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"Hormones"
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Meet your hormones
\"Explores and explains this fascinating hidden world: what hormones are, what they do and why we can't live without these super-fast chemical messengers. It includes in-depth profiles on each of the most important hormones at work in the human body and helpful advice on how we can look after our own health through greater knowledge of our hormones.\"-- Provided by publisher.
Book
Dose-Dependent Suppression of Gonadotropins and Ovarian Hormones by Elagolix in Healthy Premenopausal Women
Context:Elagolix is a nonpeptide, oral gonadotropin-releasing hormone (GnRH) antagonist being developed for sex-hormone–dependent diseases in women.Objective:We evaluated the pharmacokinetics and pharmacodynamics of elagolix.Design, Setting, and Participants:This study was a randomized, double-blind, placebo-controlled, multiple-ascending dose study in 45 healthy premenopausal women at a research unit.Interventions:Elagolix [150 mg once daily or 100, 200, 300, or 400 mg twice daily (BID)] or placebo was administered for 21 days.Main Outcome Measures:Main outcome measures were elagolix pharmacokinetics, suppression of gonadotropics [follicle-stimulating hormone (FSH), luteinizing hormone (LH)] and ovarian hormones [estradiol (E2), progesterone (P)], and adverse events.Results:Elagolix was rapidly absorbed after oral dosing, reaching maximum concentrations at 1.0 to 1.5 hours, with a half-life of 4 to 6 hours. FSH, LH, and E2 were suppressed within hours of elagolix administration on day 1. Dose-dependent suppression of E2 was observed, with maximum suppression achieved with elagolix 200 mg BID. Dose-dependent suppression of FSH and LH was also observed, with maximal or near-maximal suppression achieved at 300 mg BID and 200 mg BID, respectively. At elagolix doses ≥100 mg BID, P concentrations remained at anovulatory levels throughout 21 days of dosing. The most frequently reported adverse events were headache and hot flush.Conclusions:Elagolix administration allows for modulation of gonadotropin and ovarian hormone concentrations, from partial suppression at lower doses to nearly full suppression at higher doses. The results of this study provide a rationale for elagolix dose selection for treatment of sex hormone–dependent diseases in women.Elagolix rapidly suppressed gonadotropins and ovarian sex hormones in healthy premenopausal women in a dose-dependent manner.
Journal Article
Growth hormone-releasing hormone and its analogues in health and disease
Growth hormone-releasing hormone (GHRH) and its ability to stimulate the production and release of growth hormone from the pituitary were discovered more than four decades ago. Since then, this hormone has been studied extensively and research into its functions is still ongoing. GHRH has multifaceted roles beyond the originally identified functions that encompass a variety of direct extrapituitary effects. In this Review, we illustrate the different biological activities of GHRH, covering the effects of GHRH agonists and antagonists in physiological and pathological contexts, along with the underlying mechanisms. GHRH and GHRH analogues have been implicated in cell growth, wound healing, cell death, inflammation, immune functions, mood disorders, feeding behaviour, neuroprotection, diabetes mellitus and obesity, as well as cardiovascular, lung and neurodegenerative diseases and some cancers. The positive effects observed in preclinical models in vitro and in vivo strongly support the potential use of GHRH agonists and antagonists as clinical therapeutics.
Growth hormone-releasing hormone (GHRH) signalling modulation has shown beneficial effects in a wide range of diseases in preclinical research. This Review discusses the progression of research into the effects of GHRH agonist and antagonist treatment in several contexts, including cancer, inflammation, cardiovascular disease and metabolism.
Key points
In addition to promoting synthesis and release of growth hormone, growth hormone-releasing hormone (GHRH) exerts a wide range of extrapituitary effects in a variety of organs and tissues.
GHRH receptor (GHRHR) and the splice variant SV1 are expressed in most cell types; moreover, SV1 displays both ligand-dependent and ligand-independent proliferative effects in normal and tumour cells.
Synthetic GHRH agonists and antagonists have been developed, with high stability in vivo and strong binding affinity for GHRHRs.
GHRH agonists exert remarkable protective functions in in vitro and in vivo animal models of heart disease, wound healing, eye diseases, diabetes mellitus, cancer and neurodegenerative disorders.
GHRH antagonists have strong antitumour effects in in vitro and in vivo animal models, as well as anti-inflammatory and antioxidant functions.
Studies in humans are needed to clarify the therapeutic potential of GHRH agonistic and antagonistic analogues and their possible adverse effects.
Journal Article
Your body in balance : the new science of food, hormones, and health
\"Barnard provides readers with a way to use food to protect against chronic and terminal health problems caused by the excess hormones that are lurking in our diets\"-- Provided by publisher.
Book
GIP Receptor Antagonism Eliminates Paradoxical Growth Hormone Secretion in Some Patients With Acromegaly
About 30% of patients with active acromegaly experience paradoxically increased growth hormone (GH) secretion during the diagnostic oral glucose tolerance test (OGTT). Endogenous glucose-dependent insulinotropic polypeptide (GIP) is implicated in this paradoxical secretion.
We used the GIP receptor (GIPR) antagonist GIP(3-30)NH2 to test the hypothesis that GIP mediates this paradoxical response when GIPR is abundantly expressed in somatotropinomas.
A total of 25 treatment-naive patients with acromegaly were enrolled. Each patient underwent one OGTT during simultaneous placebo infusion and one OGTT during a GIP(3-30)NH2 infusion. Blood samples were drawn at baseline and regularly after infusions to measure GH. We assessed pituitary adenoma size by magnetic resonance imaging and GIPR expression by immunohistochemistry on resected somatotropinomas. For mechanistic confirmation, we applied in vitro and ex vivo approaches. The main outcome measure was the effect of GIP(3-30)NH2 on paradoxical GH secretion during OGTT as a measure of GIP involvement.
