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Growth Hormone: Therapeutic Possibilities

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 December 2017) | Viewed by 139129

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Prof. Dr. Steve Harvey

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Guest Editor

Department of Physiology, University of Alberta, Edmonton, AB T6G 2H7, Canada
Interests: growth hormone

Dr. Carlos G. Martinez-Moreno

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Guest Editor

Institute of Neurobiology at the National Autonomous University of Mexico, Juriquilla, Querétaro, México

Special Issue Information

Dear Colleagues,

Growth hormone (GH) actions as an endocrine are well established, particularly in post-natal growth and early development; however, its effects are not restricted to the early stages of life. In adults, endocrine GH actions were initially considered to be solely associated with metabolism and homeostasis, but it is now widely accepted that GH is also an important modulator in reproduction, immune function, renal function, neural communication, cognitive processes, and behavior. Recent evidence strongly suggests that GH administration might have positive effects in disease prevention, prognosis, progression and recovery. In different models, in both in vivo and in vitro, GH has demonstrated anti-apoptotic and pro-survival effects, which are involved in neuroprotection, neuro-regeneration, stem cell renewal, cell plasticity and tissue repair. In addition, GH has a pivotal role in oxidative stress, cancer and aging. Contributions to this Special Issue on “Growth Hormone: Therapeutic Possibilities” will provide evidence that justify the future consideration of GH as a possible treatment in different physio-pathologies. The aim of this Special Issue is to emphasize the molecular mechanisms underlying the use of GH in clinical practice.

Prof. Dr. Steve Harvey
Dr. Carlos G. Martinez-Moreno
Guest Editors

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Keywords

growth hormone (GH)
physiopathology
postnatal growth
cancer
aging
neurodegeneration
metabolism
immune function
bone and disease
hypertension
abuse

Published Papers (14 papers)

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Editorial

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3 pages, 183 KiB

Open AccessEditorial

Growth Hormone: Therapeutic Possibilities—An Overview

by Steve Harvey and Carlos G. Martinez-Moreno

Int. J. Mol. Sci. 2018, 19(7), 2015; https://doi.org/10.3390/ijms19072015 - 11 Jul 2018

Cited by 5 | Viewed by 4011

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(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

Research

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4282 KiB

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Characterization of Growth Hormone Resistance in Experimental and Ulcerative Colitis

by Christoffer Soendergaard, Peter Helding Kvist, Peter Thygesen, Mats Reslow, Ole Haagen Nielsen, John Joseph Kopchick and Thomas Lindebo Holm

Int. J. Mol. Sci. 2017, 18(10), 2046; https://doi.org/10.3390/ijms18102046 - 23 Sep 2017

Cited by 14 | Viewed by 6290

Abstract

Growth hormone (GH) resistance may develop as a consequence of inflammation during conditions such as inflammatory bowel disease, encompassing ulcerative colitis (UC). However, the specific role of the GH–insulin growth factor (IGF)-1-axis and/or the functional consequences of GH resistance in this condition are unclear. In situ hybridization targeting the GH receptor (GHR) and relevant transcriptional analyses were performed in patients with UC and in IL-10 knock-out mice with piroxicam accelerated colitis (PAC). Using cultured primary epithelial cells, the effects of inflammation on the molecular mechanisms governing GH resistance was verified. Also, the therapeutic potential of GH on mucosal healing was tested in the PAC model. Inflammation induced intestinal GH resistance in UC and experimental colitis by down-regulating GHR expression and up-regulating suppressor of cytokine signalling (SOCS) proteins. These effects are driven by pro-inflammatory mediators (tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6) as confirmed using primary epithelial cells. Treatment of experimental colitis with GH increased IGF-1 and body weight of the mice, but had no effects on colonic inflammation or mucosal healing. The high transcriptional similarity between UC and experimental colitis accentuates the formation of intestinal GH resistance during inflammation. Inflammation-induced GH resistance not only impairs general growth but induces a state of local resistance, which potentially impairs the actions of GH on mucosal healing during colitis when using long-acting GH therapy. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

