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Insulin/IGF Signaling in Early Brain Development
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Selma Yagoub, Rachel N. Lippert
Functional Insulin-like Growth Factor (IGF) is also expressed early in development and plays a significant role in the proper formation of the central nervous system (20). Both isoforms of IGF, referred to as IGF-1 and IGF-2, have varying roles in development and adulthood, promoting the growth and survival of neuronal cells through their respective receptors, IGF-1R and IGF-2R and the hybrid Insulin/IGF-1 receptor. Using bovine embryos, a protective effect- of IGF-1 was noted in the early developing embryo. However, due to the anti-apoptotic effects of IGF-1, it was indicated that IGF-1 may inhibit neurulation via the downregulation of specific genes involved in this process (25, 26). On the other hand, additional studies in vertebrates have yielded insights pertaining to IGF-2. Interestingly, IGF-2 is shown to have a high affinity and ability to signal through the IR-A isoform and points toward dynamic crosstalk of the two signaling pathways in early development (21, 27). In zebrafish, there are two co-orthologs of IGF2, igf2a and igf2b. Found primarily in and near the notochord, igf2a and igf2b, play a role in neurulation. The use of an oligomer molecule called a morpholino can decrease gene expression and morpholino-mediated knockdown of either igf2a or igf2b results in defects in dorsal midline development. This is highlighted by changes in the rate of segmentation, notochord undulations, ectopic fusion of the nephron primordia, defects in ventral forebrain development and increased ventral curvature.
Neuroendocrine Factors
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Growth hormone (GH) is a polypeptide released in a pulsatile fashion by the anterior pituitary. The release can be modified in response to a variety of stimuli including emotional stress, fasting, sleeping, certain amino acids, certain drugs, and exercise (190). Its release is activated by growth hormone-releasing factor (GH-RF), which is secreted by the hypothalamus. Growth hormone interacts with insulin-like growth factors (IGF), which are primary effector hormones for protein synthesis. These two hormones (GH and IGF) regulate each other’s secretion in a feedback system, possibly including GH-RF and the stimulation of somatotropin releasing inhibitory factor (SRIF or somatostatin) in the hypothalamus (115, 127). There are several isoforms of GH, and it appears that their effects are mediated through a single receptor, although more research is necessary to fully evaluate this phenomenon (119).
Satellite cells and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Neil R.W. Martin, Adam P. Sharples
Insulin-like growth factor I or IGF-I is an important mediator of tissue growth. IGF-I secreted by the liver in response to growth hormone acts in an endocrine fashion and drives post-natal growth and development of many organs, including the brain, spleen, kidney and bone (103). Skeletal muscle is also a source of IGF-I which can act in an autocrine/paracrine manner to induce muscle growth at the local level (104). In fact, in skeletal muscle, the IGF-I gene can be alternatively spliced during transcription to give rise (in humans) to three different IGF-I isoforms or splice variants: IGF-IEa (which is the same as the liver IGF-I), IGF-IEb and IGF-IEc (105). IGF-IEc has been termed mechano-growth factor (MGF) due to the fact that it is not detectable in resting muscle but is rapidly expressed at the mRNA level following mechanical stretch of rabbit muscle and eccentric exercise in humans (105).
Screening and characterisation of a novel efficient tumour cell-targeting peptide derived from insulin-like growth factor binding proteins
Published in Journal of Drug Targeting, 2023
Min-Lin He, Jin Lei, Xue-Wei Cao, Jian Zhao, Fu-Jun Wang
Insulin-like growth factor (IGF) is a natural growth hormone that plays a key role in cell proliferation, early development, metabolic regulation and inhibition of apoptosis [5]. IGFs are ubiquitously expressed and are important mitogens that affect cell growth and metabolism [6]. The IGF family consists of insulin and two insulin-like factors (IGF-1 and IGF-2). These factors directly regulate cellular function by interacting with specific IGF receptors and activating various intracellular signalling cascades. Numerous mutations in the IGF-1R gene and growth hormone-insulin-like growth factor (GH-IGF) axis genes have been detected in some tumours such as breast cancer, gastrointestinal stromal tumour, and osteosarcoma [7]. These findings have drawn increasing attention to the relationship between the IGF family regulation and tumorigenesis. Under normal physiological conditions, IGF signalling is tightly controlled at a stable level [8]. However, genetic abnormalities and/or chromosomal alterations can lead to disordered expression of IGF and IGF-1R and tumorigenesis [9]. Numerous experiments have shown that an increase in the concentration of IGF-1 leads to the proliferation of tumour cells [10].
