Search

Purpose: To investigate the association between insulin-like growth factor 1 ( IGF1 ) single-nucleotide polymorphisms (SNPs) and myopia in a young Chinese population., Methods: A total of 654 Chinese children aged 6-13 years from one primary school participated in our study and underwent a series of comprehensive ocular examinations, including cycloplegic refraction and measurements of axial length. Myopia was defined as a spherical equivalence (SE) ≤ -0.5 D in the worse eye. In total, six tagging SNPs of IGF1 were genotyped using the PCR-LDR (Polymerase Chain Reaction-Ligation Detection Reaction) method. We tested four different genetic modes (the allele, dominant, recessive, and additive models) of these SNPs and used multivariate logistic regression to calculate the effect of SNPs on myopia. In addition, we conducted a haplotype analysis with a variable-sized slide-window strategy., Results: Overall, 281 myopic children and 373 non-myopic controls were included in the analysis. The SNP rs2162679 showed a statistical difference between the two groups in both the allele ( p = 0.0474) and additive ( p = 0.0497) models. After adjusting for age and gender, children with the genotype AA in the SNP rs2162679 had a higher risk of myopia than those with the genotype GG (OR = 2.219, 95% CI [1.218-4.039], p = 0.009). All haplotypes that varied significantly between the two groups contained the SNP rs2162679, and the four-SNP window rs5742653-rs2162679 had the lowest p value (Chi square = 5.768, p = 0.0163). However, after permutation tests, none of the associations remained statistically significant., Conclusion: The SNP rs2162679 in IGF1 was associated with myopia in a young Chinese population. The G allele in the SNP rs2162679 may protect against myopia., Competing Interests: The authors declare there are no competing interests., (©2020 Cheng et al.)

Simple Summary: Yak is always in a malnutrition condition under pure grazing in the cold season. Many studies have suggested that provision of supplementary feed to yak cannot only be an effective approach to avoid weight loss, but also improve productivity. Growth hormone (GH) and insulin-like growth factor 1 (IGF-1) could improve yak productivity. In current work, we evaluated the effects of different energy feedstuffs on the serum concentration of GH, IGF-1, and relative hepatic expression of their associated binding proteins and receptors, as well as growth performance of yak. The results indicated that average daily gain (ADG), body weight (BW), feed conversion ratio, serum IGF-1 concentration, and relative expression of IGF-1 and IGFBP-3 were increased with an increase in dietary energy level, while serum GH concentration and hepatic growth hormone (GHR) expression were decreased. Serum IGF-1 concentration, relative hepatic expression of IGF-1, and insulin-like growth factor binding protein 3 (IGFBP-3) showed positive correlation with ADG, but serum GH concentration and GHR expression were negatively correlated with ADG. Yak offered with medium energy diet (NEg: 6.2 MJ/kg) displayed better growth by gaining 0.883 kg/d and showing a superior feed conversion ratio during experiment. The objective of this study was to investigate the effects of different dietary energy levels on serum concentrations of growth hormone (GH) and insulin-like growth factor 1 (IGF-1), as well as gene expression of their associated binding proteins and receptors in yak. Fifteen adult male yaks with BW of 276.1 ± 3.5 kg were allotted in three dietary groups and were fed with low (LE), medium (ME), and high energy (HE) level diet having different NEg of 5.5 MJ/kg, 6.2 MJ/kg, 6.9 MJ/kg, respectively. The effects of these treatments on ADG, BW, ADFI, and feed conversion ratio were significant (p < 0.05) throughout the experimental period. Serum GH concentration decreased (p < 0.05) with an increase in dietary energy level on d 30 and d 60. While IGF-1 concentration was higher (p < 0.05) in ME group, as compared to LE and HE groups on d 60. The expression level of growth hormone receptor (GHR) was decreased (p < 0.001) and IGF-1 was increased with the increase in the dietary energy level. The relative expression of insulin-like growth factor binding protein 3 (IGFBP-3) was higher (p < 0.001) in ME and HE groups, except the LE group. In conclusion, our findings provide a first insight into the combined effect of GH and IGF-1 in controlling the metabolism and productivity of yak. It also showed that medium energy level diet contributed to promote growth performance of yak during the cold season. [ABSTRACT FROM AUTHOR]

