scholarly journals DECREASED SERUM SOMATOMEDIN-C (Sm-C) RESPONSE TO GROWTH HORMONE (GH) IN HYPOPHYSECTOMIZED RATS FED A LOW PROTEIN DIET: EVIDENCE FOR A POSTRECEPTOR DEFECT

1986 ◽  
Vol 20 (11) ◽  
pp. 1185-1185
Author(s):  
M Maes ◽  
Y Amand ◽  
J M Ketelslegers
Keyword(s):  
Growth Hormone ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Somatomedin C ◽  
Low Protein ◽  
Hypophysectomized Rats

Effect of nutrition on growth and somatomedin A levels in the rat

1980 ◽  
Vol 94 (3) ◽  
pp. 321-326 ◽  
Author(s):  
Kazue Takano ◽  
Naomi Hizuka ◽  
Kazuo Shizume ◽  
Yoko Hasumi ◽  
Toshio Tsushima
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Normal Growth ◽  
Protein Diet ◽  
Low Protein Diet ◽  
High Fat ◽  
Low Protein ◽  
High Fat Diets ◽  
Hypophysectomized Rats ◽  
Fat Diets

Abstract. Serum somatomedin A was significantly reduced after 3 days of fasting in rats with a mean decrease of 23.6 ± 2.4% (N = 18) of initial values. Re-feeding for one day produced a definite increase in somatomedin A, with a rise in body weight. When re-fed isocalorically for 21 days with diets of different quality, a low protein diet led to smaller increases in both seum somatomedin A and body weight in comparison to those of control-, high-protein- and high fat-diets (P < 0.001). There is a positive correlation between the increase in body weight and serum somatomedin A levels (N = 70, r = 0.71, P< 0.001). The effect of growth hormone on somatomedin generation was abolished in hypophysectomized rats fed with low-protein diet. Our study suggests that protein in the diet is important for the generation of somatomedin A, which is necessary for normal growth.

scholarly journals Insulin-like growth factor-I, but not growth hormone, is dependent on a high protein intake to increase nitrogen balance in the rat

1999 ◽  
Vol 81 (2) ◽  
pp. 145-152 ◽  
Author(s):  
Myriam Sanchez-Gomez ◽  
Kjell Malmlöf ◽  
Wilson Mejia ◽  
Antonio Bermudez ◽  
Maria Teresa Ochoa ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Dietary Protein ◽  
Protein Diet ◽  
N Balance ◽  
Low Protein Diet ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Low Protein ◽  
Igf I

The aim of the present study was to investigate the influence of dietary protein level on the protein anabolic effects of growth hormone (GH) and insulin-like growth factor-I (IGF-I). Female growing rats were fed on either a high- or a low-protein diet with crude protein contents of 222 and 83 g/kg respectively. The diets contained the same amount of metabolizable energy (15·1 MJ/kg) and were given during a 14 d period. During the same time, three groups of rats (n 8) on each diet received subcutaneous infusions of either saline, recombinant human GH (rhGH) or recombinant human IGF-I (rhIGF-I). rhGH and rhIGF-I were given in doses of 360 and 500 μg/d respectively. The low-protein diet alone reduced significantly (P < 0·05) IGF-I concentrations in serum and in tissue taken from the gastrocnemius muscle as well as IGF-I mRNA from the same muscle. The responses to rhGH and rhIGF-I in terms of muscle IGF-I and its mRNA were variable. However, when rhIGF-I was infused into rats on the high-protein diet, significantly elevated levels of IGF-I in muscle tissues could be observed. This was associated with a significantly (P < 0·05) increased N balance, whereas rhGH significantly (P < 0·05) enhanced the N balance in rats on the low-protein diet. Thus, it can be concluded that the level of dietary protein ingested regulates not only the effect of IGF-I on whole-body N economy but also the regulation of IGF-I gene expression in muscles. The exact mechanism by which GH exerts its protein anabolic effect, however, remains to be elucidated.

