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PMID |
Sentence |
1 |
3542649
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This result provides direct confirmation that insulin is not associated with a circulating serum binding protein(s) and that insulin is present predominantly as a monomer in plasma.
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2 |
3053958
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Insulin can regulate IGF-I production, acting on the GH receptor or at a post-receptor site.
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3 |
1568530
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We conclude that IDDM is associated with low GHBP levels and that GH resistance found in this disorder may be mediated, at least in part, by a decrease in GH receptor levels.
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4 |
8421083
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To elucidate, whether reduced peripheral action of GH contributes to this phenomenon, GH-binding protein (GH-BP) activity was measured in 117 children and adolescents with IDDM (mean age 14.6 yr, range 4.5-28 yr) and 132 healthy controls (13.1 yr, 6.3-26 yr).
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5 |
8421083
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In contrast, in IDDM children, GH-BP was reduced despite a moderate degree of overweight (z-score for weight: +0.94 +/- 0.12; mean +/- SE).
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6 |
8421083
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Reduced serum GH-BP activity in IDDM children is further accentuated when compared to healthy children with a similar degree of overweight (22.8 +/- 0.5%; n = 44).
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7 |
7683512
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GH deficiency, fasting, IGF-I administration to patients with GH receptor deficiency, hepatic failure and insulinomas caused a moderate increase of serum IGFBP-2.
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8 |
8281728
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GHBP, expressed as a percentage of (125I)GH bound, was determined in 33 patients with Type 1 diabetes (M/F = 19/14, 12.3 +/- 0.4 years) before (day 0), after 5 days (day 5) and after 3 months (month 3) of insulin therapy.
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9 |
8281728
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Thus, (1) circulating GHBP is low in newly diagnosed patients with Type 1 diabetes, and increases after 3 months of insulin therapy but does not normalize and (2) the severity of biochemical derangement and residual beta-cell function at diagnosis may determine GHBP status and its recovery.
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10 |
8016174
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IGF-I may be a regulatory factor for serum GHBP activity in man.
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11 |
8091976
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We have determined GHBP activity in two cases of poorly controlled IDDM with low height velocity in relation to metabolic control in order to determine the mechanism of resistance to GH in this condition, as indicated by low levels of GH-dependent growth factor IGF-I in the face of high serum GH levels.
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12 |
8091976
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GHBP activity was within the normal range in two cases of IDDM with slow height velocity, low IGF-I and high hemoglobin-A1.
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13 |
7536205
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Before insulin therapy, serum IGF-I, IGF-II, IGF-binding protein-3 (IGFBP-3), and GH-binding protein (GHBP) levels were significantly decreased, whereas IGFBP-1 and cortisol were significantly increased in diabetic children compared to those in an age-, sex-, and stage of puberty-matched control group.
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14 |
7536205
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Improvement in glycemic control, as determined by a change in hemoglobin-A1c, correlated positively with improvement in IGF-I, IGF-II, IGFBP-3, GHBP, and weight gain after 1 month of insulin therapy.
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15 |
11422104
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IGF-I and IGF-I SDS increased significantly at 1 and 3 months (P < 0.001) after commencing GHR.
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16 |
11966735
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Individual and population-mean cosinor analysis demonstrated significant circadian rhythms for SBP, DBP and HR before and after 12 months on GHR (P < 0.001), suggesting that SBP, DBP and HR circadian rhythms were not altered by GHR.
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17 |
11966735
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However, there is a significant decrease in 24-h mean SBP and DBP and increase in 24-h mean HR after 12 months on GHR.
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18 |
11966735
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We postulate that this decrease in 24-h mean SBP and DBP may result in a reduction of cardiovascular morbidity and mortality and may explain the beneficial effects of GHR on cardiovascular system previously reported in AGHD patients.
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19 |
14510911
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Leptin correlated to kilogram fat mass in both women (r=0.55, P<0.001) and men (r=0.47, P=0.003), but in contrast, there were no significant correlations between GHBP and fat mass and GHBP and IGF-I, either in women or in men (all, r<0.24, P>0.2).
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20 |
14510911
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Insulin and leptin were significantly associated with GHBP, both in women (r=0.48, P<0.001 and r=0.43, P=0.001, respectively) and in men (r=0.40, P=0.01 and r=0.34, P=0.03, respectively).
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21 |
14510911
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In the older subjects investigated, as in younger subjects, GHBP was significantly correlated with leptin and insulin.