The insulin-like growth factor (IGF) system, which is constituted by the IGF-1 and IGF-2 peptide hormones, their corresponding receptors and several IGF binding proteins, is involved in physiological and pathophysiological processes. The IGF system promotes cancer proliferation/survival and its signaling induces the epithelial-mesenchymal transition (EMT) phenotype, which contributes to the migration, invasiveness, and metastasis of epithelial tumors. These cancers share two major IGF-1R signaling transduction pathways, PI3K/AKT and RAS/MEK/ERK. However, as far as we could review at this time, each type of cancer cell undergoes EMT through tumor-specific routes. Here, we review the tumor-specific molecular signatures of IGF-1-mediated EMT in breast, lung, and gastric cancers. [ABSTRACT FROM AUTHOR]

Anabolic androgenic steroids (AAS) are some of the most common drugs used among athletes, frequently in combination with resistance training, to improve physical performance or for aesthetic purpose. A great number of scientific reports showed the detrimental effects of anabolic androgenic steroids on different organs and tissues. In this literature review, we analyzed the AAS-mediated carcinogenicity, focusing on Leydig cell tumor. AAS-induced carcinogenicity can affect DNA transcription through two pathways. It can act directly via the androgen receptor, by means of dihydrotestosterone (DHT) produced by the action of 5-a-reductase. It can also work through the estrogen receptor, by means of estradiol produced by CYP19 aromatase. In addition, nandrolone and stanazolol can activate the PI3K/AKT and PLC/PKC pathways via IGF-1 . This would result in cell proliferation in Leydig cell cancer, or magnify cyclin D1 concentration inducing breast cell proliferation. AAS abuse is becoming a serious public health concern in view of the severe health consequences secondary to AAS abuse. The negative role of AAS in supraphysiological dosage impairs the expression of enzymes involved in testosterone biosynthesis. Abnormal synthesis of testosterone plays has a negative effect on the hormonal changes/regulation, and might be involved in certain carcinogenic mechanisms. At the light of this review, it could become very interesting to perform an information campaign more strengthened in gyms and schools in order to prevent male fertility impairment and other tissues damage., Competing Interests: CONFLICTS OF INTEREST The authors declare that there are no conflict of interests, financial or otherwise, regarding the publication of this paper.

Stem cell treatment for critical limb ischemia yields a limited therapeutic effect due to cell loss and dysfunction caused by local ischemic environment. Biomimetic scaffolds emerge as ideal cell delivery vehicles for regulating cell fate via mimicking the components of stem cell niche. Herein, we prepared a bioactive hydrogel by mixing chitosan and hyaluronic acid that is immobilized with C domain peptide of insulin-like growth factor 1 (IGF-1C) and examined whether this hydrogel could augment stem cell survival and therapeutic potential. Our results showed that IGF-1C-modified hydrogel increased in vitro viability and proangiogenic activity of adipose-derived stromal cells (ADSCs). Moreover, cotransplantation of hydrogel and ADSCs into ischemic hind limbs of mice effectively ameliorated blood perfusion and muscle regeneration, leading to superior limb salvage. These therapeutic effects can be ascribed to improved ADSC retention, angiopoientin-1 secretion, and neovascularization, as well as reduced inflammatory cell infiltration. Additionally, hydrogel enhanced antifibrotic activity of ADSCs, as evidenced by decreased collagen accumulation at late stage. Together, our findings indicate that composite hydrogel modified by IGF-1C could promote survival and proangiogenic capacity of ADSCs and thereby represents a feasible option for cell-based treatment for critical limb ischemia.

Background: Metformin is widely used for management of Type 2 Diabetes Mellitus (T2DM). Recently growing evidences have shown its anti-cancer effects. The results are mainly from observational studies and thus few information is available concerning the mechanisms of action., Method: This paper reviews recent available evidences for anti-cancer effects of metformin. The effects of metformin in specific cancers including colorectal, prostate, pancreatic, renal, cervical, endometrial, gastric, lung, breast, and ovarian cancer are reviewed., Results: Adenosine Monophosphate (AMP)-Activated Protein Kinase (AMPK) plays an important role in mechanism of action of metformin. The anti-cancer mechanisms of metformin include direct and indirect effects. The direct effects of metformin include AMPK-independent and AMPK-dependent effects whereas decrease in glucose level, hyperinsulinemia, and Insulin-like Growth Factor 1 (IGF-1) level are considered its indirect effects. Metformin also decreases both pro-inflammatory cytokines and Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF- κB) and improves the immune response to cancer cells., Conclusion: Although the results of recent trials confirm the efficacy of metformin in prevention and treatment of different cancers, the evidences are not adequate enough., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

