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GH/IGF-1 Abnormalities and Muscle Impairment: from Basic Research to Clinical Practice

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GH/IGF-1 Abnormalities and Muscle Impairment: from Basic Research to Clinical Practice International Journal of Molecular Sciences Review GH/IGF-1 Abnormalities and Muscle Impairment: From Basic Research to Clinical Practice Betina Biagetti * and Rafael Simó * Diabetes and Metabolism Research Unit, Vall d’Hebron Research Institute and CIBERDEM (ISCIII), Universidad Autónoma de Barcelona, 08193 Bellaterra, Spain * Correspondence: [email protected] (B.B.); [email protected] (R.S.); Tel.: +34-934894172 (B.B.); +34-934894172 (R.S.) Abstract: The impairment of skeletal muscle function is one of the most debilitating least understood co-morbidity that accompanies acromegaly (ACRO). Despite being one of the major determinants of these patients’ poor quality of life, there is limited evidence related to the underlying mechanisms and treatment options. Although growth hormone (GH) and insulin-like growth factor-1 (IGF-1) levels are associated, albeit not indisputable, with the presence and severity of ACRO myopathies the precise effects attributed to increased GH or IGF-1 levels are still unclear. Yet, cell lines and animal models can help us bridge these gaps. This review aims to describe the evidence regarding the role of GH and IGF-1 in muscle anabolism, from the basic to the clinical setting with special emphasis on ACRO. We also pinpoint future perspectives and research lines that should be considered for improving our knowledge in the field. Keywords: acromegaly; myopathy; review; growth hormone; IGF-1 1. Introduction Acromegaly (ACRO) is a rare chronic disfiguring and multisystem disease due to Citation: Biagetti, B.; Simó, R. non-suppressible growth hormone (GH) over-secretion, commonly caused by a pituitary GH/IGF-1 Abnormalities and Muscle tumour [1]. The autonomous production of GH leads to an increase in the synthesis Impairment: From Basic Research to and secretion of insulin-like growth factor-1 (IGF-1), mainly by the liver, which results in Clinical Practice. Int. J. Mol. Sci. 2021, 22, 415. https://doi.org/10.3390/ somatic overgrowth, metabolic changes, and several comorbidities [1]. ijms22010415 One of the significant disabling co-morbidities accompanying ACRO is myopathy and its related musculoskeletal symptoms [2,3], which are significant determinants of the low Received: 4 December 2020 quality of life (QoL) of these patients and may persist despite disease remission [2,4–6]. Accepted: 28 December 2020 However, we do not know the exact underlying mechanisms involved in its develop- Published: 2 January 2021 ment. Although the duration of the disease and serum GH/IGF-1 levels were shown to be independent predictors of overall mortality and co-morbidities of ACRO [7–11], their spe- Publisher’s Note: MDPI stays neu- cific role in the pathogenesis of myopathy remains to be elucidated. Besides, both GH tral with regard to jurisdictional clai- and IGF-1 levels are not always directly and unequivocally associated with patient QoL ms in published maps and institutio- and the presence and severity of co-morbidities [4,12]. For this reason, numerous efforts nal affiliations. are currently being made to detect active disease, pointing to other variables apart from GH/IGF-1 [13,14]. Experimental research using cell lines and animal models is necessary to understand better the mechanisms involved in the myopathy induced by ACRO. In this regard, there is Copyright: © 2021 by the authors. Li- some evidence regarding the effects of the GH/IGF-1 axis in the muscular system and the censee MDPI, Basel, Switzerland. This article is an open access article mechanisms by which different conditions could impact on muscle performance. distributed under the terms and con- This review aims to describe the evidence regarding the role of GH and IGF-1 in ditions of the Creative Commons At- muscle anabolism, from the basic to the clinical setting, taking ACRO as the leading tribution (CC BY) license (https:// paradigm in the clinical setting. The new perspectives and scientific gaps in this field to be creativecommons.org/licenses/by/ covered are also underlined. 4.0/). Int. J. Mol. Sci. 2021, 22, 415. https://doi.org/10.3390/ijms22010415 https://www.mdpi.com/journal/ijms Int. J. Mol. Sci. 2021, 22, x FOR PEER REVIEW 2 of 18 This review aims to describe the evidence regarding the role of GH and IGF‐1 in muscle anabolism, from the basic to the clinical setting, taking ACRO as the leading par‐ adigm in the clinical setting. The new perspectives and scientific gaps in this field to be Int. J. Mol. Sci. 2021, 22, 415 2 of 18 covered are also underlined. 