Objective: To explore the effect of insulin-like growth factor-I (IGF-I), insulin-like growth factor-II (IGF-II) and insulin-like growth factor-binding protein-3 (IGFBP-3) on the fetal growth.
Methods: Samples of maternal blood and matched umbilical cord blood were collected at time of delivery from twenty pairs of mothers and newborns with normal birth weight (control group) twenty pairs with fetal growth restriction (FGR group) and ten pairs with macrosomia (macrosomia group). Serum IGF-I, IGF-II and IGFBP-3 were measured by radioimmunoassay (RIA) and immunoradiometric analysis (IRMA).
Results: (1) Levels of maternal serum IGF-I, IGF-II and IGFBP-3 in GFR group were (130.5 +/- 26.0) microgram/L, (2.40 +/- 0.42) microgram/L, (5 579 +/- 848) microgram/L respectively; IGF-I, IGF-II and IGFBP-3 levels of fetal serum in this group were (6.6 +/- 1.7) microgram/L, (1.54 +/- 0.31) microgram/L, (869 +/- 183) microgram/L respectively. (2) In macrosomia group the levels of maternal serum IGF-I, IGF-II and IGFBP-3 were (309.7 +/- 44.6) microgram/L, (2.43 +/- 0.25) microgram/L, (5 562 +/- 742) microgram/L respectively. In fetal serum that were (69.6 +/- 23.9) microgram/L, (2.19 +/- 0.29) microgram/L, (1 682 +/- 130) microgram/L respectively. (3) In control group the levels of maternal serum IGF-I, IGF-II and IGFBP-3 were (307.9 +/- 70.7) microgram/L, (2.41 +/- 0.36) microgram/L, (5 586 +/- 678) microgram/L respectively;That were (68.9 +/- 32.9) microgram/L, (1.95 +/- 0.26) microgram/L, (1 624 +/- 296) microgram/L in fetal serum respectively. (4) In three group the levels of maternal IGF-I, IGF-II and IGFBP-3 were significantly higher than that of fetal levels (P < 0.01). The fetal IGF-I, IGF-II and IGFBP-3 levels in FGR group were significantly lower than those in control group (P < 0.01). (5) The levels of fetal IGF-I, IGF-II, IGFBP-3 were positively correlated with birth weight (r = 0.61, r = 0.51 and 0.63, P < 0.01) and placental weight (r = 0.47, r = 0.56 and 0.48, P < 0.01). The levels of fetal IGF-I, IGF-II and IGFBP-3 were no different between macrosomia group and control group.
Conclusions: This study suggest that (1) IGF-I, IGF-II and IGFBP-3 cannot pass through the placenta. (2) The betal IGF-I, IGF-II and IGFBP-3 may have the close relationship with the fetal growth. The decrease of IGF-I, IGF-II and IGFBP-3 may be one of the causes of FGR.
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J Clin Endocrinol Metab
December 2024
Department of Endocrinology, Metabolism and Nephrology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Context: In most cases of non-islet cell tumor hypoglycemia (NICTH), high molecular weight forms of insulin-like growth factor II, commonly referred to as big IGF-II, cause hypoglycemia. MicroRNA-483 (miR-483), encoded within an intron of IGF2 gene, has been suggested to be co-expressed with IGF-II.
Objective: The aim of this study is to demonstrate the utility and reliability of circulating miR-483 as a biomarker for diagnosis and therapeutic outcome of NICTH.
Clin Endocrinol (Oxf)
February 2025
Department of Pediatric Endocrinology and Genetics, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Mol Med
November 2024
URT "Genomic of Diabetes", Institute for Experimental Endocrinology and Oncology "G. Salvatore", National Research Council (IEOS-CNR), Via Pansini 5, 80131, Naples, Italy.
The adipose tissue (AT) surrounding breast cancer (BC) plays a pivotal role in cancer progression and represents an optimal source for new biomarker discovery. The aim of this work was to investigate whether specific AT factors may have prognostic value in estrogen receptor-positive (ER+) BC. Proteoglycan Versican (VCAN), Insulin-like Growth Factor 1 (IGF1), Reticulon 4B (RTN4), chemokines CCL5 (also known as RANTES) and interleukin 8 (IL-8) are expressed in AT and may play important roles in BC progression.
View Article and Find Full Text PDFInt Immunopharmacol
December 2024
Cancer Center, Renmin Hospital of Wuhan University, Wuhan, Hubei, China. Electronic address:
IGFALS forms stable ternary complexes with insulin-like growth factors (IGF1 and IGF2) and IGF-binding proteins (IGFBP3 and IGFBP5), which prolong the half-lives of IGFs. Through immunohistochemical analysis of 90 pairs of clinical samples and bioinformatics analysis, we observed downregulation of IGFALS in hepatocellular carcinoma tissues, which was associated with poor patient prognosis. This prompted us to explore the specific molecular mechanism of action of IGFALS in the inhibition of hepatocellular carcinoma (HCC), which could be a potential new target for the treatment of HCC.
View Article and Find Full Text PDFMediterr J Rheumatol
September 2024
Rheumatology Department, KAT General Hospital, Attica, Greece.
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