Identification of insulin-like growth factor (IGF) and glucose transporter-1 and -3 mRNA in CNS tumors

1993 ◽  
Vol 48 (1-2) ◽  
pp. 251-256 ◽  
Author(s):  
Roberta P. Glick ◽  
Terry G. Unterman ◽  
Raul Lacson
Keyword(s):  
Growth Factor ◽  
Glucose Transporter ◽  
Cns Tumors ◽  
Insulin Like Growth Factor ◽  
Glucose Transporter 1

scholarly journals Regulation of Human Trophoblast GLUT1 Glucose Transporter by Insulin-Like Growth Factor I (IGF-I)

PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e106037 ◽  
Author(s):  
Marc U. Baumann ◽  
Henning Schneider ◽  
Antoine Malek ◽  
Vidya Palta ◽  
Daniel V. Surbek ◽  
...  
Keyword(s):  
Growth Factor ◽  
Glucose Transporter ◽  
Insulin Like Growth Factor ◽  
Human Trophoblast ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
Glut1 Glucose Transporter

scholarly journals Regulation of lactate production and glucose transport as well as of glucose transporter 1 and lactate dehydrogenase A mRNA levels by basic fibroblast growth factor in rat Sertoli cells

2002 ◽  
Vol 173 (2) ◽  
pp. 335-343 ◽  
Author(s):  
MF Riera ◽  
SB Meroni ◽  
HF Schteingart ◽  
EH Pellizzari ◽  
SB Cigorraga
Keyword(s):  
Growth Factor ◽  
Glucose Transport ◽  
Glucose Transporter ◽  
Lactate Production ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Short Term ◽  
Glucose Transporter 1 ◽  
Ldh Activity

By using cultured rat Sertoli cells as a model, both the action of basic fibroblast growth factor (bFGF) on lactate production and the site of this action were studied. bFGF stimulated Sertoli cell lactate production in a dose-dependent manner (basal: 7.3+/-0.5; 0.1 ng/ml bFGF: 7.5+/-0.5; 1 ng/ml bFGF: 7.5+/-0.6; 10 ng/ml bFGF: 10.3+/-1.0; 30 ng/ml bFGF: 15.2+/-1.5; 50 ng/ml bFGF: 15.4+/-1.6 microg/microg DNA). Two major sites for the action of this growth factor were identified. First, bFGF was shown to exert short- and long-term stimulatory effects on glucose transport (basal: 1170+/-102; 30 ng/ml bFGF for 120 min: 1718+/-152 and basal: 718+/-64; 30 ng/ml bFGF for 48 h: 1069+/-69 d.p.m./microg DNA respectively). Short-term bFGF stimulation of glucose transport was not inhibited by the protein synthesis inhibitor cycloheximide. These results indicate that short-term bFGF stimulation of glucose uptake does not involve an increase in the number of glucose transporters. On the other hand, stimulation with bFGF for periods of time longer than 12 h increased glucose transporter 1 (GLUT1) mRNA levels. These increased mRNA levels were probably ultimately responsible for the increments in glucose uptake that are observed in long-term treated cultures. Secondly, bFGF increased lactate dehydrogenase (LDH) activity (basal: 31.0+/-1.4; 30 ng/ml bFGF: 45.7+/- 2.4 mIU/microg DNA). The principal subunit component of those LDH isozymes that favors the transformation of pyruvate to lactate is subunit A. bFGF increased LDH A mRNA levels in a dose- and time-dependent manner. In summary, the results presented herein show that glucose transport, LDH activity and GLUT1 and LDH A mRNA levels are regulated by bFGF to achieve an increase in lactate production. These observed regulatory actions provide unequivocal evidence of the participation of bFGF in Sertoli cell lactate production which may be related to normal germ cell development.

scholarly journals Insulin and insulin-like growth factor 1 antagonize the stimulation of ob gene expression by dexamethasone in cultured rat adipose tissue

