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Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to design an approach for localizing IGF-I receptors within the intact CNS, the effect of paraformaldehyde (PAF) fixation on receptor binding was examined. Cryostat sections of rat brains, which were perfused with 0 to 10% PAF, were incubated in 125I-IGF-I and assayed for binding under equilibrium conditions. Binding was quantified from 10 brain regions, involving laminae and nuclei from median eminence, thalamus, hippocampus, choroid plexus, pyriform cortex, and cerebral cortex, by computer densitometry of film autoradiographs. The specific binding, saturation curves, Bmax and Ka, ligand specificity, and binding reversibility of IGF-I binding sites were not significantly affected by 1% or 2% PAF. However, 4% PAF elevated IGF-I receptor total binding, nonspecific binding, and Ka, and decreased Bmax, presumably by increasing the number of tissue-receptor interconnections. Only nonspecific 125I-IGF-I binding persisted when 10% PAF was used. These results indicate that tissue perfused with 2% PAF can be used for localizing IGF-I receptors by autoradiographic binding methods.
Anat Rec 1991 Dec
PMID:Effect of paraformaldehyde fixation on localization and characterization of insulin-like growth factor-I (IGF-I) receptors in the rat brain. 166 20

Removal of the ocular lens in adult newts (Notophthalmus viridescens) is followed by a series of cellular events leading to regeneration of a new lens by cell type conversion of pigmented iris epithelial cells at the dorsal pupillary margin (Yamada, Curr. Top. Dev. Biol. 2:247-283, 1967). Following depigmentation and five to seven cell divisions, iris epithelial cells redifferentiate into lens fiber cells and synthesize crystallin proteins (Yamada, Curr. Top. Dev. Biol. 2:247-283, 1967). This process is dependent upon neural retina in vivo (Stone, Anat. Rec. 131:151-172, 1958; Reyer, Dev. Biol. 14:214-225, 1966) and in vitro (Yamada et al., Differentiation 1:65-82, 1973). Acting on the hypothesis that the role of the neural retina is to promote passage of iris epithelial cells through the requisite number of cell cycles which will then allow them to redifferentiate as lens fiber cells (Yamada, in: Cell Biology of the Eye. Academic Press, New York, 1982), we undertook testing of the effects of eye-derived mitogenic substances, as well as other mitogens, on regeneration of lens from iris in organ culture. We have previously defined a critical period for the retinal influence in vivo and in vitro, and have shown that crude extracts of retina can enhance regeneration of lenses in culture (Connelly et al., J. Exp. Zool., 240:343-351, 1986). In this paper, we report on the lens regeneration enhancing activity (LRA) of more highly purified fractions of the retinal extracts. Heparin-sepharose chromatography of the crude retinal extract yields three fractions (Courty et al., Biochemie 67:265-269, 1985) called EDGF I, II, and III. EDGF I and II have affinity for heparin, while EDGF III does not. In our bioassay, LRA appears only in the EDGF III fraction. Dialysis of EDGF III against 0.1 N acetic acid yields a fraction which has affinity for cibacron blue sepharose (eluting at 2.15 M salt) and also has significant LRA. Because insulin at high doses has a marginal effect on lens regeneration in culture (Williams and McGlinn, Am. Zool. 19:923, 1979; Connelly, Differentiation 16:85-91, 1980), we tested IGF-I. Because of the putative neurotrophic effects of transferrin (Tf) (Mescher and Munaim, J. Exp. Zool., 230:485-490, 1986), we tested Tf for its ability to enhance regeneration of the lens in culture. IGF-I seems to have an enhancing effect on lens regeneration; Tf does not.
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PMID:Influence of chromatographic fractions of extracts derived from bovine neural retina on newt (Notophthalmus viridescens) lens regeneration in vitro. 365 82

