Effects of dietary recombinant human insulin-like growth factor-I on concentrations of hormones and growth factors in the blood of newborn calves

1994 ◽  
Vol 140 (1) ◽  
pp. 15-21 ◽  
Author(s):  
C R Baumrucker ◽  
J W Blum
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Milk Replacer ◽  
Insulin Like Growth Factor ◽  
Recombinant Human Insulin ◽  
Blood Concentrations ◽  
Factor I ◽  
First Feeding ◽  
Igf I ◽  
Growth Factor I

Abstract Colostrum is rich in insulin-like growth factor-I (IGF-I) and IGF-II and the dietary effects of recombinant human IGF-I (rhIGF-I) on the newborn are of interest. The objective of this study was to examine the effects of dietary rhIGF-I upon selected hormones and growth factors in the blood. Calves were fed for the first 2 days of life with one of three experimental diets: (1) milk replacer plus isolated colostrum-derived globulin (MR−), (2) as (1) plus 98 μmol rhIGF-I/l (MR+) or (3) pooled cow colostrum. Thereafter, all animals received only milk replacer at 5% of body weight/feeding twice a day with only treatment 2 having the continued addition of 98 μmol rhIGF-I/l until completion of the experiment 7 days after birth. Radioimmunoassays for insulin, prolactin, IGF-I, IGF-II, GH, l-thyroxine, 3,5,3′-l-triiodothyroline and cortisol were conducted. With the exception of GH, all hormones and growth factors examined showed some form of dietary effect, but many were transient, changing only with the first feeding. Both insulin and prolactin concentrations exhibited a transient increase in blood at the first feeding, but insulin increased with the MR− treatment whereas prolactin increased with the MR+ treatment. Total IGF-I concentration in blood did not show any diet-induced changes for the first 4 days, but thereafter a rise in blood concentrations of IGF-I was observed. These data indirectly support the hypothesis that dietary IGF-I may be absorbed and causes transient systemic effects in the newborn calf. Journal of Endocrinology (1994) 140, 15–21

Insulin-like growth factor I accelerates protein synthesis in skeletal muscle during sepsis

1995 ◽  
Vol 269 (5) ◽  
pp. E977-E981 ◽  
Author(s):  
C. V. Jurasinski ◽  
T. C. Vary
Keyword(s):  
Protein Synthesis ◽  
Growth Factor ◽  
Peptide Chain ◽  
Translational Efficiency ◽  
Insulin Like Growth Factor ◽  
Recombinant Human Insulin ◽  
Chain Initiation ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

Sepsis causes an inhibition of protein synthesis in gastrocnemius that is resistant to the anabolic effects of insulin. The purpose of the present studies was to investigate the effect of recombinant human insulin-like growth factor I (IGF-I) on protein synthesis during a 30-min perfusion of the isolated rat hindlimb from septic rats. Inclusion of IGF-I (1 or 10 nM) in the perfusate stimulated protein synthesis in gastrocnemius of septic rats 2.5-fold and restored rates of protein synthesis to those observed in control rats. The stimulation of protein synthesis did not result from an increase in the RNA content but was correlated with a 2.5-fold increase in the translational efficiency. The enhanced translational efficiency was accompanied by a 33 and 55% decrease in the abundance of free 40S and 60S ribosomal subunits, respectively, indicating that IGF-I accelerated peptide-chain initiation relative to elongation/termination. These studies provide evidence that IGF-I can accelerate protein synthesis in gastrocnemius during chronic sepsis by reversing the sepsis-induced inhibition of peptide-chain initiation.

Insulin and insulin-like growth factor I (IGF I) in early mouse embryogenesis

Development ◽  
1990 ◽  
Vol 108 (3) ◽  
pp. 491-495
Author(s):  
R. Spaventi ◽  
M. Antica ◽  
K. Pavelic
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Indirect Evidence ◽  
Mouse Embryos ◽  
Insulin Like Growth Factor ◽  
Embryonic Cells ◽  
Mouse Development ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

Growth factors have an important role in the regulation of cell growth, division and differentiation. They are also involved in the regulation of embryonic growth and differentiation. Insulin and insulin-like growth factor I (IGF I) play an important part in these events in the later stages of embryogenesis, when organogenesis is completed. In this study, we are presenting evidence that insulin and IGF I are also secreted by embryonic tissues during the prepancreatic stage of mouse development. We found measurable amounts of insulin and IGF I in 8- to 12-day-old mouse embryos. We also showed that embryonic cells derived from 8-, 9- and 10-day-old mouse embryos secrete insulin, IGF I and/or related molecules. Furthermore, the same growth factors, when added to the culture of 9-day-old mouse embryonic cells, stimulate their proliferation. These results lead to the conclusion that insulin can stimulate the growth of embryonic cells during the period when pancreas is not yet formed, which is indirect evidence for a paracrine (or autocrine) type of action.