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3841 KiB

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Autocrine Human Growth Hormone Promotes Invasive and Cancer Stem Cell-Like Behavior of Hepatocellular Carcinoma Cells by STAT3 Dependent Inhibition of CLAUDIN-1 Expression

by Yi-Jun Chen, Ming-Liang You, Qing-Yun Chong, Vijay Pandey, Qiu-Shi Zhuang, Dong-Xu Liu, Lan Ma, Tao Zhu and Peter E. Lobie

Int. J. Mol. Sci. 2017, 18(6), 1274; https://doi.org/10.3390/ijms18061274 - 15 Jun 2017

Cited by 33 | Viewed by 7383

Abstract

Despite progress in diagnosis and treatment of hepatocellular carcinoma (HCC), the clinical outcome is still unsatisfactory. Increased expression of human growth hormone (hGH) in HCC has been reported and is associated with poor survival outcome in HCC patients. Herein, we investigated the mechanism of the oncogenic effects of hGH in HCC cell lines. In vitro functional assays demonstrated that forced expression of hGH in these HCC cell lines promoted cell proliferation, cell survival, anchorage-independent growth, cell migration, and invasion, as previously reported. In addition, forced expression of hGH promoted cancer stem cell (CSC)-like properties of HCC cells. The increased invasive and CSC-like properties of HCC cells with forced expression of hGH were mediated by inhibition of the expression of the tight junction component CLAUDIN-1. Consistently, depletion of CLAUDIN-1 expression increased the invasive and CSC-like properties of HCC cell lines. Moreover, forced expression of CLAUDIN-1 abrogated the acquired invasive and CSC-like properties of HCC cell lines with forced expression of hGH. We further demonstrated that forced expression of hGH inhibited CLAUDIN-1 expression in HCC cell lines via signal transducer and activator of transcription 3 (STAT3) mediated inhibition of CLAUDIN-1 transcription. Hence, we have elucidated a novel hGH-STAT3-CLAUDIN-1 axis responsible for invasive and CSC-like properties in HCC. Inhibition of hGH should be considered as a therapeutic option to hinder progression and relapse of HCC. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

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Essential Role of Growth Hormone and IGF-1 in Therapeutic Effect of Ghrelin in the Course of Acetic Acid-Induced Colitis

by Piotr Ceranowicz, Zygmunt Warzecha, Jakub Cieszkowski, Dagmara Ceranowicz, Beata Kuśnierz-Cabala, Joanna Bonior, Jolanta Jaworek, Tadeusz Ambroży, Krzysztof Gil, Rafał Olszanecki, Małgorzata Pihut and Artur Dembiński

Int. J. Mol. Sci. 2017, 18(6), 1118; https://doi.org/10.3390/ijms18061118 - 24 May 2017

Cited by 23 | Viewed by 4931

Abstract

Previous studies have shown that ghrelin exhibits a protective and therapeutic effect in the gut. The aim of the present study was to examine whether administration of ghrelin affects the course of acetic acid-induced colitis and to determine what is the role of growth hormone (GH) and insulin-like growth factor-1 (IGF-1) in this effect. In sham-operated or hypophysectomized male Wistar rats, colitis was induced by enema with 1 mL of 3% solution of acetic acid. Saline or ghrelin (given at the dose of 8 nmol/kg/dose) was administered intraperitoneally twice a day. Seven days after colitis induction, rats were anesthetized and the severity of the colitis was assessed. Treatment with ghrelin reduced the area of colonic mucosa damage in pituitary-intact rat. This effect was associated with increase in serum levels of GH and IGF-1. Moreover, administration of ghrelin improved blood flow in colonic mucosa and mucosal cell proliferation, as well as reduced mucosal concentration of proinflammatory interleukin-1β (IL-1β) and activity of myeloperoxidase. Hypophysectomy reduced serum levels of GH and IGF-1 and increased the area of colonic damage in rats with colitis. These effects were associated with additional reduction in mucosal blood follow and DNA synthesis when compared to pituitary-intact rats. Mucosal concentration of IL-1β and mucosal activity of myeloperoxidase were maximally increased. Moreover, in hypophysectomized rats, administration of ghrelin failed to affect serum levels of GH or IGF-1, as well as the healing rate of colitis, mucosal cell proliferation, and mucosal concentration of IL-1β, or activity of myeloperoxidase. We conclude that administration of ghrelin accelerates the healing of the acetic acid-induced colitis. Therapeutic effect of ghrelin in experimental colitis is mainly mediated by the release of endogenous growth hormone and IGF-1. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

