scholarly journals Insulin-like growth factor I and insulin induce adipogenic-related gene expression in fetal brown adipocyte primary cultures

1996 ◽  
Vol 319 (2) ◽  
pp. 627-632 ◽  
Author(s):  
Teresa TERUEL ◽  
Angela M VALVERDE ◽  
Manuel BENITO ◽  
Margarita LORENZO
Keyword(s):  
Growth Factor ◽  
Fatty Acid Synthase ◽  
Brown Adipocyte ◽  
Dependent Manner ◽  
Insulin Like Growth Factor ◽  
Brown Adipocytes ◽  
Factor I ◽  
Fetal Rat ◽  
Igf I ◽  
Growth Factor I

Fetal rat brown adipocytes show high-affinity binding sites for both insulin-like growth factor I (IGF-I) and insulin. Cell culture for 24 h in the presence of IGF-I or insulin, independently, up-regulated the mRNA expression of adipogenic-related genes, such as fatty acid synthase (FAS), glycerol-3-phosphate dehydrogenase and insulin-regulated glucose transporter Glut4, and down-regulated the expression of phosphoenolpyruvate carboxykinase mRNA in a dose-dependent manner. Moreover, both IGF-I and insulin increased the FAS gene transcription rate at 2 h, producing a time-dependent accumulation of FAS mRNA. Furthermore IGF-I or insulin increased glucose uptake and lipid content throughout the 24 h culture period. Our results suggest that both IGF-I and insulin are major signals involved in initiating and/or maintaining the expression of adipogenic-related genes in fetal rat brown adipocytes.

scholarly journals Evidence for modulation of osteocalcin containing gamma-carboxyglutamic acid residues synthesis by insulin-like growth factor-I and vitamin K2 in human osteosarcoma cell line MG-63

1998 ◽  
pp. 443-448 ◽  
Author(s):  
Y Kudo ◽  
M Iwashita ◽  
Y Takeda ◽  
T Muraki
Keyword(s):  
Growth Factor ◽  
Vitamin K2 ◽  
Osteosarcoma Cell ◽  
Dependent Manner ◽  
Insulin Like Growth Factor ◽  
Concentration Dependent Manner ◽  
Factor I ◽  
Carboxyglutamic Acid ◽  
Igf I ◽  
Growth Factor I

The effect of insulin-like growth factor-I (IGF-I) and 2-methyl-3-all-trans-tetraphenyl-1,4-naphtoquinone (vitamin K2) on the synthesis of osteocalcin containing gamma-carboxyglutamic acid (Gla) residues which is the physiologically relevant form in bone metabolism was studied in cultured human osteoblast-like (MG-63) cells. Both IGF-I and vitamin K2 stimulated 1,25-dihydroxyvitamin D3 (1,25(OH)2D3)-induced osteocalcin containing Gla secretion in a concentration-dependent manner. This stimulatory effect of IGF-I and vitamin K2 was additive. Vitamin K2-enhanced osteocalcin containing Gla secretion was selectively suppressed by 3-(alpha-acetonyl-benzyl)-4-hydroxy-coumarin (warfarin). The stimulatory effect of IGF-I was completely abolished by the presence of cycloheximide; in contrast the effect of vitamin K2 was still observed in the presence of cycloheximide. Treatment of MG-63 cells with IGF-I caused an approximately 2.2-fold increase in osteocalcin mRNA levels (determined by reverse transcription-polymerase chain reaction). Vitamin K2 had no effect on either the stimulation of mRNA level by IGF-I or the basal level. IGF-I-stimulated osteocalcin containing Gla secretion was inhibited by one of its binding proteins (insulin-like growth factor binding protein-4) in a concentration-dependent manner. These findings suggest that the modes of action of IGF-I and vitamin K2 on 1.25(OH)2D3-induced osteocalcin containing Gla secretion in MG-63 cells are different.