2. GH/IGF‐1 Axis in Humans Pituitary2. synthesis GH/IGF-1 and Axis secretion in Humans of GH is stimulated by the episodic hypothalamic secretion of GH releasingPituitary factor synthesis and mainly and secretion inhabited of GHby somatostatin is stimulated [15]. by theGH episodicstimulates hypothalamic the synthesissecretion of IGF‐1 ofmostly GH releasing by the liver, factor and and both mainly circulating inhabited GH by and somatostatin IGF‐1 inhibit [15 ].GH GH stimulates secretion by thea negative synthesis loop of IGF-1at both mostly hypothalamic by the liver, and and pituitary both circulating levels. In addition, GH and IGF-1 age, inhibit GH gender, pubertalsecretion status, by food, a negative exercise, loop fasting, at both insulin, hypothalamic sleep and and body pituitary composition levels. play In addition, age, important regulatorygender, pubertal roles in the status, GH/IGF food,‐1 exercise, axis [15]. fasting, insulin, sleep and body composition play important regulatory roles in the GH/IGF-1 axis [15]. 2.1. GH Circulation, GH Receptor and Intracellular Signalling 2.1. GH Circulation, GH Receptor and Intracellular Signalling In the circulation, GH binds to growth hormone binding protein (GHBP) which is a In the circulation, GH binds to growth hormone binding protein (GHBP) which soluble truncated form of the extracellular domain of the GH receptor (GHR) [16]. There‐ is a soluble truncated form of the extracellular domain of the GH receptor (GHR) [16]. fore, bound and free GH both exist in the circulation, and GH bioavailability depends on Therefore, bound and free GH both exist in the circulation, and GH bioavailability depends the pulsatile pattern of its secretion. on the pulsatile pattern of its secretion. GHR belongs to the so‐called “cytokine receptor family”, specifically part of the class GHR belongs to the so-called “cytokine receptor family”, specifically part of the class I cytokine receptor family. Cytokine receptors lack intrinsic protein tyrosine kinase (PTK) I cytokine receptor family. Cytokine receptors lack intrinsic protein tyrosine kinase (PTK) activity and therefore rely on binding non‐receptor PTKs for their signal transduction, the activity and therefore rely on binding non-receptor PTKs for their signal transduction, so‐called Janus Kinase (JAK) (Figure 1). The dimerisation induced by the binding of GHR the so-called Janus Kinase (JAK) (Figure1). The dimerisation induced by the binding of is the critical step in activating the signalling pathway JAK/STAT (Janus kinase/signal GHR is the critical step in activating the signalling pathway JAK/STAT (Janus kinase/signal transducer and activator of transcription), and binding to GHR brings two JAK2 mole‐ transducer and activator of transcription), and binding to GHR brings two JAK2 molecules cules close enough to initiate their trans‐phosphorylation by recruiting STAT[17,18]. Phos‐ close enough to initiate their trans-phosphorylation by recruiting STAT [17,18]. Phosphory- phorylated STATSs,lated STATSs, translocate translocate to the to nucleus, the nucleus, binding binding to specific to specific DNA DNA sequences sequences and and induce induce the transcriptionthe transcription of specific of specific GH‐dependent GH-dependent genes, genes, thus thuspromoting promoting not only not onlythe the synthe- synthesis of sisIGF of‐1, IGF-1, IGF‐1 IGF-1 binding binding protein protein (IGFBP) (IGFBP) acid‐ acid-labilelabile sub‐units sub-units (ALS), (ALS), but also but also directly directly stimulatingstimulating proliferative proliferative and andmetabolic metabolic actions actions (Figure (Figure 1). 1). Figure 1. Growth hormone (GH) receptor. The GH receptor’s dimerisation is the critical step in activating the signalling Figure 1. Growth hormone (GH) receptor. The GH receptor’s dimerisation is the critical step in pathway JAK/STAT.activating Phosphorylated the signalling STATS pathway translocate JAK/STAT. to the Phosphorylated nucleus, inducing STATS the transcription translocate to of the specific nucleus, GH-dependent genes, promotinginducing mainly the the transcription synthesis ofof IGF-1,specific IGFBP GH‐dependent acid-labile genes, sub-units, promoting but also, mainly stimulating the synthesis other of pathways (i.e., IRIS and SHC)IGF that‐1, regulateIGFBP acid cellular‐labile proliferation, sub‐units, but growth also, stimulating and metabolic other events. pathways In addition,(i.e., IRIS newlyand SHC) synthesised that IGF-1 promotes metabolicregulate and cellular cellular proliferation, events. IGF-1: growth insulin-like and metabolic growth events. factor, In GH: addition, growth newly hormone synthesised IGFBP3: IGF IGF-1‐1 binding protein type 3,promotes JAK/STAT: metabolic Janus kinase/signal and cellular events. transducer IGF‐ and1: insulin transcription‐like growth activator factor, IRS: GH: insulin growth receptor hormone substrate; PI3K: phosphatidylinositolIGFBP3: 3-kinase; IGF‐1 binding SHC: (adaptor protein type proteins). 3, JAK/STAT: Janus kinase/signal transducer and transcription activator IRS: insulin receptor substrate; PI3K: phosphatidylinositol 3‐kinase; SHC: (adaptor pro‐ teins). GHR is widely distributed throughout the body. Although GHR expression is particu- larly important in the liver, GH receptors are found in other tissues like muscle, fat, heart, kidney, brain and pancreas [19]. The actions of GH depend not only on the receptor but also on the organ it stimulates; specifically, GH actions in the muscle are controversial and depend, among other factors, on GH quantity, the time of exposition and the condition of the subjects. Int. J. Mol. Sci. 2021, 22, x FOR PEER REVIEW 3 of 18 GHR is widely distributed throughout the body.
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