1997 ◽  
Vol 324 (2) ◽  
pp. 605-610 ◽  
Author(s):  
Bénédicte A. REUL ◽  
Lumbe N. ONGEMBA ◽  
Anne-Marie Marie ◽  
Jean-Claude HENQUIN ◽  
Sonia M. BRICHARD
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Growth Factor ◽  
Fatty Acid Synthase ◽  
Glucose Transporter ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Insulin Like Growth Factor ◽  
Ob Gene ◽  
Rat Adipose Tissue

The ob gene, specifically expressed in fat cells, encodes leptin, a hormone that induces satiety and increases energy expenditure. In this study, we investigated the interactions between glucocorticoids and insulin on ob gene expression in cultured explants of rat adipose tissue. Only low levels of ob mRNA were detected when adipose tissue from fasted rats was cultured for 12–24 h in minimal essential medium. However, the addition of dexamethasone to the medium increased ob gene expression in a concentration-dependent manner (EC50 10 nM). With 1 μM dexamethasone, ob mRNA levels were similar to those in fresh fat pads from fed rats, reaching a maximum after 12 h. The effect of dexamethasone was blocked by actinomycin D, which indicates an action on transcription. This effect was increased when a minimum amount of fuel (glucose or a mixture of lactate and pyruvate) was supplied in the medium. Unlike dexamethasone, insulin, even when combined with high glucose concentrations, did not induce ob expression, although it strongly increased the accumulation of mRNA species for fatty acid synthase (FAS), the insulin-sensitive glucose transporter GLUT4 and the γ isoform of peroxisome proliferator-activated receptor (PPARγ). Unexpectedly, insulin dose-dependently inhibited dexamethasone-induced ob mRNA accumulation. This effect was observed at low concentrations of insulin (IC50 1 nM) and was delayed in onset, beginning after 6–9 h of culture. It was mimicked by insulin-like growth factor 1 (IGF-1) (100 nM). The inhibition by insulin was only detectable when fuels were present and/or when a critical level of ob expression was reached. As this inhibitory effect was reversed by cycloheximide, this suggests that it required ongoing protein synthesis. In conclusion, unlike dexamethasone, insulin had no direct stimulatory effect on ob gene expression. On the other hand, insulin (and IGF-1) even inhibited the dexamethasone-induced accumulation of ob mRNA. The underlying mechanism involved ongoing synthesis of an inhibitory protein by insulin, which is in keeping with its delayed effect. Moreover, the expression of genes for FAS, GLUT4 and PPARγ may be inversely related to that of ob.

Insulin and insulin-like growth factors in central nervous system tumors

1992 ◽  
Vol 77 (3) ◽  
pp. 445-450 ◽  
Author(s):  
Roberta P. Glick ◽  
Terry G. Unterman ◽  
Mary Van der Woude ◽  
Lisa Zollner Blaydes
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Growth Factor ◽  
Tumor Cell ◽  
Cns Tumors ◽  
Insulin Like Growth Factor ◽  
Content Type ◽  
Igf I ◽  
Fine Print

✓ The authors have previously reported the presence of insulin-like growth factor (IGF) receptors in central nervous system (CNS) tumors and the production of IGF's and their binding proteins by CNS tumors in situ. This study was designed to investigate whether CNS tumor cells are capable of autocrine secretion of IGF-I and IGF-II in vitro. Production of IGF's was studied by specific radioimmunoassay of tumor-cell-conditioned serum-free media from 34 CNS tumors: 12 gliomas, 12 meningiomas, and 10 miscellaneous tumors. Normal human serum and cerebrospinal fluid served as controls. Insulin-like growth factor I was detected in five of 12 meningiomas but in none of the gliomas studied. In contrast, IGF-II was detected in four of 12 gliomas and in six of 11 meningiomas studied. Four miscellaneous tumors produced IGF-I and/or IGF-II. These results suggest that CNS tumors differentially produce IGF-I and IGF-II in vitro. Preferential production of IGF's may be an important marker of the tumor-cell differentiation or malignancy and may be useful as a clinical diagnostic tool. These results add further support to the concept that IGF's may play a role in the regulation of the behavior of CNS tumors.

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