Effects of insulin-like growth factor-I and insulin on the in-vitro uptake of sulphate by eel branchial cartilage: evidence for the presence of independent hepatic and pancreatic sulphation factors

1992 ◽  
Vol 133 (2) ◽  
pp. 211-219 ◽  
Author(s):  
C. Duan ◽  
T. Hirano
Keyword(s):  
Growth Factor ◽  
Coho Salmon ◽  
Bovine Insulin ◽  
Dependent Manner ◽  
Insulin Like Growth Factor ◽  
Cartilage Growth ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

ABSTRACT The possible roles of insulin-like growth factor-I (IGF-I) and insulin in regulating cartilage growth were studied in the teleost Anguilla japonica. Significant sulphation activity was found in the extracts of pancreas, liver and muscle, but not in those of kidney, intestine or spleen. The hepatic sulphation activity was significantly decreased by hypophysectomy or by fasting for 14 days, suggesting that this activity is regulated by pituitary function and nutritional status. Northern blot analysis revealed that the hepatic IGF-I mRNA in the eel consists of a major 4·0 kb band. This mRNA was GH-dependent and was significantly decreased by fasting for 14 days. On the other hand, fasting for 14 days had no significant effect on pancreatic sulphation activity. Pancreatic extracts from both intact and hypophysectomized eels exhibited equally significant stimulating activity. Addition of bovine or human insulin (1–250 ng/ml) to the culture medium significantly stimulated sulphate uptake in a dose-dependent manner. Teleost (coho salmon) insulin was as effective as bovine insulin. Bovine insulin was more effective than IGF-I at lower concentrations (1–4 ng/ml) but less effective at higher concentrations (10–250 ng/ml). These results indicate that not only IGF-I but also insulin are likely to be involved in the regulation of cartilage growth in the eel. Journal of Endocrinology (1992) 133, 211–219

scholarly journals Gq-coupled Purinergic Receptors Inhibit Insulin-like Growth Factor-I/Phosphoinositide 3-Kinase Pathway-dependent Keratinocyte Migration

2010 ◽  
Vol 21 (6) ◽  
pp. 946-955 ◽  
Author(s):  
Salma Taboubi ◽  
Françoise Garrouste ◽  
Fabrice Parat ◽  
Gilbert Pommier ◽  
Emilie Faure ◽  
...  
Keyword(s):  
Growth Factor ◽  
Purinergic Receptors ◽  
Purinergic Signaling ◽  
Extracellular Nucleotides ◽  
Dependent Manner ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Keratinocyte Migration ◽  
Igf I ◽  
Growth Factor I

Insulin-like growth factor-I (IGF-I) activation of phosphoinositol 3-kinase (PI3K) is an essential pathway for keratinocyte migration that is required for epidermis wound healing. We have previously reported that activation of Gα(q/11)-coupled-P2Y2purinergic receptors by extracellular nucleotides delays keratinocyte wound closure. Here, we report that activation of P2Y2receptors by extracellular UTP inhibits the IGF-I–induced p110α-PI3K activation. Using siRNA and pharmacological inhibitors, we demonstrate that the UTP antagonistic effects on PI3K pathway are mediated by Gα(q/11)—and not G(i/o)—independently of phospholipase Cβ. Purinergic signaling does not affect the formation of the IGF-I receptor/insulin receptor substrate-I/p85 complex, but blocks the activity of a membrane-targeted active p110α mutant, indicating that UTP acts downstream of PI3K membrane recruitment. UTP was also found to efficiently attenuate, within few minutes, the IGF-I–induced PI3K-controlled translocation of the actin-nucleating protein cortactin to the plasma membrane. This supports the UTP ability to alter later migratory events. Indeed, UTP inhibits keratinocyte spreading and migration promoted by either IGF-I or a membrane-targeted active p110α mutant, in a Gα(q/11)-dependent manner both. These findings provide new insight into the signaling cross-talk between receptor tyrosine kinase and Gα(q/11)-coupled receptors, which mediate opposite effects on p110α-PI3K activity and keratinocyte migration.

scholarly journals Circulating insulin-like growth factor I is involved in the effect of diet on peripheral amyloid β clearance

2020 ◽  
Author(s):  
Raquel Herrero-Labrador ◽  
Angel Trueba-Saiz ◽  
Laura Martinez-Rachadell ◽  
Maria Estrella Fernandez de Sevilla ◽  
Jonathan A Zegarra-Valdivia ◽  
...  
Keyword(s):  
Growth Factor ◽  
Amyloid Β ◽  
Dependent Manner ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Peripheral Clearance ◽  
Aβ Clearance ◽  
Growth Factor I ◽  
The Brain