The common variant of rs6214 in insulin like growth factor 1 (IGF1) gene: a potential protective factor for non-alcoholic fatty liver disease
Published in Archives of Physiology and Biochemistry, 2023
Mohammad Sabzikarian, Touraj Mahmoudi, Seidamir Pasha Tabaeian, Gholamreza Rezamand, Asadollah Asadi, Hamid Farahani, Hossein Nobakht, Reza Dabiri, Fariborz Mansour-Ghanaei, Faramarz Derakhshan, Mohammad Reza Zali
The insulin axis and insulin-like growth factor (IGF) axis are biologically interrelated. Insulin like growth factor 1 (product of the IGF1 gene) and insulin-like growth factor-binding protein 3 (product of the IGFBP3 gene) are directly involved in insulin-signalling pathway. IGF1 is mostly synthesised and secreted by the liver and is similar in molecular structure and function to insulin. On the other hand, IGFBP3 regulates the bioavailability of IGF1 to the target tissues. Furthermore, insulin increases the expression and bioavailability of IGF1 via decreases the synthesis of IGFBPs, especially IGFBP3 (Giovannucci 2001). Circulating IGF1 level is inversely associated with reduced insulin sensitivity (Succurro et al. 2009), and its low level is an independent predictor for the development of glucose intolerance (Sandhu et al. 2002). Consistently, liver-specific IGF1 knockout mice exhibit IR and hyperinsulinemia (Yakar et al. 2001). More interestingly, circulating levels of IGF1 and its mRNA expression levels are lower in patients with NAFLD than in the controls (Sumida et al. 2015, Chishima et al. 2017, Yao et al. 2019). Based on these considerations, we designed the present study to examine the possible association of IGF1 (rs6214) and IGFBP3 (rs3110697) gene variants with NAFLD risk.
Advances in adrenocortical carcinoma pharmacotherapy: what is the current state of the art?
Published in Expert Opinion on Pharmacotherapy, 2022
Valentina Cremaschi, Andrea Abate, Deborah Cosentini, Salvatore Grisanti, Elisa Rossini, Marta Laganà, Mariangela Tamburello, Antonella Turla, Sandra Sigala, Alfredo Berruti
Molecular screenings have provided some promising insights on proteins involved in the cell cycle as potential targets in the ACC treatment [36]. In particular, the CDK4 gene was found overexpressed in 62% of ACC samples [37]. Therefore, the cyclin dependent kinases (CDK) seem to be a druggable target in ACC. An overview of preclinical studies involving CDK inhibitor is presented in Table 1. Commercially available CDK inhibitors, such as palbociclib and ribociclib, as well as the non-commercially available alvocidib, either alone or in combination with other targeted therapies, demonstrated a clear cytotoxic effect on ACC cells in vitro. IGF (insulin-like growth factor) pathway is frequently mutated in ACC [38], being a potential target. The effect of molecules interfering with this pathway in the context of ACC has been under evaluation for several years both at preclinical and clinical level, although disappointing results have been reported in clinics [39]. Looking at the preclinical data, encouraging results were obtained using a combination approach of linsitinib with mTOR (mammalian target of rapamycin) inhibitors. In NCI-H295R cells and in its sub-clone HAC15, linsitinib showed an antiproliferative effect, which was increased by the combination with sirolimus and everolimus [40].