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Growth Hormone (GH) and Rehabilitation Promoted Distal Innervation in a Child Affected by Caudal Regression Syndrome

by Jesús Devesa, Alba Alonso, Natalia López, José García, Carlos I. Puell, Tamara Pablos and Pablo Devesa

Int. J. Mol. Sci. 2017, 18(1), 230; https://doi.org/10.3390/ijms18010230 - 23 Jan 2017

Cited by 17 | Viewed by 9039

Abstract

Caudal regression syndrome (CRS) is a malformation occurring during the fetal period and mainly characterized by an incomplete development of the spinal cord (SC), which is often accompanied by other developmental anomalies. We studied a 9-month old child with CRS who presented interruption of the SC at the L2–L3 level, sacral agenesis, a lack of innervation of the inferior limbs (flaccid paraplegia), and neurogenic bladder and bowel. Given the known positive effects of growth hormone (GH) on neural stem cells (NSCs), we treated him with GH and rehabilitation, trying to induce recovery from the aforementioned sequelae. The Gross Motor Function Test (GMFM)-88 test score was 12.31%. After a blood analysis, GH treatment (0.3 mg/day, 5 days/week, during 3 months and then 15 days without GH) and rehabilitation commenced. This protocol was followed for 5 years, the last GH dose being 1 mg/day. Blood analysis and physical exams were performed every 3 months initially and then every 6 months. Six months after commencing the treatment the GMFM-88 score increased to 39.48%. Responses to sensitive stimuli appeared in most of the territories explored; 18 months later sensitive innervation was complete and the patient moved all muscles over the knees and controlled his sphincters. Three years later he began to walk with crutches, there was plantar flexion, and the GMFM-88 score was 78.48%. In summary, GH plus rehabilitation may be useful for innervating distal areas below the level of the incomplete spinal cord in CRS. It is likely that GH acted on the ependymal SC NSCs, as the hormone does in the neurogenic niches of the brain, and rehabilitation helped to achieve practically full functionality. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

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Review

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20 pages, 2707 KiB

Open AccessReview

Growth Hormone Receptor Mutations Related to Individual Dwarfism

by Shudai Lin, Congjun Li, Charles Li and Xiquan Zhang

Int. J. Mol. Sci. 2018, 19(5), 1433; https://doi.org/10.3390/ijms19051433 - 10 May 2018

Cited by 43 | Viewed by 8238

Abstract

Growth hormone (GH) promotes body growth by binding with two GH receptors (GHRs) at the cell surface. GHRs interact with Janus kinase, signal transducers, and transcription activators to stimulate metabolic effects and insulin‐like growth factor (IGF) synthesis. However, process dysfunctions in the GH–GHR–IGF-1 axis cause animal dwarfism. If, during the GH process, GHR is not successfully recognized and/or bound, or GHR fails to transmit the GH signal to IGF-1, the GH dysfunction occurs. The goal of this review was to focus on the GHR mutations that lead to failures in the GH–GHR–IGF-1 signal transaction process in the dwarf phenotype. Until now, more than 90 GHR mutations relevant to human short stature (Laron syndrome and idiopathic short stature), including deletions, missense, nonsense, frameshift, and splice site mutations, and four GHR defects associated with chicken dwarfism, have been described. Among the 93 identified mutations of human GHR, 68 occur extracellularly, 13 occur in GHR introns, 10 occur intracellularly, and two occur in the transmembrane. These mutations interfere with the interaction between GH and GHRs, GHR dimerization, downstream signaling, and the expression of GHR. These mutations cause aberrant functioning in the GH-GHR-IGF-1 axis, resulting in defects in the number and diameter of muscle fibers as well as bone development. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

