• 한국수정란이식학회:학술대회논문집
• /
• 한국수정란이식학회 2002년도 국제심포지엄
• /
• pp.34-36
• /
• 2002

Epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I) have been shown to stimulate proliferation and differentiation of various somatic cells, including placental trophoblasts and also to enhance fetal growth and development when maternally administered. Since an increase of the expression of placental EGF and IGF-I receptors in rat, mouse, and human with the gestation advanced, both EGF and IGF-I were considered to play pivotal roles on fetal growth by regulating some function of placental cells. Amino acids are crucial importance for both maternal and fetal requirements of energy source and essential constituent of fetal mass during pregnancy. Impaired fetal and placental uptake of amino acids has been observed in several models of growth retardation in the rat. Amino acid is concentrated in the fetal side through active transport by amino acid transporters and is one of the important metabolic fuels for the fatal growth. Therefore, at first plasma amino acid concentrations in mothers and fetuses were measured as an index of uphill transport across the placenta associated with EGF and IGF-1. The EGF administration at the concentration of 0, 0.1, or 0.2 $\mu\textrm{g}$/g to pregnant rats from day 18 to 21 of gestation apparently increased fetal/maternal ratio of serum proline concentration and also fatal growth in EGF dose-dependent manner. When IGF-I in doses of 0, 1, 2, and 4 $\mu\textrm{g}$/g were administrated, the ratio of leucine, isoleucine, tryptophan, phenylalanine, tyrosine and also fetal growth significantly increased with a dose-dependent manner. These results suggested that EGF and IGF-I enhanced fatal growth by, as one of its possible mechanisms, promoting placental activity to transfer some amino acid supplies from the mother to the fetus in late pregnancy.

• 대한생식의학회:학술대회논문집
• /
• 대한불임학회 1995년도 추계 학술대회 및 정기총회
• /
• pp.70.1-70.1
• /
• 1995

• 한국가축번식학회지
• /
• 제23권4호
• /
• pp.323-331
• /
• 1999

본 연구는 돼지난자의 체외성숙동안 insulin-like growth factor-I (IGF-I)과 난구세포의 영향을 검토하기 위하여 실시하였다. 미성숙난자를 0(60%), 1(61%), 5(62%) 및 l0ng/$m\ell$(72%)의 서로 다른 IGF-I의 농도로 첨가하여 배양했을 때 체외성숙율은 큰 차이를 나타내지 않았다. 또한 10ng/$m\ell$의 IGF-I이 첨가된 배양액내에서 난자를 배양한 경우, 난구세포부착시 (68%) 제거 (52%)된 난자에 비해 높은성숙율을 나타냈지만 유의적인 차이는 인정되지 않았다. 그러나 IGF-I이 첨가되지 않은 경우에는 난구세포 부착 (63%) 난자가 제거 (32%)된 난자에 비해 유의적 (P＜0.05)으로 높은 성숙율을 나타냈으며, IGF-I를 성숙 배양기간중 전반기 24시간 또는 후반기 24시간 동안만 첨가했을 때의 난구세포 부착시 (61과 49%) 제거된 (45 와 49%) 난자에 비해 높은 성숙융올 나타냈다. 한편, IGF-I의 존재 여부에 관계없이 FCS와 돼지난포액 (PFF)이 무첨가된 배양액에서 48시간동안 또는 배양전반기 24시간동안 난구세포를 제거한 경우 (16과 18%)로 난구세포 부착시 (46과 63%)에 비해 유의적 (P＜0.01)으로 낮은 성숙율을 나타냈다. 이와 같은 결과는 난구세포가 IGF-I의 존재 유무에 관계없이 난자의 체외성숙에 필수적이며, FCS와 PFF 첨가시 난구세포가 제거된 난자의 체외성숙을 촉진하는 것으로 밝혀졌다.