Low-Protein Diet Suppresses Serum Insulin-Like Growth Factor-1 and Decelerates the Progression of Growth Hormone-Induced Glomerulosclerosis

2001 ◽  
Vol 21 (4) ◽  
pp. 331-339 ◽  
Author(s):  
Sonia Q. Doi ◽  
Suvi Rasaiah ◽  
Ivan Tack ◽  
Jagannatha Mysore ◽  
John J. Kopchick ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Serum Insulin ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Insulin Like Growth Factor ◽  
Low Protein

scholarly journals Somatomedin-C and zinc status in rats as affected by Zn, protein and food intake

1986 ◽  
Vol 56 (1) ◽  
pp. 163-169 ◽  
Author(s):  
Zafrallah T. Cossack
Keyword(s):  
Food Intake ◽  
Body Weight Gain ◽  
Experimental Period ◽  
Optimal Level ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Control Group ◽  
Somatomedin C ◽  
Low Protein ◽  
Adequate Food

1. The objective of the present experiment was to study the level of plasma somatomedin-C (SM-C) and the status of zinc in rats as affected by three levels of Zn given in combinations with two levels of protein.2. Six groups of rats were fed, for 21 d, on six different diets based on combinations of two levels of dietary protein (low protein, 75 g/kg; high protein, 200 g/kg) and three levels of zinc (low Zn, 0.9 pglkg; moderate Zn, 55 pg/kg; high Zn, 110 pglkg). All groups were pair-fed with the group receiving the low-Zn-low-protein diet. An additional group of six rats served as an ad lib.-fed control group and was fed on a diet that contained 55 pg Zn/kg and 200 g protein/kg ad lib.3. Body-weight gain and food intake were recorded daily. Rats were killed at the end of the experimental period (21 d). Zn was assayed in plasma, tibia and liver by atomic absorption technique. Plasma SM-C was assayed by radioimmunoassay.4. In rats given the low-Zn-low-protein diet, the level of plasma SM-C increased in response to the increase in the amount of Zn or Zn and protein in the diet. However, no change was observed when the level of protein alone was increased.5. Among all groups tested, adlib.-fed rats showed the highest level of plasma SM-C. Thus it may be concluded that a balanced diet combined with adequate food intake is necessary to maintain an optimal level of plasma SM-C.

Decreased serum insulin-like growth factor I response to growth hormone in hypophysectomized rats fed a low protein diet: evidence for a postreceptor defect

1988 ◽  
Vol 117 (3) ◽  
pp. 320-326 ◽  
Author(s):  
M. Maes ◽  
Y. Amand ◽  
L. E. Underwood ◽  
D. Maiter ◽  
J.-M. Ketelslegers
Keyword(s):  
Binding Sites ◽  
Protein Diet ◽  
Female Rats ◽  
Low Protein Diet ◽  
Affinity Constant ◽  
Protein Calorie Malnutrition ◽  
Low Protein ◽  
Igf I ◽  
Hypophysectomized Rats ◽  
Gh Resistance