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19 pages, 355 KiB

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Treatment with Growth Hormone for Adults with Growth Hormone Deficiency Syndrome: Benefits and Risks

by Juan J. Díez, Susana Sangiao-Alvarellos and Fernando Cordido

Int. J. Mol. Sci. 2018, 19(3), 893; https://doi.org/10.3390/ijms19030893 - 17 Mar 2018

Cited by 54 | Viewed by 9030

Abstract

Pharmacological treatment of growth hormone deficiency (GHD) in adults began in clinical practice more than 20 years ago. Since then, a great volume of experience has been accumulated on its effects on the symptoms and biochemical alterations that characterize this hormonal deficiency. The effects on body composition, muscle mass and strength, exercise capacity, glucose and lipid profile, bone metabolism, and quality of life have been fully demonstrated. The advance of knowledge has also taken place in the biological and molecular aspects of the action of this hormone in patients who have completed longitudinal growth. In recent years, several epidemiological studies have reported interesting information about the long-term effects of GH replacement therapy in regard to the possible induction of neoplasms and the potential development of diabetes. In addition, GH hormone receptor polymorphism could potentially influence GH therapy. Long-acting GH are under development to create a more convenient GH dosing profile, while retaining the excellent safety, efficacy, and tolerability of daily GH. In this article we compile the most recent data of GH replacement therapy in adults, as well as the molecular aspects that may condition a different sensitivity to this treatment. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

21 pages, 1175 KiB

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Growth Hormone (GH) and Gonadotropin-Releasing Hormone (GnRH) in the Central Nervous System: A Potential Neurological Combinatory Therapy?

by Carlos G. Martínez-Moreno, Denisse Calderón-Vallejo, Steve Harvey, Carlos Arámburo and José Luis Quintanar

Int. J. Mol. Sci. 2018, 19(2), 375; https://doi.org/10.3390/ijms19020375 - 26 Jan 2018

Cited by 38 | Viewed by 7400

Abstract

This brief review of the neurological effects of growth hormone (GH) and gonadotropin-releasing hormone (GnRH) in the brain, particularly in the cerebral cortex, hypothalamus, hippocampus, cerebellum, spinal cord, neural retina, and brain tumors, summarizes recent information about their therapeutic potential as treatments for different neuropathologies and neurodegenerative processes. The effect of GH and GnRH (by independent administration) has been associated with beneficial impacts in patients with brain trauma and spinal cord injuries. Both GH and GnRH have demonstrated potent neurotrophic, neuroprotective, and neuroregenerative action. Positive behavioral and cognitive effects are also associated with GH and GnRH administration. Increasing evidence suggests the possibility of a multifactorial therapy that includes both GH and GnRH. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

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40 pages, 3962 KiB

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Growth Hormone (GH) and Cardiovascular System

by Diego Caicedo, Oscar Díaz, Pablo Devesa and Jesús Devesa

Int. J. Mol. Sci. 2018, 19(1), 290; https://doi.org/10.3390/ijms19010290 - 18 Jan 2018

Cited by 53 | Viewed by 25657

Abstract

This review describes the positive effects of growth hormone (GH) on the cardiovascular system. We analyze why the vascular endothelium is a real internal secretion gland, whose inflammation is the first step for developing atherosclerosis, as well as the mechanisms by which GH acts on vessels improving oxidative stress imbalance and endothelial dysfunction. We also report how GH acts on coronary arterial disease and heart failure, and on peripheral arterial disease, inducing a neovascularization process that finally increases flow in ischemic tissues. We include some preliminary data from a trial in which GH or placebo is given to elderly people suffering from critical limb ischemia, showing some of the benefits of the hormone on plasma markers of inflammation, and the safety of GH administration during short periods of time, even in diabetic patients. We also analyze how Klotho is strongly related to GH, inducing, after being released from the damaged vascular endothelium, the pituitary secretion of GH, most likely to repair the injury in the ischemic tissues. We also show how GH can help during wound healing by increasing the blood flow and some neurotrophic and growth factors. In summary, we postulate that short-term GH administration could be useful to treat cardiovascular diseases. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