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22 |
15140756
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We investigated the endogenous parathyroid hormone [PTH-(1-84)] response to hypocalcemic and hypercalcemic stimuli induced by sodium EDTA and calcium gluconate infusion, respectively, and to PTH-(1-34) infusion in AGHD patients before and during GH replacement (GHR).
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23 |
15140756
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The calcemic response to the effects of PTH-(1-34) infusion significantly increased after GHR.
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24 |
15140756
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Our results suggest increased parathyroid gland sensitivity to smaller changes in serum calcium and increased end-organ sensitivity to the effects of PTH in AGHD patients after GHR.
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25 |
15921943
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Neither total nor weight adjusted insulin requirements correlated to total PGH, calculated free PGH, nor GHBP.
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26 |
16613824
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Furthermore, no difference was noted in ALS and GHBP values between patients successfully treated with either somatostatin analogues or another type of treatment. a) Successfully treated acromegalic patients demonstrate lower ALS and higher GHBP levels than patients before treatment, and b) somatostatin analogue treatment does not have a direct effect on GHBP and ALS concentration in acromegaly.
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27 |
17492951
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To isolate and define the impact of GH, GH receptor (GHR) blockade and intravenous FFA infusion on total circulating ghrelin levels during a hyperinsulinaemic glucose clamp with identical insulin levels.
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28 |
17488973
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GH receptor (GHR) is a cytokine receptor family member that responds to GH by activation of the receptor-associated tyrosine kinase, JAK2 (Janus family of tyrosine kinase 2).
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29 |
17488973
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We previously showed that JAK2, in addition to being a signal transducer, dramatically increases the half-life of mature GHR, partly by preventing constitutive GHR down-regulation.
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30 |
17488973
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In cells that expressed JAK2, but not cells lacking JAK2, GH markedly enhanced GHR degradation.
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31 |
17488973
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Interestingly, GH-induced GHR ubiquitination, like down-regulation, was prevented in cells expressing a kinase-deficient JAK2 protein.
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32 |
17488973
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Collectively, our data suggest that determinants required for JAK2 to protect mature GHR from constitutive degradation differ from those that drive GH-induced GHR down-regulation.
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33 |
17488973
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The latter requires GH-induced JAK2 activation and GHR tyrosine phosphorylation and is correlated to GHR ubiquitination in our reconstitution system.
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34 |
17573420
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The GHR fl/d3 genotype modulates the relationship between GH and IGF-1 concentrations in patients presenting with acromegaly.
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35 |
17537658
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In the larger subset of T2DM, GHR(d3) was associated with higher CRP levels as well as age adjusted IGF-I, with a trend of higher C-peptide secretion and impaired lipid levels, indicating a phenotype with metabolic disorder when compared to the GHR(fl/fl) T2DM subjects.
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36 |
17534717
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Pegvisomant, a growth hormone receptor antagonist, suppresses IGF-1 levels into the normal range in over ninety percent of patients.
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37 |
18586085
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Here we overview downregulation of the growth hormone receptor as the most specific and potent mechanism of restricting cellular responses to growth hormone and analyze the role of several proteolytic systems and, specifically, ubiquitin-dependent pathways in this regulation.
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38 |
19907080
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Moreover, gene silencing of either endogenous Leprot or Leprotl1 in H4IIE hepatocytes increased GH signaling and enhanced cell-surface GH receptor.
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39 |
20502324
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Newer longer-acting somatostatin analogues are in development and combination regimes with the growth hormone receptor antagonist, pegvisomant, given at more cost-effective weekly doses show promising results.
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40 |
21325617
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Serum from GHR-deficient subjects also caused reduced expression of RAS, PKA (protein kinase A), and TOR (target of rapamycin) and up-regulation of SOD2 (superoxide dismutase 2) in treated cells, changes that promote cellular protection and life-span extension in model organisms.
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41 |
18431372
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Pegvisomant, a recombinant growth-hormone-receptor antagonist, suppresses production of insulin-like growth factor I.
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42 |
21555853
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Here we have employed a rat insulin II promoter-driven (RIP-driven) Cre recombinase to disrupt the GH receptor in ? cells (?GHRKO). ?GHRKO mice fed a standard chow diet exhibited impaired glucose-stimulated insulin secretion but had no changes in ? cell mass.
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43 |
22034225
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GH and IGF-I exert their biological effects through binding to respective receptors (GHR and IGF-IR) and subsequently engaging downstream signaling pathways.
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