Relationship between Insulin-Like Growth Factor Type 1 and Intrauterine Growth

Banjac, Lidija; Kotur‐Stevuljević, Jelena; Gojković, Tamara; Bokan-Mirković, Vesna; Banjac, Goran; Banjac, Gorica

doi:10.20471/acc.2020.59.01.11

Cited by 7 publications

(9 citation statements)

References 21 publications

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“…Rapid uptake of AFB1 in rat and dog prostate [548] Commercial milk is contaminated with aflatoxins; AFM1 levels rise in maize-fed cows [537- Major mineral of milk; questionable influence of dairy calcium on the prostate as circulatory calcium levels are maintained within close limits [116] derived IGF-1, constituting a major part of circulating IGF-1, is an important endocrine factor involved in a variety of physiological and pathological processes [567] . Notably, locally derived IGF-1 cannot replace liver-derived IGF-1 for the regulation of a large number of other parameters including GH secretion, cortical bone mass, and prostate size [567] .…”

Section: Fetal Prostate Growthmentioning

confidence: 99%

The endocrine and epigenetic impact of persistent cow milk consumption on prostate carcinogenesis

Melnik¹,

John²,

Weiskirchen³

et al. 2022

jtgg

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This review analyzes the potential impact of milk-induced signal transduction on the pathogenesis of prostate cancer (PCa). Articles in PubMed until November 2021 reporting on milk intake and PCa were reviewed. Epidemiological studies identified commercial cow milk consumption as a potential risk factor of PCa. The potential impact of cow milk consumption on the pathogenesis of PCa may already begin during fetal and pubertal prostate growth, critical windows with increased vulnerability. Milk is a promotor of growth and anabolism via activating insulin-like growth factor-1 (IGF-1)/phosphatidylinositol-3 kinase (PI3K)/AKT/mechanistic target of rapamycin complex 1 (mTORC1) signaling. Estrogens, major steroid hormone components of commercial milk of persistently pregnant dairy cows, activate IGF-1 and mTORC1. Milk-derived signaling synergizes with common driver mutations of the PI3K/AKT/mTORC1 signaling pathway that intersect with androgen receptor, MFG-E8, MAPK, RUNX2, MDM4, TP53, and WNT signaling, respectively. Potential exogenously induced drivers of PCa are milk-induced elevations of growth hormone, IGF-1, MFG-E8, estrogens, phytanic acid, and aflatoxins, as well as milk exosome-derived oncogenic microRNAs including miR-148a, miR-21, and miR-29b. Commercial cow milk intake, especially the consumption of pasteurized milk, which represents the closest replica of native milk, activates PI3K-AKT-mTORC1 signaling via cow milk’s endocrine and epigenetic modes of action. Vulnerable periods for adverse nutrigenomic impacts on prostate health appear to be the fetal and pubertal growth periods, potentially priming the initiation of PCa. Cow milk-mediated overactivation of PI3K-AKT-mTORC1 signaling synergizes with the most common genetic deviations in PCa, promoting PCa initiation, progression, and early recurrence.

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Section: Fetal Prostate Growthmentioning

confidence: 99%

The endocrine and epigenetic impact of persistent cow milk consumption on prostate carcinogenesis

Melnik¹,

John²,

Weiskirchen³

et al. 2022

jtgg

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“…Single nucleotide polymorphisms rs2234693-rs9340799 ESR1 variants MTHFR 677C > T variant [74,75] [ [76][77][78][79] Genetic causes of preeclampsia IGF-1-insulin growth factor 1; IGF-2-insulin growth factor 2; IGFBP-3-IGF-binding protein 3; IGF1R-insulinlike growth factor receptor type 1; ET-1-endothelin 1; TNFα-tumor necrosis factor α; ESR1-estrogen receptor α; MTHFR-methylenetetrahydrofolate reductase.…”