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GH/IGF-1 Signaling and Current Knowledge of Epigenetics; a Review and Considerations on Possible Therapeutic Options

by Francisco Álvarez-Nava and Roberto Lanes

Int. J. Mol. Sci. 2017, 18(10), 1624; https://doi.org/10.3390/ijms18101624 - 05 Oct 2017

Cited by 27 | Viewed by 5994

Abstract

Epigenetic mechanisms play an important role in the regulation of the Growth Hormone- Insulin-like Growth Factor 1 (GH-IGF1) axis and in processes for controlling long bone growth, and carbohydrate and lipid metabolism. Improvement of methodologies that allow for the assessment of epigenetic regulation have contributed enormously to the understanding of GH action, but many questions still remain to be clarified. The reversible nature of epigenetic factors and, particularly, their role as mediators between the genome and the environment, make them viable therapeutic target candidates. Rather than reviewing the molecular and epigenetic pathways regulated by GH action, in this review we have focused on the use of epigenetic modulators as potential drugs to improve the GH response. We first discuss recent progress in the understanding of intracellular molecular mechanisms controlling GH and IGF-I action. We then emphasize current advances in genetic and epigenetic mechanisms that control gene expression, and which support a key role for epigenetic regulation in the cascade of intracellular events that trigger GH action when coupled to its receptor. Thirdly, we focus on fetal programming and epigenetic regulation at the IGF1 locus. We then discuss epigenetic alterations in intrauterine growth retardation, and the possibility for a potential epigenetic pharmaceutical approach in short stature associated with this fetal condition. Lastly, we review an example of epigenetic therapeutics in the context of growth-related epigenetic deregulation disorders. The advance of our understanding of epigenetic changes and the impact they are having on new forms of therapy creates exciting prospects for the future. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

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Manipulation of the Growth Hormone-Insulin-Like Growth Factor (GH-IGF) Axis: A Treatment Strategy to Reverse the Effects of Early Life Developmental Programming

by Clare M. Reynolds, Jo K. Perry and Mark H. Vickers

Int. J. Mol. Sci. 2017, 18(8), 1729; https://doi.org/10.3390/ijms18081729 - 08 Aug 2017

Cited by 19 | Viewed by 4855

Abstract

Evidence from human clinical, epidemiological, and experimental animal models has clearly highlighted a link between the early life environment and an increased risk for a range of cardiometabolic disorders in later life. In particular, altered maternal nutrition, including both undernutrition and overnutrition, spanning exposure windows that cover the period from preconception through to early infancy, clearly highlight an increased risk for a range of disorders in offspring in later life. This process, preferentially termed “developmental programming” as part of the developmental origins of health and disease (DOHaD) framework, leads to phenotypic outcomes in offspring that closely resemble those of individuals with untreated growth hormone (GH) deficiency, including increased adiposity and cardiovascular disorders. As such, the use of GH as a potential intervention strategy to mitigate the effects of developmental malprogramming has received some attention in the DOHaD field. In particular, experimental animal models have shown that early GH treatment in the setting of poor maternal nutrition can partially rescue the programmed phenotype, albeit in a sex-specific manner. Although the mechanisms remain poorly defined, they include changes to endothelial function, an altered inflammasome, changes in adipogenesis and cardiovascular function, neuroendocrine effects, and changes in the epigenetic regulation of gene expression. Similarly, GH treatment to adult offspring, where an adverse metabolic phenotype is already manifest, has shown efficacy in reversing some of the metabolic disorders arising from a poor early life environment. Components of the GH-insulin-like growth factor (IGF)-IGF binding protein (GH-IGF-IGFBP) system, including insulin-like growth factor 1 (IGF-1), have also shown promise in ameliorating programmed metabolic disorders, potentially acting via epigenetic processes including changes in miRNA profiles and altered DNA methylation. However, as with the use of GH in the clinical setting of short stature and GH-deficiency, the benefits of treatment are also, in some cases, associated with potential unwanted side effects that need to be taken into account before effective translation as an intervention modality in the DOHaD context can be undertaken. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

