·4 units/day), bovine GH and 0·9% NaCl were injected once daily in a volume of 0·1 ml for 10 days. Treatment with bovine GH promoted a significant dose-dependent increase in body-weight and tail-length velocities and 35SO2−4 uptake into costal cartilage in vivo. Somatomedin also promoted a significant increase in body-weight velocity and 35SO2−4 uptake, both responses were between that observed with the lowest dose of bovine GH and control values. Somatomedin did not promote increase in tail-length velocity. Organ weights did not differ significantly between any of the treatment groups when expressed as mg/g body weight. In the second experiment somatomedin (a daily total of 21·6 units/day) and 0·9% NaCl were injected three times per day in a volume of 0·033 ml, bovine GH was again injected once daily in a volume of 0·1 ml, and the treatment period was 12 days. As in the first experiment all doses of bovine GH and somatomedin promoted a significant increase in body-weight velocity. These results are consistent with the somatomedin hypothesis.

EFFECT OF GROWTH HORMONE AND PEPTIDE FRACTIONS CONTAINING SOMATOMEDIN ACTIVITY ON GROWTH AND CARTILAGE METABOLISM OF SNELL DWARFMICE

1979 ◽  
Vol 92 (2) ◽  
pp. 242-257 ◽  
Author(s):  
Sylvia van Buul-Offers ◽  
Jan Leo Van den Brande ◽  
C. M. Hoogerbrugge ◽  
L. Dumoleijn ◽  
P. L. M. v.d. Klundert
Keyword(s):  
Growth Hormone ◽  
Thymidine Incorporation ◽  
Costal Cartilage ◽  
Human Growth ◽  
Liver Weight ◽  
Skinfold Thickness ◽  
Treated Group ◽  
Serum Glucose ◽  
Significant Rise

ABSTRACT In order to obtain more information about a possible role of somatomedin (SM) in vivo, increase in length and weight, costal cartilage activity (35SO4 = and 3H-methyl-thymidine incorporation), organ weight and serum glucose levels were studied in Snell dwarfmice, during treatment with human growth hormone (hGH), l-thyroxine (T4), insulin and a semipurified SM-preparation (SM-P1). SM-P1, hGH and T4 caused a significant increase in length and weight, whereas insulin was not effective in a dosage similar to the insulinlikeactivity of the SM-P1 preparation measured by radioreceptorassay. The effect obtained with the SM-preparation cannot be due to contamination of GH, prolactin, T4, insulin or testosterone. Costal cartilage activity was measured three days after initiation of treatment by incubation immediately after sacrifice in plasma free medium. Both sulphate and thymidine incorporation were increased by the administration of SM-Pl and hGH, compared to buffer treated controls. After treatment for four weeks no differences between treated and untreated animals in cartilage activity could be observed anymore. Both SM-P1 and hGH induced weight gain in most organs. An outspoken effect was seen on lymphoid organs, the submandibular salivary glands and muscle, a sizable effect was present on the kidneys and a small effect, not reaching significance for the SM-Pl treated group on brain weight. An impression of divergence was seen with liver weight, which increased on hGH while there was a small and not significant rise on SM-P1. A definite discrepancy was found in skinfold thickness, which was essentially unchanged on hGH and increased on SM-P1. Testes and epididymal fat, though probably increasing their weights, were in insufficient number to do statistics on. Serum T4 is low in untreated dwarfmice. It is increased to a subnormal level after hGH administration whereas no effect is observed with SM-P1. The dose dependent effect of insulin, measured by radioimmunoassay, on the induction of hypoglycaemia is markedly similar to the effect of nonradioimmunoactive insulin-like activity of SM-P1 as measured by radioreceptorassay. The hypoglycaemia induced with insulin and the SM-preparation is reduced by adding 10 % glucose to the diet. In conclusion: SM-P1 shows growth stimulating and insulin-like actions in vivo. The pattern of effects obtained with hGH, T4 and insulin differs from that of SM-P1.

scholarly journals Role of insulin-like growth factor-1 and growth hormone in growth inhibition induced by magnesium and zinc deficiencies

1991 ◽  
Vol 66 (3) ◽  
pp. 505-521 ◽  
Author(s):  
Inge Dørup ◽  
Allan Flyvbjerg ◽  
Maria E. Everts ◽  
Torben Clausen
Keyword(s):  
Growth Hormone ◽  
Growth Rate ◽  
Body Weight ◽  
Growth Inhibition ◽  
Zn Deficiency ◽  
Relative Pair ◽  
Mg Deficiency ◽  
And Zn Deficiency ◽  
Old Rats ◽  
Catch Up

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.

scholarly journals Growth and survival of giant gourami juvenile immersed in freshwater containing growth hormone