O-Mannosylation of recombinant human insulin-like growth factor I (IGF-I) produced inSaccharomyces cerevisiae

FEBS Letters ◽  
1989 ◽  
Vol 248 (1-2) ◽  
pp. 111-114 ◽  
Author(s):  
Karl Hård ◽  
Wilbert Bitter ◽  
Johannis P. Kamerling ◽  
Johannes F.G. Vliegenthart
Keyword(s):  
Growth Factor ◽  
Human Insulin ◽  
Insulin Like Growth Factor ◽  
Recombinant Human Insulin ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

scholarly journals Effects of Recombinant Human Insulin-Like Growth Factor I Administration on Spontaneous and Growth Hormone (GH)-Releasing Hormone-Stimulated GH Secretion in Anorexia Nervosa1

2000 ◽  
Vol 85 (8) ◽  
pp. 2805-2809
Author(s):  
Laura Gianotti ◽  
Angela I. Pincelli ◽  
Massimo Scacchi ◽  
Mimma Rolla ◽  
Deanna Bellitti ◽  
...  
Keyword(s):  
Growth Factor ◽  
Normal Weight ◽  
Insulin Like Growth Factor ◽  
Recombinant Human Insulin ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
Igfbp 3

Exaggerated GH and reduced insulin-like growth factor I (IGF-I) levels are common features in anorexia nervosa (AN). A reduction of the negative IGF-I feedback could account, in part, for GH hypersecretion. To ascertain this, we studied the effects of recombinant human (rh)IGF-I on spontaneous and GH-releasing hormone (GHRH)-stimulated GH secretion in nine women with AN [body mass index, 14.1 ± 0.6 kg/m2] and in weight matched controls (normal weight). Mean basal GH concentrations (mGHc) and GHRH (2.0μ g/kg, iv) stimulation were significantly higher in AN. rhIGF-I administration (20 μg/kg, sc) significantly reduced mGHc in AN (P < 0.01), but not normal weight, and inhibited peak GH response to GHRH in both groups; mGHc and peak GH, however, persisted at a significantly higher level in AN. Insulin, glucose, and IGFBP-1 basal levels were similar in both groups. rhIGF-I inhibited insulin in AN, whereas glucose remained unaffected in both groups. IGFBP-1 increased in both groups (P < 0.05), with significantly higher levels in AN. IGFBP-3 was under basal conditions at a lower level in AN (P < 0.05) and remained unaffected by rhIGF-I. This study demonstrates that a low rhIGF-I dose inhibits, but does not normalize, spontaneous and GHRH-stimulated GH secretion in AN, pointing also to the existence of a defective hypothalamic control of GH release. Moreover, the increased IGFBP-1 levels might curtail the negative IGF-I feedback in AN.

scholarly journals Effects of Recombinant Human Insulin-Like Growth Factor I Administration on Growth Hormone (GH) Secretion, Both Spontaneous and Stimulated by GH-Releasing Hormone or Hexarelin, a Peptidyl GH Secretagogue, in Humans1

1999 ◽  
Vol 84 (1) ◽  
pp. 285-290
Author(s):  
E. Ghigo ◽  
L. Gianotti ◽  
E. Arvat ◽  
J. Ramunni ◽  
M. R. Valetto ◽  
...  
Keyword(s):  
Growth Factor ◽  
Negative Feedback ◽  
Inhibitory Effect ◽  
Insulin Like Growth Factor ◽  
Recombinant Human Insulin ◽  
Gh Secretion ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
Hypothalamic Level