• Animal Bioscience
• /
• 제34권12호
• /
• pp.1886-1894
• /
• 2021

Objective: Growth hormone (GH) and insulin-like growth factor I (IGF-I) play a critical role in animal growth rates. We aimed to investigate the effect of GH and IGF-I genotypes on body weight (BW), dominance, and gene expression in slow-growing chickens at different ages. Methods: A total of 613 Korat chickens (KRs) were bred and divided into three groups by genotype - A1A1, A1A3, and A3A3 for GH and AA, AC, and CC for IGF-I. Chickens were weighed every two weeks, and liver and breast muscle tissues were collected at 10 weeks of age. Genetic parameters of KRs were estimated using ASReml software. The GH and IGF-I mRNA levels were measured by quantitative polymerase chain reaction. Significant differences between traits were analyzed using the generalized linear model. Results: A significant effect of GH genotypes on BW was found at most ages, and the A1A1 genotype had the highest value of BW. Compared with the A3A3 genotype, the A1A1 and A1A3 genotypes showed a higher dominance effect at 0 and 2 weeks, and genotype A1A1 had the highest value of dominance at 8 weeks of age. A difference in GH mRNA levels between genotypes was detected in breast muscle at 6 weeks and in the liver tissue at 2 weeks. In the case of IGF-I gene, the AA genotype had the highest BW at the beginning of life. Significant differences in BW dominance were found at 2 weeks. However, IGF-I mRNA levels were not different among genotypes in both breast muscles and liver tissues. Conclusion: Our results revealed that GH and IGF-I influence growth, but may not be involved in heterosis. GH can be used as a marker gene in selection programs for growth because the homozygous genotype (A1A1) had the highest BW at all ages. The IGF-I is not a useful marker gene for selection programs.

• Tuberculosis and Respiratory Diseases
• /
• 제48권3호
• /
• pp.324-330
• /
• 2000

연구배경 : IGFs는 다양한 종양세포에서 세포분열 및 성장에 관여하는 것으로 알려진 펩티드로써 폐암 조직에서 IGF-1에 대한 항체를 이용하여 면역조직화학염색을 실시하여 폐암세포에서 이의 발현 및 조직학적 형태에 따라 발현의 정도를 비교해 보고자 하였다. 방 법 : 15명의 소세포성 폐암 환자와 42명의 비소세포성 폐암 환자를 대상으로 IGF-1에 대한 면역조직화학적 염색을 실시하였다. 결 과 : 모든 폐암 조직애서 IGF-1의 발현을 보였고 비소세포성 폐암조직은 소세포성 폐암조직보다 IGF-1에 대한 발현의 정도가 유의하게 증가되어 있었다. 결 론 : 폐암세포는 IGF-1의 발현을 보이며 이에 대한 면역조직화학염색은 폐암세포의 조직학적 형태를 감별하는데 도움을 줄 수 있다.

• 한국식품영양학회지
• /
• 제34권6호
• /
• pp.568-575
• /
• 2021

The purpose of this study was to investigate the effects of extract mixture of C. wilfordii and P. umbrosa (IPLUS-CWPU) on bone growth in 4-week old young male SD rats. To confirm the effect of IPLUS-CWPU, we measured the length of bone growth plate, the ratio of proliferative zone to the length of growth plate and the expression level of insulin-like growth factor, IGF-1. The IPLUS-CWPU treatment shows a significant increase of tibial and femoral growth plate and the ratio of proliferative zone in growth plate. Especially, the length increased by 13.9% and 25.3% in the tibia and femur, respectively, in the high-dose group compared to the normal group. Moreover, the expression of IGF-1 gene in liver was upregulated in IPLUS-CWPU treated groups. These results indicated that IPLUS-CWPU administration could increase the proliferative zone of bone growth plate in early developmental stage by upregulation of IGF-1 gene.

• Molecules and Cells
• /
• 제28권6호
• /
• pp.589-593
• /
• 2009

In this study, the roles of the p38 MAPK, ERK1/2 and JNK signaling pathway in IGF-I-induced AR induction and activation were examined. C2C12 cells were treated with IGF-I in the absence or presence of various inhibitors of p38 MAPK (SB203580), ERK1/2 (PD98059), and JNK (SP600125). Inhibition of the MAPK pathway with SB203580, PD98059, or SP600125 significantly decreased IGF-I-induced AR phosphorylation and total AR protein expression. IGF-I-induced nuclear fraction of total AR and phosphorylated AR were significantly inhibited by SB203580, PD98059, or SP600125. Furthermore, IGF-I-induced AR mRNA and skeletal ${\alpha}-actin$ mRNA were blocked by those inhibitors in dose-dependent manner. Confocal images showed that IGF-I-induced AR nuclear translocation from cytosol was significantly blocked by SB203580, PD98059, or SP600125, suggesting that the MAPK pathway regulates IGF-I-induced AR nuclear localization in skeletal muscle cells. The present results suggest that the MAPK pathways are required for the ligand-independent activation of AR by IGF-I in C2C12 skeletal muscle cells.