Previous studies have shown that insulin-like growth factor 1 (IGF-1) may be responsible for the higher risk for developing endometrial carcinoma (EMC) in insulin-resistant type 2 diabetes mellitus (T2DM) patients. However, the underlying mechanisms are not understood. Here, we compared T2DM patients with or without EMC. We did not find difference in the serum levels of IGF-1, insulin-like growth factor 2 (IGF-2), IGF-1 binding protein 3, as well as the activation of IGF-1 receptor (IGF1R) in endometrial cells between T2DM patients with or without EMC. However, the levels of IGF2R activation and activation of PI3k, an IGF1R downstream factor, were significantly higher in endometrial cells in T2DM patients with EMC. In vitro analyses of activation of IGF1R, IGF2R, PI3k and CCND1 in EMC cells or IGF2R-overexpressing EMC cells by IGF-1 or IGF-2 suggest that increases in IGF2R in endometrial cells in T2DM may increase PI3k/CCND1-dependent cell growth through loss of competitive binding of IGF-2 to IGF1R, as a possible explanation for the higher risk for developing EMC in T2DM.

Accurate measurement of height and weight using standardized techniques is a fundamental component of pediatric medical visits. Calculation of height velocity over time enables comparison with standardized growth charts to identify potential deviations from normal. Growth deviations may be expressed as SD from the normal population mean for children of comparable age and sex; children with heights >2 SD below the mean are generally classified as short stature. In a child with suspected impaired growth, a detailed evaluation should be conducted to identify the cause. Such an evaluation may include a combination of personal, family, and social history; physical examination; general and perhaps specialized laboratory evaluations; radiologic examinations; genetic testing; and consultation with a pediatric subspecialist, such as a pediatric endocrinologist. Variants of normal growth include familial short stature, constitutional delay of growth and puberty, and small for gestational age with catch-up growth. Pathological causes of abnormal growth include many systemic diseases and their treatments, growth hormone deficiency, and a series of genetic syndromes, including Noonan syndrome and Turner syndrome. Children with short stature in whom no specific cause is identified may be diagnosed with idiopathic short stature. Early identification of abnormal growth patterns and prompt referral to specialist care offer children with growth failure and/or short stature the greatest chance for appropriate diagnosis, treatment, and improved clinical outcomes. [Copyright &y& Elsevier]

Background: Recent evidence suggests a role for the insulin-like growth factor-1Ec (IGF-IEc) transcript variant in cancer biology. The aim of the present study was to investigate whether IGF-IEc expression is associated with prostate cancer stage., Materials and Methods: Formalin-fixed and paraffin-embedded prostate cancer surgical specimens from 83 patients were assessed by immunohistochemistry for IGF-IEc expression., Results: Normal prostate epithelium was negative or demonstrated mild IGF-IEc cytoplasmic expression whereas prostate cancer exhibited mild to strong cytoplasmic immunoexpression. The mean IGF-1Ec expression, was significantly lower (p=0.004) in localized (stage ≤ IIb) prostate cancer, compared to locally advanced tumors (stage ≥ III). Only one out of 83 (1.2%) prostate cancer samples was completely negative for IGF-IEc. A weak-positive correlation was also observed between IGF-IEc expression levels and Gleason score (r=0.247; p=0.024)., Conclusion: The present data demonstrate that the expression of IGF-IEc is positively-associated with more advanced stage and higher Gleason score of prostate carcinomas.

The Insulin-like Growth Factor 1 (IGF-1) signaling pathway activates several downstream signals important to lung cancer development and survival. IGF-1R activation has been linked to cancer risk in epidemiological studies and tumorigenesis in preclinical models. Several inhibitors of the insulin-like growth factor 1 receptor (IGF-1R) have been tested in clinical trials. Despite promising data in early phase studies, most studies of IGF-1R antagonists in combination with chemotherapy or with epidermal growth factor receptor (EGFR) inhibitors in non-small cell lung cancer (NSCLC) yielded disappointing results. Biomarker studies of clinical trials have identified IGF-1 levels as a potential marker of sensitivity to IGF-1R inhibition. Further study will need to focus on selection of NSCLC patients most likely to benefit from the addition of IGF-1R antagonists to standard therapy and the development of rational strategies for combination therapy in NSCLC.