2013 ◽  
Vol 11 (2) ◽  
pp. 162
Author(s):  
Pustika Ratnawati ◽  
. Alimuddin ◽  
Harton Arfah ◽  
Agus Oman Sudrajat
Keyword(s):  
Growth Hormone ◽  
Growth Rate ◽  
Body Weight ◽  
Immersion Time ◽  
Egg Yolk ◽  
Recombinant Growth Hormone ◽  
Fish Hatchery ◽  
Growth And Survival ◽  
Controlled Conditions

<p>Growth of giant gourami is relatively slow. Administration of recombinant growth hormone (rGH) by several<br />times immersion in water containing 0.9% NaCl for one hour can significantly increase the growth. In this<br />study, giant gourami juvenile were immersed in freshwater containing 120 mg/L rGH to determine the long<br />immersion time that provides higher growth and survival. Juvenile at seventh-day-old after egg yolk absorbed<br />was immersed for 0.5, 1.0, 2.0, and 3.0 hours in rGH solution. As controls, fish was immersed in freshwater<br />without rGH (control 1: C1), and water containing 0.9% NaCl, and 120 mg/L rGH (control 2: C2). Fish was<br />kept under controlled conditions in 20 L aquarium for three weeks, then in 50 L aquarium until at end of<br />experiment, and fed at satiation. The results showed that highest growth in body weight, survival, and biomass<br />(p&lt;0.05) were obtained in rGH immersion treatment for 0.5 hour. Biomass of fish immersed by rGH for 0.5<br />hour was about 32% higher compared to control C1, and 13% compared to C2. Survival of the 0.5 hour rGHimmersed<br />fish (100%) was similar to control C1 and C2. Thus, immersion of giant gourami juvenile in<br />freshwater containing rGH for 0.5 hour allowed highest growth rate, and this method is relatively easy to be<br />adopted by fish hatchery.</p><p>Keywords: immersion, hormone, growth, freshwater, giant gourami</p>

scholarly journals Selective β2-Adrenoceptor Blockade Rescues Mandibular Growth Retardation in Adolescent Rats Exposed to Chronic Intermittent Hypoxia

2021 ◽  
Vol 12 ◽  
Author(s):  
Haixin Hong ◽  
Jun Hosomichi ◽  
Hideyuki Maeda ◽  
Yuji Ishida ◽  
Risa Usumi-Fujita ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Growth Retardation ◽  
Adrenergic Receptors ◽  
Intermittent Hypoxia ◽  
Skeletal Growth ◽  
Chronic Intermittent Hypoxia ◽  
Rankl Expression ◽  
Mandibular Growth ◽  
Condylar Head

Activation of the sympathoadrenal system is associated with sleep apnea-related symptoms and metabolic dysfunction induced by chronic intermittent hypoxia (IH). IH can induce hormonal imbalances and growth retardation of the craniofacial bones. However, the relationship between IH and β2-adrenergic receptor signaling in the context of skeletal growth regulation is unclear. This study aimed to investigate the role of β2-adrenergic receptors in IH-induced mandibular growth retardation and bone metabolic alterations. Male 7-week-old Sprague–Dawley rats were subjected to IH for 3 weeks. IH conditions were established using original customized hypoxic chambers; IH was induced at a rate of 20 cycles per hour (oxygen levels changed from 4 to 21% in one cycle) for 8 h per day during the 12 h “lights on” period. The rats received intraperitoneal administration of a β2-adrenergic antagonist (butoxamine) or saline. To exclude dietary effects on general growth, the normoxic rats with saline, normoxic rats with butoxamine, and IH rats with butoxamine were subjected to food restriction to match the body weight gains between IH and other three groups. Body weight, heart rate, blood pressure, and plasma concentrations of leptin, serotonin, and growth hormone were measured. Bone growth and metabolism were evaluated using radiography, microcomputed tomography, and immunohistochemical staining. Plasma leptin levels were significantly increased, whereas that of serotonin and growth hormone were significantly decreased following IH exposure. Leptin levels recovered following butoxamine administration. Butoxamine rescued IH-induced mandibular growth retardation, with alterations in bone mineral density at the condylar head of the mandible. Immunohistochemical analysis revealed significantly lower expression levels of receptor activator of nuclear factor-kappa B ligand (RANKL) in the condylar head of IH-exposed rats. Conversely, recovery of RANKL expression was observed in IH-exposed rats administered with butoxamine. Collectively, our findings suggest that the activation of β2-adrenergic receptors and leptin signaling during growth may be involved in IH-induced skeletal growth retardation of the mandible, which may be mediated by concomitant changes in RANKL expression at the growing condyle.

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
Keyword(s):  
Growth Hormone ◽  
Growth Rate ◽  
Body Weight ◽  
Coho Salmon ◽  
Lower Percentage ◽  
Bovine Growth Hormone ◽  
Growth Promoter ◽  
Ration Level ◽  
Diet Formulation ◽  
Treated Fish

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.

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