In 4 of 7 patients with paradoxical GH secretion, GIP(3-30)NH2 infusion completely abolished the paradoxical response (P = .0003). Somatotrophs were available from 3 of 4 of these patients, all showing abundant GIPR expression. Adenoma size did not differ between patients with and without paradoxical GH secretion.
Of 25 patients with acromegaly, 7 had paradoxical GH secretion during OGTT, and pharmaceutical GIPR blockade abolished this secretion in 4. Corresponding somatotroph adenomas abundantly expressed GIPR, suggesting a therapeutic target in this subpopulation of patients. In vitro and ex vivo analyses confirmed the role of GIP and the effects of the antagonist.
Journal Article
Relationship of IGF-1 and IGF-Binding Proteins to Disease Severity and Glycemia in Nonalcoholic Fatty Liver Disease
Abstract
Context
Growth hormone (GH) and IGF-1 help regulate hepatic glucose and lipid metabolism, and reductions in these hormones may contribute to development of nonalcoholic fatty liver disease (NAFLD).
Objective
To assess relationships between hepatic expression of IGF1 and IGF-binding proteins (IGFBPs) and measures of glycemia and liver disease in adults with NAFLD. Secondarily to assess effects of GH-releasing hormone (GHRH) on circulating IGFBPs.
Design
Analysis of data from a randomized clinical trial of GHRH.
Setting
Two US academic medical centers.
Participants
Participants were 61 men and women 18 to 70 years of age with HIV-infection, ≥5% hepatic fat fraction, including 39 with RNA-Seq data from liver biopsy.
Main Outcome Measures
Hepatic steatosis, inflammation, and fibrosis by histopathology and measures of glucose homeostasis.
Results
Hepatic IGF1 mRNA was significantly lower in individuals with higher steatosis and NAFLD Activity Score (NAS) and was inversely related to glucose parameters, independent of circulating IGF-1. Among the IGFBPs, IGFBP2 and IGFBP4 were lower and IGFBP6 and IGFBP7 (also known as IGFBP-related protein 1) were higher with increasing steatosis. Hepatic IGFBP6 and IGFBP7 mRNA levels were positively associated with NAS. IGFBP7 mRNA increased with increasing fibrosis. Hepatic IGFBP1 mRNA was inversely associated with glycemia and insulin resistance, with opposite relationships present for IGFBP3 and IGFBP7. GHRH increased circulating IGFBP-1 and IGFBP-3, but decreased IGFBP-2 and IGFBP-6.
Conclusions
These data demonstrate novel relationships of IGF-1 and IGFBPs with NAFLD severity and glucose control, with divergent roles seen for different IGFBPs. Moreover, the data provide new information on the complex effects of GHRH on IGFBPs.
Journal Article
The heart of the brain : the hypothalamus and its hormones
\"This book is about the neuroendocrine brain - about the hypothalamus, the seat of our passions, and about the control that this small structure exerts on our physiology and behavior. The hypothalamus contains a vast diversity of neuronal types, and these signal not only though conventional messengers but by a wide range of other signals, many of which act as hormones within the brain. Behaviors important to who we are - love and hate, how much we eat and what we eat, how we respond to threat and to stress - are governed by the hypothalamus, and not by the map of how the neurons are connected, but by where the receptors for these peptide signals are found. Neurotransmitter signals are ephemeral and confined by anatomical connectivity, but the peptide signals that hypothalamic neurons generate are potent, wide reaching and long-lasting, and they affect not just neuronal excitability but also the genes that neurons express. Remarkably, different peptides when injected into the brain induce coherent, meaningful behaviors - some trigger eating, others induce a longing for salt, or initiate maternal behavior or aggression or sleep. This book describes the frontiers of current research into the hypothalamus, and does so in a way that makes it accessible to readers with no specialized knowledge.\"-- Provided by publisher.
BOOK
Sex steroids and autoimmune rheumatic diseases: state of the art
In autoimmune rheumatic diseases, oestrogens can stimulate certain immune responses (including effects on B cells and innate immunity), but can also have dose-related anti-inflammatory effects on T cells, macrophages and other immune cells. By contrast, androgens and progesterone have predominantly immunosuppressive and anti-inflammatory effects. Hormone replacement therapies and oral contraception (and also pregnancy) enhance or decrease the severity of autoimmune rheumatic diseases at a genetic or epigenetic level. Serum androgen concentrations are often low in men and in women with autoimmune rheumatic diseases, suggesting that androgen-like compounds might be a promising therapeutic approach. However, androgen-to-oestrogen conversion (known as intracrinology) is enhanced in inflamed tissues, such as those present in patients with autoimmune rheumatic diseases. In addition, it is becoming evident that the gut microbiota differs between the sexes (known as the microgenderome) and leads to sex-dependent genetic and epigenetic changes in gastrointestinal inflammation, systemic immunity and, potentially, susceptibility to autoimmune or inflammatory rheumatic diseases. Future clinical research needs to focus on the therapeutic use of androgens and progestins or their downstream signalling cascades and on new oestrogenic compounds such as tissue-selective oestrogen complex to modulate altered immune responses.The effects of sex steroids (oestrogens, androgens and progesterone) on immune responses contribute to the sex bias in autoimmune rheumatic diseases in complex ways. Targeting these effects could hold potential for treating patients with autoimmune rheumatic diseases.
Journal Article