Abstract BackgroundObesity is a risk factor for Alzheimer´s disease (AD), but underlying mechanisms are not clear.MethodsWe analyzed peripheral clearance of amyloid β (Aβ) in overweight mice because its systemic elimination may impact on brain Aβ load, a major landmark of AD pathology. We also analyzed whether circulating insulin-like growth factor I (IGF-I) intervenes in the effects of overweight as this growth factor modulates brain Aβ clearance, and is increased in serum of overweight mice. Results Overweight mice showed increased peripheral Aβ clearance by the liver, the major site of elimination of systemic Aβ, but unaltered brain Aβ levels. We also found that Aβ clearance by hepatocytes is stimulated by IGF-I, and that mice with low serum IGF-I levels show reduced peripheral Aβ clearance and unchanged brain Aβ levels. In the brain, IGF-I favored association of its receptor (IGF-IR) with Aβ precursor protein (APP), and at the same time stimulated non-amyloidogenic processing of APP in astrocytes, as indicated by an increased sAPPα/sAPPβ ratio after IGF-I treatment. Since serum IGF-I enters into the brain in an activity-dependent manner, we analyzed in overweight mice the effect of brain activation by environmental enrichment (EE) on brain IGF-IR phosphorylation and its association to APP, as a readout of IGF-I activity. After EE, significantly reduced brain IGF-IR phosphorylation and APP/IGF-IR association was found in overweight mice as compared to lean controls. Conclusions Collectively, these results indicate that diet influences peripheral clearance of Aβ without affecting brain Aβ load. Increased serum IGF-I likely contributes to enhanced peripheral Aβ clearance in overweight mice, without affecting brain Aβ clearance probably because its brain entrance is reduced.

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 Dephosphorylation of human insulin-like growth factor I (IGF-I) receptors by membrane-associated tyrosine phosphatases

1992 ◽  
Vol 285 (1) ◽  
pp. 71-78 ◽  
Author(s):  
P Peraldi ◽  
S Hauguel-de Mouzon ◽  
F Alengrin ◽  
E Van Obberghen
Keyword(s):  
Growth Factor ◽  
Tyrosine Kinase ◽  
Insulin Receptor ◽  
Dependent Manner ◽  
Insulin Like Growth Factor ◽  
Tyrosine Phosphatases ◽  
Insulin Receptor Tyrosine Kinase ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

The insulin-like growth factor-I (IGF-I) receptor exhibits structural and functional similarities to the insulin receptor. Although the regulation of the insulin-receptor tyrosine kinase has been extensively investigated, the mechanisms involved in phosphorylation/dephosphorylation of the IGF-I receptor have received only little attention. To obtain a better understanding of the mode of IGF-I action, we have investigated the effects of protein phosphotyrosine phosphatases (PTPases) on the phosphorylation status of the IGF-I receptor. The dephosphorylation of the human IGF-I receptor by membrane-associated tyrosine phosphatases was studied by an immuno-enzymic assay based on the recognition of phosphotyrosine residues by anti-phosphotyrosine antibodies. Using intact IGF-I receptors as substrates, we show that they could be completely dephosphorylated by different cellular PTPases. Three pieces of evidence indicate that receptor dephosphorylation takes place on phosphotyrosine, i.e. the inhibition profile of phosphatase activity by zinc and vanadate, its absolute requirement for thiol compounds and the diminution of [32P]phosphotyrosine labelling of the beta subunit assessed by SDS/PAGE and phosphoamino acid analysis. Tyrosine kinase activity and autophosphorylation of the IGF-I receptor were decreased in a dose-dependent manner by PTPases, indicating that partial dephosphorylation of the receptor was associated with a decrease in its intrinsic activity. The sensitivity of the activated human IGF-I receptor to dephosphorylation on tyrosine leads to the speculation that IGF-I receptor activity might be regulated by mechanisms such as those described for the insulin receptor. Further investigation of the pathways of IGF-I receptor dephosphorylation will contribute to define the role(s) of PTPases in the overall mechanism of IGF-I signalling.

scholarly journals Differentiation of rat brown adipocytes during late foetal development: role of insulin-like growth factor I