• Journal of Microbiology and Biotechnology
• /
• 제9권1호
• /
• pp.113-118
• /
• 1999

The insulin-like growth factor (IGF) is found in all vertebrates and its type-II molecule is regarded as a fundamental embryonic growth factor during development. We have firstly identified, in this study, a cDNA clone corresponding to IGF-II (flIGF-II) from the adult brain of the teleost, Paralichthys olivaceus. We also examined the tissue expression of flIGF-II in several adult tissues by RT-PCR. The flIGF-II cDNA contained a complete ORF consisting of 215 amino acids and one stop codon. Its molecular characteristics appear to be similar to the previously identified IGF-II molecules, in which a common primary structure exhibiting B, C, A, D, and E domains is evidently observed. This cDNA clone seems to be cleaved at $Ala_{52}$ for the $NH_2$-end signal peptide and appears to produce a 98 amino acid-long E-peptide from the $Arg^{118}$. The functional B-D domain regions, therefore, include 65 amino acids and is able to encode a 7.4-kDa protein. The most prominent structural difference between IGF-I and IGF-II was that the D domain of IGF-II exhibits a two-codon-deleted pattern compared to the 8 amino acid-containing IGF-I. The insulin family signature in the A domain and six cysteins forming three disulfide bridges between the B and A domains were evolutionary-conserved from teleosts to mammalian IGF-II. Interestingly, the E-peptide region appears to provide a distinct hallmark between teleosts in amino acid composition. The flIGF-II shows 85.1% of sequence identity to salmon and trout, 90.6% to tilapia, and 98.4% to perch in amino acid level. In tissue expressions of IGF-II, it is very likely that flIGF-II has a significant expression in the adult brain. However, liver seems to be the main source for IGF-II production, and relatively low signals were observed in the adult muscle and kidney. Taken together, it would be concluded that the functional region for IGF-II mRNA is highly similar in phylogeny and is evolutionary, conserved as a mediator for the growth of vertebrates.

• The Korean Journal of Physiology and Pharmacology
• /
• 제20권6호
• /
• pp.613-619
• /
• 2016

Diabetic cardiomyopathy (DCM), a serious complication of diabetes mellitus, is associated with changes in myocardial structure and function. This study sought to explore the ability of insulin-like growth factor-1 (IGF-1) to modulate DCM and its related mechanisms. Twenty-four male Wistar rats were injected with streptozotocin (STZ, 60 mg/kg) to mimic diabetes mellitus. Myocardial fibrosis and apoptosis were evaluated by histopathologic analyses, and relevant proteins were analyzed by Western blotting. Inflammatory factors were assessed by ELISA. Markers of oxidative stress were tested by colorimetric analysis. Rats with DCM displayed decreased body weight, metabolic abnormalities, elevated apoptosis (as assessed by the bcl-2/bax ratio and TUNEL assays), increased fibrosis, increased markers of oxidative stress (MDA and SOD) and inflammatory factors (TNF-${\alpha}$ and IL-$1{\beta}$), and decreased phosphorylation of Akt and glycogen synthase kinase (GSK-$3{\beta}$). IGF-1 treatment, however, attenuated the metabolic abnormalities and myocardial apoptosis, interstitial fibrosis, oxidative stress and inflammation seen in diabetic rats, while also increasing the phosphorylation levels of Akt and GSK-$3{\beta}$. These findings suggest that IGF-1 ameliorates the pathophysiological progress of DCM along with an activation of the Akt/GSK-$3{\beta}$ signaling pathway. Our findings suggest that IGF-1 could be a potential therapeutic choice for controlling DCM.

• The Korean Journal of Physiology and Pharmacology
• /
• 제17권2호
• /
• pp.157-162
• /
• 2013

Insulin-like growth factor binding proteins (IGFBPs) are important components of insulin growth factor (IGF) signaling pathways. One of the binding proteins, IGFBP-5, enhances the actions of IGF-1, which include the enhanced proliferation of smooth muscle cells. In the present study, we examined the expression and the biological effects of IGFBP-5 in vascular smooth muscle cells (VSMCs) from spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). The levels of IGFBP-5 mRNA and protein were found to be higher in the VSMC from SHR than in those from WKY. Treatment with recombinant IGFBP-5-stimulated VSMC proliferation in WKY to the levels observed in SHR. In the VSMCs of WKY, incubation with angiotensin (Ang) II or IGF-1 dose dependently increased IGFBP-5 protein levels. Transfection with IGFBP-5 siRNA reduced VSMC proliferation in SHR to the levels exhibited in WKY. In addition, recombinant IGFBP-5 significantly up-regulated ERK1/2 phosphorylation in the VSMCs of WKY as much as those of SHR. Concurrent treatment with the MEK1/2 inhibitors, PD98059 or U0126 completely inhibited recombinant IGFBP-5-induced VSMC proliferation in WKY, while concurrent treatment with the phosphatidylinositol-3 kinase inhibitor, LY294002, had no effect. Furthermore, knockdown with IGFBP-5 siRNA inhibited ERK1/2 phosphorylation in VSMC of SHR. These results suggest that IGFBP-5 plays a role in the regulation of VSMC proliferation via ERK1/2 MAPK signaling in hypertensive rats.