Section: Fetal Chromosomal Aberrationsmentioning

confidence: 99%

“…During pregnancy, estrogen stimulates i.a. the activation of IGF-1 receptor, promoting fetal growth and response to different signals, such as hypoxia, hormones and nutrients [ 63 , 75 ]. Although in the last few years a lot of studies have been published concerning the potential association of methylenetetrahydrofolate reductase (MTHFR) 677C > T polymorphism with the risk of FGR and placental abruption, they didn’t bring enough evidence to support introducing MTHFR genetic testing into routine clinical practice [ 76 , 77 , 78 ].…”

Section: Maternal Fgr Causesmentioning

confidence: 99%

Genetic Background of Fetal Growth Restriction

Nowakowska¹,

Pankiewicz²,

Nowacka³

et al. 2021

IJMS

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Fetal growth restriction (FGR) is one of the most formidable challenges in present-day antenatal care. Pathological fetal growth is a well-known factor of not only in utero demise in the third trimester, but also postnatal morbidity and unfavorable developmental outcomes, including long-term sequalae such as metabolic diseases, diabetic mellitus or hypertension. In this review, the authors present the current state of knowledge about the genetic disturbances responsible for FGR diagnosis, divided into fetal, placental and maternal causes (including preeclampsia), as well as their impact on prenatal diagnostics, with particular attention on chromosomal microarray (CMA) and noninvasive prenatal testing technique (NIPT).

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“…Hyperoxia can interfere with the binding of IGF-1 and its receptor, IGF-1R, affect the development of lung tissues, and subsequently hamper the normal alveolar and microvascular development, causing pathological changes similar to those seen in BPD ( 22 , 24 ). In addition, studies have shown that the serum levels of IGF-1 are associated with the risk of developing BPD ( 25 , 26 ). These studies have highlighted that IGF-1 could be used as a novel anti-BPD therapeutic target.…”

Section: Introductionmentioning

confidence: 99%

Insulin‑like growth factor‑1: A potential target for bronchopulmonary dysplasia treatment (Review)

Zhang

Xue

et al. 2022

Exp Ther Med

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Bronchopulmonary dysplasia (BPD) is a common respiratory disorder among preterm infants, particularly low-birth-weight infants (LBWIs) and very-low-birth-weight infants (VLBWIs). Although BPD was first reported 50 years ago, no specific drugs or efficient measures are yet available for prevention or treatment. Insulin-like growth factor-1 (IGF-1) belongs to the insulin family. It promotes mitosis and stimulates cell proliferation and DNA synthesis, the primary factors involved in pulmonary development during the fetal and postnatal periods. Several studies have reported that IGF-1 exerts certain effects on BPD genesis and progression by regulating BPD-related biological processes. In addition, exogenous addition of IGF-1 can alleviate lung inflammation, cell apoptosis and eliminate alveolar development disorders in children with BPD. These findings suggest that IGF-1 could be a new target for treating BPD. Here, we summarize and analyze the definition, pathogenesis, and research status of BPD, as well as the pathogenesis of IGF-1 in BPD and the latest findings in related biological processes. Contents 1. Introduction 2. Definition and naming of BPD 3. Pathogenesis and current situation of BPD 4. Biological characteristics and activity of IGF-1 5. IGF-1 in lung development 6. IGF-1 and lung injury 7. Possible underlying mechanisms of IGF-1 in BPD development 8. IGF-1 as a new option for BPD treatment 9. Challenges and prospects of IGF-1 10. Conclusion

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Relationship between Insulin-Like Growth Factor Type 1 and Intrauterine Growth

Cited by 7 publications

References 21 publications

The endocrine and epigenetic impact of persistent cow milk consumption on prostate carcinogenesis

The endocrine and epigenetic impact of persistent cow milk consumption on prostate carcinogenesis

Genetic Background of Fetal Growth Restriction

Insulin‑like growth factor‑1: A potential target for bronchopulmonary dysplasia treatment (Review)

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