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Organ Cross-Talk Regulates (Brain) Insulin Action
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Insulin-like growth factors were discovered in 1957 when Salmon and Daughaday began studying the effect of biological substances to stimulate cartilage sulfation in vitro (151). IGFs are hormones similar to insulin with regard to molecular structure and functionality and increase insulin sensitivity. IGFs play a pivotal role in growth and development in an autocrine, paracrine and endocrine manner. The two main IGFs, IGF1 and IGF2, are evolutionarily conserved peptide hormones with structural homology to proinsulin (152). The three ligands IGF1, IGF2, and insulin bind with different affinities to four types of receptors; the IGF1-R, the IGF2-R, the hybrid receptor, and the insulin receptor (153). Finally, the binding of the ligand to the receptor elicits a phosphorylation of intracellular adaptor proteins and activation of the MAPK and PI3K/AKT signaling pathways, which leads to GLUT4 translocation from an intracellular compartment to the plasma membrane, enhancing glucose uptake (153, 154). In comparison to insulin, IGFs are about 90% less potent to stimulate glucose transport and induce hypoglycemia in vitro and in vivo, respectively, but are about 100 times higher concentrated (155, 156). Furthermore, IGFs are regulated by a family of seven IGF-binding proteins (IGFBP) that transport IGFs, extend their half-life, and regulate their clearance (157). Besides limiting the hypoglycemic effects of the circulating IGF1 and IGF2, IGFBP fulfills IGF-independent functions (158).
Prelabor rupture of the membranes
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Roberto Romero, Lami Yeo, Francesca Gotsch, Eleazar Soto, Sonia S. Hassan, Juan Pedro Kusanovic, Ray Bahado-Singh
Additional biochemical tests for the diagnosis of PROM include diamine oxidase (DAO) activity (150), prolactin concentration (151–153), alpha-fetoprotein (AFP; sensitivity: 94.5% and specificity: 95.4%) (151,154), and insulin-like growth factor-binding protein-1 (IGFBP-1) (155). AFP has been reported to be better than prolactin and more practical than DAO assay with an overall accuracy of 98% (156,157). IGFBP-1 determinations have a sensitivity of 74.4% and specificity of 92.6% (155). Overall, the sensitivity, specificity, and positive and negative predictive values of the different diagnostic tests presented today in comparison with the nitrazine test are good (158–163).
Endocrine, paracrine and intracrine mechanisms of growth regulation in normal and malignant endometrial epithelium
Published in A. R. Genazzani, Hormone Replacement Therapy and Cancer, 2020
The IGF system consists of two IGFs (IGF-I and IGF-II), type 1 and type 2 IGF receptors, and at least six soluble IGF binding proteins (IGFBP), which specifically bind IGFs with affinities similar to those of IGF receptors. IGFBPs modulate IGF receptor binding and thus IGF actions at the cellular level16. IGFBPs are regulated in a tissue-specific manner. IGF-I and IGF-II are highly expressed in reproductive organs and especially in the endometrium17. IGF-I and IGF-II mRNAs were first described in human endometrium more than 10 years ago18. Both IGFs are produced by endometrial stromal cells as evidenced by in situ hybridization19.
Biomarkers and their potential functions in idiopathic pulmonary fibrosis
Published in Expert Review of Respiratory Medicine, 2020
Shanshan Ni, Min Song, Wei Guo, Ting Guo, Qinxue Shen, Hong Peng
Insulin-like growth factor binding proteins (IGFBPs) are a family of secreted proteins binding to insulin-like growth factors (IGFs), generally including IGFBP1-IGFBP6 and IGFBP8-10, which also named as IGFBP-related proteins (IGFBP-rPs) [35,36]. There is now a broad consensus that only IGFBP-1-IGFBP-6 are recognized as true members of the IGFBP family because of their conserved protein structures and high binding affinity to IGF-I and IGF-II [35]. Analyses showed that the serum and sputum supernatant concentrations of IGFBP-2 were significantly higher in IPF compared to patients with chronic obstructive pulmonary disease and HCs, and the same results occurred in sputum gene expression analysis [37,38]. After anti-fibrotic therapy, although the level of IGFBP-2 in IPF group was still higher than HCs, a significant reduction compared to untreated patients was observed [37]. Besides, serum levels of IGFBP-1 were obviously elevated in IPF patients than in the HCs [37]. In IPF lung tissues and in fibroblasts cultured from IPF lung, the levels of IGFBP-3 and −5 were increased [39]. Taken together, IGFBPs may contribute to the development of fibrosis in IPF.
Associations of Current, Childhood, and Adolescent Milk Intake with Serum Insulin-like Growth Factor (IGF)-1 and IGF Binding Protein 3 Concentrations in Adulthood
Published in Nutrition and Cancer, 2019
Vishnu Srinivasan, Katharina Nimptsch, Sabine Rohrmann
Serum samples collected from NHANES III participants were stored under appropriate refrigerated or frozen conditions until they were shipped to Diagnostic Systems Laboratories (DSL) in Webster, Texas, USA for analytical testing (21). Data on the storage history and quality control of the serum samples were reported by Berrigan et al (22). Serum IGF-1 concentrations were quantified using the IGF-1 ELISA assay (DSL 10-5600) and serum IGFBP-3 concentrations were quantified using the IGFBP-3 immunoradiometric assay (DSL 6600) (21). The following equations were used to compute the IGF-1:IGFBP-3 molar ratio:1 ng/mL IGF-1 = 0.130 nM IGF-11 ng/mL IGFBP-3 = 0.036 nM IGFBP-3.
Exploring the link between diabetes and pancreatic cancer
Published in Expert Review of Anticancer Therapy, 2019
Margherita Pizzato, Federica Turati, Valentina Rosato, Carlo La Vecchia
Both a direct effect of insulin and an indirect action involving growth hormone (GH)/insulin-like growth factor (IGF) axis could explain the increase in risk of hyperinsulinemic patients. Pancreatic β-cells release insulin in the intrapancreatic portal vessels [51] that lap acinar and ductal cells [57]. Thus, insulin exerts a proxicrine effect on receptors of exocrine pancreatic cells that, once activated, convey survival and proliferation signals [19] involved in carcinogenesis [58]. Insulin may also indirectly promote cancerogenesis acting on GH/IGF axis [19]. IGF receptors, expressed in pancreatic cancer cells, codify antiapoptotic and angiogenic signals which promote tumor development. Insulin increases levels of free and bioactive IGF-1, reducing hepatic production of IGF binding protein (IGFBP). Further, IGF-1 and insulin receptors are structurally similar, thus insulin and IGF-1 could activate both receptors. High IGF-1 and hyperinsulinemia, that occurs in insulin resistant individuals, act synergically in promoting cancerogenesis [28]. In line with the hyperinsulinemic hypothesis [53], treatments improving insulin resistance, namely metformin, might reduce pancreatic cancer risk, whereas therapies that stimulate endogenous release of insulin, such as sulfunylureas, may increase the risk [59], although evidence is unclear [60].