The negative feedback exerted by insulin-like growth factor I (IGF-I) on GH secretion occurs at the pituitary, as well as the hypothalamic level, via stimulation of SS and/or inhibition of GHRH release. In fact, recombinant human IGF-I (rhIGF-I) administration inhibits basal GH secretion, at least in fasted humans, though its effect on the GH response to GHRH is still controversial. GH secretagogues (GHS) are peptidyl and nonpeptidyl molecules that act on specific receptors at the pituitary and/or the hypothalamic level. Contrary to GHRH, the GH-releasing activity of GHS is strong, reproducible, and even partially refractory to inhibitory influences such as exogenous somatostatin. We studied the effects of rhIGF-I administration (20μ g/kg sc at 0 min) on GH secretion, either spontaneous or stimulated by GHRH (2 μg/kg iv at +180 min) or Hexarelin (HEX, 2.0 μg/kg iv at+ 180 min), a GHS, in eight normal young women (age, mean ± sem, 28.3 ± 1.2 yr; body mass index, 20.1± 0.5 kg/m2). rhIGF-I administration increased IGF-I levels (peak vs. baseline: 420.3 ± 30.5 vs. 274.4 ± 25.3 μg/L, P < 0.05) within the physiological range from +120 to +300 min. No variation in glucose or insulin levels was recorded. rhIGF-I did not reduce spontaneous GH secretion [areas under curves (AUC)0–300 min 140.6± 66.3 vs. 114.6 ± 32.1 μg/L·h], whereas it inhibited the GH response to both GHRH (AUC180–300 min 447.7 ± 159.4 vs. 715.9 ± 104.3 μg/L·h, P < 0.05) and HEX (620.3 ± 110.4 vs. 1705.9 ± 328.9 μg/L·h, P < 0.03). The percent inhibitory effect of rhIGF-I on the GH response to GHRH (41.7 ± 12.8%) was lower than that on the response to HEX (57.7 ± 11.0%). In fact, the GH response to GHRH alone was clearly lower than that to HEX alone (P < 0.05), whereas the GH responses to GHRH and HEX were similar after rhIGF-I. Our findings show that the sc administration of low rhIGF-I doses inhibits the GH response to GHRH and, even more, that to HEX; whereas, at least in this experimental design in fed conditions, it does not modify the spontaneous GH secretion. Because GHS generally show partial refractoriness to inhibitory inputs, including exogenous somatostatin, the present results point toward a peculiar sensitivity of GHS to the negative feedback action of IGF-I.

Insulin-like growth factor-I stimulates oxytocin and progesterone production by bovine granulosa cells in culture

1988 ◽  
Vol 116 (1) ◽  
pp. 97-100 ◽  
Author(s):  
D. Schams ◽  
R. Koll ◽  
C. H. Li
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Corpora Lutea ◽  
Dependent Manner ◽  
Insulin Like Growth Factor ◽  
Luteal Cells ◽  
Factor I ◽  
Igf I ◽  
Epidermal Growth ◽  
Growth Factor I

ABSTRACT The effect of insulin-like growth factor-I (IGF-I), epidermal growth factor (EGF), fibroblast growth factor (FGF) and nerve growth factor (NGF) on production of oxytocin and progesterone by cultured bovine granulosa and luteal cells was studied. Secretion of oxytocin was stimulated, in a dose-dependent manner, by IGF-I at 48 and 120 h of culture to levels much higher than those after stimulation with LH, FSH, EGF, FGF or NGF. A similar effect of IGF-I was observed for progesterone but, in contrast to oxytocin, secretion of progesterone was not increased by EGF, NGF or FGF. During primary culture, for 4 h, of dispersed bovine luteal cells obtained from corpora lutea between days 4 and 10 of the oestrous cycle, all the growth factors tested failed to stimulate secretion of oxytocin or progesterone. The data suggest the relevance of growth factors (especially IGF-I) for ovarian physiology and their possible importance for differentiation of follicles and luteinization. J. Endocr. (1988) 116, 97–100

scholarly journals Plasma GH, TSH and PRL Responses to Recombinant Human Insulin-Like Growth Factor-I (IGF-I) in Normal and Acromegalic Subjects.

1996 ◽  
Vol 43 (Suppl) ◽  
pp. S81-S83
Author(s):  
KUNIHIKO HANEW ◽  
AKI TANAKA ◽  
AKIRA SUGAWARA ◽  
KEIICHI ITOI ◽  
KEISHI ABE
Keyword(s):  
Growth Factor ◽  
Human Insulin ◽  
Insulin Like Growth Factor ◽  
Recombinant Human Insulin ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
Plasma Gh
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