Abstract. In protein-calorie malnutrition, serum IGF-I concentrations are low despite high GH. This GH resistance might be due to a reduced number of liver GH binding sites as suggested by studies performed in fasted rats that were refed a low protein diet. To determine whether a postreceptor defect in GH action might also contribute to the GH resistance, we measured the number and the affinity constant of the liver GH binding sites and the serum IGF-I responses to injections of recombinant bGH in hypophysectomized female rats, fed a standard (15% protein) diet (N = 25) or a low (5%) protein diet (N = 25) for 8 days. There were no significant differences in the liver GH binding capacities between the 15% and the 5% protein-fed rats, whether expressed as pmol per liver (20.6 ± 3.5 vs 14.4 ± 1.3; mean ± sem; P < 0.2; N = 5, respectively), pmol per mg DNA (1.08 ± 0.16 vs 0.84 ± 0.07; P <0.4) or fmol per mg of protein (28.98 ± 5.04 vs 30.26 ± 2.00; P > 0.5). Likewise, the affinity constants of the GH binding sites of the 15% and the 5% protein-fed rats were not significantly different (0.78 ± 0.05 vs 0.78 ± 0.07 × 109 l/mol; P > 0.5). Despite these non-significant reductions in liver GH binding sites, the IGF-I responses 24 h after sc injections of increasing doses of bovine GH were blunted in the rats fed the 5% protein diet. The maximal IGF-I response in the rats with the normal protein intake was 360 ± 30 U/I, but only 130 ± 40 U/l in the 5% protein-fed animals (P < 0.001). The blunted serum IGF-I responses to GH, together with decreased maximal stimulation in the 5% protein-fed hypophysectomized rats, support the possibility that a postreceptor defect in GH action contributes to the GH resistance in protein-calorie malnutrition.

Effects of a low-protein diet on prolactin- and growth hormone-producing cells in the rat pituitary gland

1998 ◽  
Vol 251 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Masayuki Hara ◽  
Damon C. Herbert ◽  
Takashi Taniguchi ◽  
Atsuhiko Hattori ◽  
Ritsuko Ohtani-Kaneko ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Pituitary Gland ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Low Protein ◽  
Rat Pituitary

Immunohistochemical detection of changes in growth hormone cells in rat pituitaries in protein deficiency

1975 ◽  
Vol 33 (1) ◽  
pp. 11-15 ◽  
Author(s):  
Therese Drummond
Keyword(s):  
Growth Hormone ◽  
Normal Diet ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Immunohistochemical Method ◽  
Deficient Diet ◽  
Low Protein ◽  
Gh Cells ◽  
Protein Free Diet ◽  
Cell Changes

1. An immunohistochemical method was used to study the effect of a low-protein diet on growth hormone (GH) cells in the pituitaries of developing rats. The deficient diet (80 g protein/kg) was administered during gestation and lactation, or during the time after weaning until 90 d of age, or during both periods.2. GH-cell changes were much more striking in males than in females.3. In males, GH-producing cells were usually reduced in size and number in all treatments. The effect was most intense when protein deprivation occurred throughout gestation and sucking, and continued until 90 d of age, but it was also evident in animals given the low protein diet only after weaning. Recuperation appeared to be almost complete when offspring of deprived dams were fed on a normal diet after weaning.4. It is concluded that a low-protein diet reduces the amount of GH in the rat pituitary in a way similar to that with a protein-free diet.

Hepatic Ultrastructure Changes Induced by Lithocholic Acid

1967 ◽  
Vol 25 ◽  
pp. 162-163 ◽  
Author(s):  
F. G. Zaki
Keyword(s):  
Endoplasmic Reticulum ◽  
Lithocholic Acid ◽  
Smooth Endoplasmic Reticulum ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Electron Microscopic ◽  
Hydropic Degeneration ◽  
Hepatic Cells ◽  
Low Protein ◽  
Microscopic Studies

Addition of lithocholic acid (LCA), a naturally occurring bile acid in mammals, to a low protein diet fed to rats induced marked inflammatory reaction in the hepatic cells followed by hydropic degeneration and ductular cell proliferation. These changes were accompanied by dilatation and hyperplasia of the common bile duct and formation of “gallstones”. All these changes were reversible when LCA was withdrawn from the low protein diet except for the hardened gallstones which persisted.Electron microscopic studies revealed marked alterations in the hepatic cells. Early changes included disorganization, fragmentation of the rough endoplasmic reticulum and detachment of its ribosomes. Free ribosomes, either singly or arranged in small clusters were frequently seen in most of the hepatic cells. Vesiculation of the smooth endoplasmic reticulum was often encountered as early as one week after the administration of LCA (Fig. 1).

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