An Escherichia coli derived somatomedin-C/IGF-I preparation (rec-IGF-I) with an amino acid sequence identical to the natural IGF-I derived from human plasma, increases body length and weight, as well as the growth of several organs of Snell dwarf mice, when administered for 4 wk. After 2 wk of treatment rec-IGF-I (22.2 micrograms/day) induced a significant increase over buffer treated controls, to a comparable degree as obtained with bacterially synthesized human growth hormone (bhGH; 8.4 micrograms/day). The weight/length ratio of rec-IGF-I and bhGH-treated dwarf mice after 4 wk of treatment were not significantly different. A significant increase over controls was obtained with both preparations. Organs with increased weights after bhGH treatment (brain; submandibular salivary glands; heart, liver, kidneys, thymus, and spleen) were also heavier after rec-IGF-I. Significance was only reached for the kidneys and the spleen and the musculus quadriceps femoris. Organ weights expressed as a percentage of body weight of bhGH and rec-IGF-I treated dwarfs were similar except for the relative weight of the heart of the bhGH group, which was significantly increased compared to the controls and the rec-IGF-I group. These data resolve the issue as to whether or not pure SM-C/IGF-I will induce growth in length and demonstrate the usefulness of recombinant IGF-I in the studies of growth regulation.
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PMID:Biosynthetic somatomedin C (SM-C/IGF-I) increases the length and weight of Snell dwarf mice. 374 55

The study was designed to be an open test for short-term efficacy of rec hGH-therapy on spermatogenesis of ten infertile men with idiopathic severe oligozoospermia (1-5 x 10(6)) and normogonadotropinemia or moderate ipergonadotropinemia (FSH: range 1.90-9.60 IU/L, mean +/- SD 5.78 +/- 2.84; LH: 2.70-12.70 IU/L, mean +/- SD 6.60 +/- 3.61). FSH, LH, Testosterone, GH, and IGF-I were evaluated. Seminal parameters: sperm concentration, sperm motility and morphology were studied before and after therapy. Five responder patients showed an increase of seminal parameters both in sperm concentration and total number of motile spermatozoa. The short-term rec-hGH therapy significantly increased sperm concentration and total motile spermatozoa in five out of ten infertile patients who didn't show any modification in seminal parameters to other preavious treatment.
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PMID:Recombinant-growth hormone (rec-hGH) therapy in infertile men with idiopathic oligozoospermia. 766 Jul 21

Eight gluten-sensitive Irish setters underwent a gluten challenge to investigate changes in the insulin-like growth factor (IGF) axis. In the first study, they were challenged with an acute intraduodenal administration of tryptic-peptic gluten digest and then maintained on dietary gluten for three months. In the second study, the challenge came solely from dietary gluten fed for three months. After the acute intraduodenal administration of gluten, serum IGF-I levels decreased significantly by 21.8 per cent, (P = 0.01) on day 3 after challenge and then returned to normal. There was also a decrease (52.5 per cent, P < 0.03) in the levels of serum IGF-binding protein-3 (IGFBP-3) until day 14 after challenge but they had returned to normal by day 28. In two dogs IGFBP-3 levels decreased through specific serum protease activity. There were no changes in serum IGF-I or IGFBP levels during the second study after the dietary gluten challenge alone, or in four non-gluten-sensitive beagles studied as controls during the acute intraduodenal/dietary gluten challenge.
Vet Rec 1998 Jul 18
PMID:Insulin-like growth factor axis of gluten-sensitive dogs during a gluten challenge. 971 21