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Growth Hormone’s Effect on Adipose Tissue: Quality versus Quantity

by Darlene E. Berryman and Edward O. List

Int. J. Mol. Sci. 2017, 18(8), 1621; https://doi.org/10.3390/ijms18081621 - 26 Jul 2017

Cited by 48 | Viewed by 19463

Abstract

Obesity is an excessive accumulation or expansion of adipose tissue (AT) due to an increase in either the size and/or number of its characteristic cell type, the adipocyte. As one of the most significant public health problems of our time, obesity and its associated metabolic complications have demanded that attention be given to finding effective therapeutic options aimed at reducing adiposity or the metabolic dysfunction associated with its accumulation. Growth hormone (GH) has therapeutic potential due to its potent lipolytic effect and resultant ability to reduce AT mass while preserving lean body mass. However, AT and its resident adipocytes are significantly more dynamic and elaborate than once thought and require one not to use the reduction in absolute mass as a readout of efficacy alone. Paradoxically, therapies that reduce GH action may ultimately prove to be healthier, in part because GH also possesses potent anti-insulin activities along with concerns that GH may promote the growth of certain cancers. This review will briefly summarize some of the newer complexities of AT relevant to GH action and describe the current understanding of how GH influences this tissue using data from both humans and mice. We will conclude by considering the therapeutic use of GH or GH antagonists in obesity, as well as important gaps in knowledge regarding GH and AT. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

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The Role of Growth Hormone and Insulin-Like Growth Factor-I in the Liver

by Yutaka Takahashi

Int. J. Mol. Sci. 2017, 18(7), 1447; https://doi.org/10.3390/ijms18071447 - 05 Jul 2017

Cited by 131 | Viewed by 16215

Abstract

Adult growth hormone deficiency (GHD) is characterized by metabolic abnormalities associated with visceral obesity, impaired quality of life, and increased mortality. Patients with adult GHD show increased prevalence of non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH), and growth hormone (GH) replacement therapy has been shown to improve these conditions. It has also been demonstrated that a decrease in the GH insulin-like growth factor-I (IGF-I) axis is closely associated with the progression of general NAFLD, suggesting a physiological role of these hormones for the maintenance of the liver. NASH histologically demonstrates inflammation, necrosis, and fibrosis, in addition to steatosis (and is a serious disease because it can progress to liver cirrhosis and hepatocellular carcinoma in a subset of cases). While fibrosis determines the prognosis of the patient, efficacious treatment for fibrosis is crucial; however, it has not yet been established. Recent studies have clarified the essential roles of GH and IGF-I in the liver. GH profoundly reduces visceral fat, which plays an important role in the development of NAFLD. Furthermore, GH directly reduces lipogenesis in the hepatocytes. IGF-I induces cellular senescence and inactivates hepatic stellate cells, therefore ameliorating fibrosis. IGF-I treatment has been shown to improve animal models of NASH and cirrhosis, suggesting potential clinical applications of IGF-I in these conditions. In this review, I will focus on the important roles of GH and IGF-I in the liver, their underlying mechanisms, and their potential therapeutic applications. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

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Growth Hormone Resistance—Special Focus on Inflammatory Bowel Disease

by Christoffer Soendergaard, Jonathan A. Young and John J. Kopchick

Int. J. Mol. Sci. 2017, 18(5), 1019; https://doi.org/10.3390/ijms18051019 - 09 May 2017

Cited by 30 | Viewed by 9663

Abstract

Growth hormone (GH) plays major anabolic and catabolic roles in the body and is important for regulating several aspects of growth. During an inflammatory process, cells may develop a state of GH resistance during which their response to GH stimulation is limited. In this review, we will emphasize specific mechanisms governing the formation of GH resistance in the active phase of inflammatory bowel disease. The specific molecular effects mediated through individual inflammatory mediators and processes will be highlighted to provide an overview of the transcriptional, translational and post-translational inflammation-mediated impacts on the GH receptor (GHR) along with the impacts on GH-induced intracellular signaling. We also will review GH’s effects on mucosal healing and immune cells in the context of experimental colitis, human inflammatory bowel disease and in patients with short bowel syndrome. Full article

(This article belongs to the Special Issue Growth Hormone: Therapeutic Possibilities)

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