1995 ◽  
Vol 310 (3) ◽  
pp. 771-776 ◽  
Author(s):  
T Teruel ◽  
A M Valverde ◽  
A Alvarez ◽  
M Benito ◽  
M Lorenzo
Keyword(s):  
Adipose Tissue ◽  
Growth Factor ◽  
Brown Adipose Tissue ◽  
Insulin Like Growth Factor ◽  
Foetal Development ◽  
Brown Adipocytes ◽  
Factor I ◽  
Brown Adipose ◽  
Igf I ◽  
Growth Factor I

Rat brown adipocytes at day 22 of foetal development showed greater size, higher mitochondria content and larger amounts of lipids, as determined by flow cytometry, than 20-day foetal cells. Simultaneously, an inhibition on the percentage of brown adipocytes into S+G2/M phases of the cell cycle was observed between days 20 and 22 of foetal development. The expression of several adipogenesis-related genes, such as fatty acid synthase, malic enzyme, glucose-6-phosphate dehydrogenase and insulin-regulated glucose transporter, increased at the end of foetal life in brown adipose tissue. In addition, the lipogenic enzyme activities and the lipogenic flux increased during late foetal development, resulting in mature brown adipocytes showing a multilocular fat droplet phenotype. Concurrently, brown adipocytes induced the expression of the uncoupling protein (UP) mRNA and UP protein, as visualized by immunofluorescence. The three isoforms of CCAAT enhancer-binding proteins (C/EBPs) were expressed at the mRNA level in brown adipose tissue at day 20. C/EBP alpha decreased and C/EBP beta and delta increased their expression between days 20 and 22 of foetal development, respectively. Brown adipose tissue constitutively expressed insulin-like growth factor I (IGF-I) and IGF-I receptor (IGF-IR) mRNAs. Moreover, IGF-IR mRNA content increased between days 20 and 22 in parallel with the occurrence of tissue differentiation.

scholarly journals DIET INFLUENCES PERIPHERAL AMYLOID β METABOLISM: A ROLE FOR CIRCULATING INSULIN-LIKE GROWTH FACTOR I

2020 ◽  
Author(s):  
R. Herrero-Labrador ◽  
A. Trueba-Saiz ◽  
L. Martinez-Rachadell ◽  
E. Fernandez de Sevilla ◽  
S. Diaz-Pacheco ◽  
...  
Keyword(s):  
Growth Factor ◽  
Amyloid Β ◽  
Dependent Manner ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Peripheral Clearance ◽  
Aβ Clearance ◽  
Growth Factor I ◽  
The Brain

AbstractObesity is a risk factor for Alzheimer’s disease (AD), but underlying mechanisms are not clear. We analyzed peripheral clearance of amyloid β (Aβ) in overweight mice because its systemic elimination may impact on brain Aβ load, a major landmark of AD pathology. Overweight mice showed increased peripheral Aβ clearance by the liver, the major site of elimination of systemic Aβ, but unaltered brain Aβ levels. Since circulating insulin-like growth factor I (IGF-I) modulates brain Aβ clearance, and is increased in serum of overweight mice, we determined whether it affects peripheral Aβ clearance. We found that Aβ uptake by hepatocytes is stimulated by IGF-I. Moreover, mice with low serum IGF-I levels show reduced peripheral Aβ clearance. In the brain, IGF-I favored association of its receptor (IGF-IR) with Aβ precursor protein (APP), and at the same time stimulated non-amyloidogenic processing of APP in astrocytes, as indicated by an increased sAPPα/sAPPβ ratio after IGF-I treatment. Since serum IGF-I enters into the brain in an activity-dependent manner, we analyzed in overweight mice the effect of brain activation by environmental enrichment (EE) on brain IGF-IR phosphorylation and its association to APP, as a readout of IGF-I activity. After EE, significantly less activation of brain IGF-IR phosphorylation and APP/IGF-IR association was found in overweight mice as compared to lean controls. Collectively, these results indicate that diet influences peripheral clearance of Aβ without affecting brain Aβ load. Increased serum IGF-I likely contributes to enhanced peripheral Aβ clearance in overweight mice, without affecting brain Aβ clearance probably because its brain entrance is reduced.

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