Children suffering from thalassaemia major are reported to have growth delay and bone alterations even when well transfused and chelated. In the present study we evaluated bone and collagen turnover (bone Gla-protein, BGP; carboxyterminal telopeptide of type I collagen, ICTP; aminoterminal propeptide of type III procollagen, PIIINP, respectively) and bone mineral density (BMD) in 5 pre-pubertal GH deficient thalassaemic children before and during rec-GH treatment (0.6 IU/kg/week). Data were compared with those recorded in an age- and sex-matched control group. Before treatment, serum BGP and ICTP levels were significantly lower (p<0.0001) in children with thalassaemia (9.3+/-0.7 ng/ml and 5.3+/-0.5 ng/ml, respectively) than in healthy controls (18.9+/-0.9 ng/ml and 14.4+/-0.6 ng/ml, respectively), while serum PIIINP levels did not significantly differ in the two groups (6.7+/-0.7 ng/ml vs 6.7+/-0.7 ng/ml). Mean lumbar BMD values of patients (0.62+/-0.05 g/cm2) were significantly lower (p<0.05) than those recorded in healthy controls (0.78+/-0.01 g/cm2), while femoral BMD values were similar in the two groups (patients: 0.70+/-0.08 g/cm2 vs controls: 0.74+/-0.01 g/cm2). One-year GH therapy significantly increased height velocity (from 2.3+/-0.2 cm/year to 6.1+/-0.4 cm/yr, p<0.0001) and IGF-I levels (from 61.6+/-15.4 to 342+/-38.5 ng/ml, p<0.005). Serum BGP (basal: 9.3+/-0.7 ng/ml, 6th month: 10.8+/-0.6 ng/ml, 12th month: 14.9+/-1.4 ng/ml), ICTP (basal: 5.3+/-0.5 ng/ml, 6th month: 7.9+/-0.8 ng/ml, 12th month: 10.9+/-1.7 ng/ml) and PIIINP levels (basal: 6.7+/-0.7 ng/ml, 6th month: 9.9+/-1.0 ng/ml, 12th month: 9.6+/-1.4 ng/ml) significantly increased (p<0.05), while no significant effects were observed on lumbar and femoral BMD values. Although the GH-induced stimulation of bone turnover markedly increased BGP (+60%) and ICTP (+105%) levels, one-year GH therapy was not sufficient to completely normalize these parameters, which remained significantly lower than in healthy controls. In conclusion, our study shows that pre-pubertal GH deficient children with thalassaemia major have reduced bone turnover (both bone formation and resorption) and lumbar BMD values, thus indicating that bone metabolism should be monitored and improved even in well-transfused patients. One-year GH treatment is able to increase, but not normalize, bone turnover, this effect being insufficient to improve BMD values. More prolonged periods of GH therapy are probably requested to positively affect both bone turnover and BMD values in GH deficient thalassaemic patients, as occurs in children and adults with GH deficiency.
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PMID:Effects of 12 months rec-GH therapy on bone and collagen turnover and bone mineral density in GH deficient children with thalassaemia major. 1090 62

Diabetes mellitus results in various complications, also compromising the salivary glands. Hormone levels and interactions with cellular receptors are altered, intensifying the damage caused by this disease. Hormone replacement therapy alone or combined with other treatments may reverse this damage, but doubts still exist regarding the efficacy of this procedure. The objective of this study was to evaluate the effect of estrogen replacement therapy combined with insulin treatment on salivary secretory cells and on the expression of insulin-like growth factor (IGF)-I receptors in salivary glands of spontaneously diabetic (NOD) mice. Twenty-five mice were divided into five groups of five animals each: group I (NOD diabetic), group II (NOD diabetic treated with insulin), group III (NOD diabetic treated with estrogen), group IV (NOD diabetic treated with insulin and estrogen), and group V (control Balb/c mice). Group II received insulin, group III received estrogen, and group IV received insulin plus estrogen administered daily for 20 days. Groups I and V received saline for the same period of time to simulate treatment. Glucose and estrogen levels were monitored during treatment, and salivary gland samples were collected at the end of treatment for stereological analysis and immunofluorescence detection of IGF-I receptors. Tissue restructuring and regulation of IGF-I receptors expression were observed in animals submitted to estrogen replacement therapy plus insulin. Estrogen effectively promoted the recovery of salivary secretory cells, demonstrating that this hormone alone, and especially when combined with insulin, might be important for the reversal of hyperglycemia-induced tissue injury.
Anat Rec (Hoboken) 2011 Nov
PMID:Estrogen and insulin replacement therapy modulates the expression of insulin-like growth factor-I receptors in the salivary glands of diabetic mice. 2196 57