Journal of Endocrinology

  1479-6805

  0022-0795

  Anh Quốc

Cơ quản chủ quản:  BioScientifica Ltd.

Lĩnh vực:
Endocrinology, Diabetes and MetabolismEndocrinology

Các bài báo tiêu biểu

The role of corticotropin-releasing factor in depression and anxiety disorders
Tập 160 Số 1 - Trang 1-12 - 1999
Lotta Arborelius, M J Owens, PM Plotsky, Charles B. Nemeroff
Corticotropin-releasing factor (CRF), a 41 amino acid-containing peptide, appears to mediate not only the endocrine but also the autonomic and behavioral responses to stress. Stress, in particular early-life stress such as childhood abuse and neglect, has been associated with a higher prevalence rate of affective and anxiety disorders in adulthood. In the present review, we describe the evidence suggesting that CRF is hypersecreted from hypothalamic as well as from extrahypothalamic neurons in depression, resulting in hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis and elevations of cerebrospinal fluid (CSF) concentrations of CRF. This increase in CRF neuronal activity is also believed to mediate certain of the behavioral symptoms of depression involving sleep and appetite disturbances, reduced libido, and psychomotor changes. The hyperactivity of CRF neuronal systems appears to be a state marker for depression because HPA axis hyperactivity normalizes following successful antidepressant treatment. Similar biochemical and behavioral findings have been observed in adult rats and monkeys that have been subjected to early-life stress. In contrast, clinical studies have not revealed any consistent changes in CSF CRF concentrations in patients with anxiety disorders; however, preclinical findings strongly implicate a role for CRF in the pathophysiology of certain anxiety disorders, probably through its effects on central noradrenergic systems. The findings reviewed here support the hypothesis that CRF receptor antagonists may represent a novel class of antidepressants and/or anxiolytics.
Extracellular matrix and cell signalling: the dynamic cooperation of integrin, proteoglycan and growth factor receptor
Tập 209 Số 2 - Trang 139-151 - 2011
Soo‐Hyun Kim, Jeremy E. Turnbull, Scott E. Guimond
Extracellular matrices (ECM) are secreted molecules that constitute the cell microenvironment, composed of a dynamic and complex array of glycoproteins, collagens, glycosaminoglycans and proteoglycans. ECM provides the bulk, shape and strength of many tissues in vivo, such as basement membrane, bone and cartilage. In vitro, most animal cells can only grow when they are attached to surfaces through ECM. ECM is also the substrate for cell migration. However, ECM provides much more than just mechanical and structural support, with implications in developmental patterning, stem cell niches and cancer. ECM imparts spatial context for signalling events by various cell surface growth factor receptors and adhesion molecules such as integrins. The external physical properties of ECM may also have a role in the signalling process. ECM molecules can be flexible and extendable, and mechanical tension can expose cryptic sites, which could further interact with growth factors or their receptors. ECM proteins and structures can determine the cell behaviour, polarity, migration, differentiation, proliferation and survival by communicating with the intracellular cytoskeleton and transmission of growth factor signals. Integrins and proteoglycans are the major ECM adhesion receptors which cooperate in signalling events, determining the signalling outcomes, and thus the cell fate. This review focuses on the emerging concept of spatial cell biology of ECM, especially the current understanding of integrins and heparan sulphate proteoglycans as the essential cellular machineries that sense, integrate and respond to the physical and chemical environmental information either by directly connecting with the local adhesion sites or by regulating global cellular processes through growth factor receptor signalling pathways, leading to the integration of both external and internal signals in space and time.
Adipocytokines in obesity and metabolic disease
Tập 220 Số 2 - Trang T47-T59 - 2014
Haiming Cao
The current global obesity pandemic is the leading cause for the soaring rates of metabolic diseases, especially diabetes, cardiovascular disease, hypertension, and non-alcoholic hepatosteatosis. Efforts devoted to find cures for obesity and associated disorders in the past two decades have prompted intensive interest in adipocyte biology, and have led to major advances in the mechanistic understanding of adipose tissue as an essential endocrine organ. Adipose tissue secretes an array of hormones (adipokines) that signal key organs to maintain metabolic homeostasis, and their dysfunction has been causally linked to a wide range of metabolic diseases. In addition, obesity induces production of inflammatory cytokines (often referred to together with adipokines as adipocytokines) and infiltration of immune cells into adipose tissue, which creates a state of chronic low-grade inflammation. Metabolic inflammation has been increasingly recognized as a unifying mechanism linking obesity to a broad spectrum of pathological conditions. This review focuses on classic examples of adipocytokines that have helped to form the basis of the endocrine and inflammatory roles of adipose tissue, and it also details a few newly characterized adipocytokines that provide fresh insights into adipose biology. Studies of adipocytokines in clinical settings and their therapeutic potential are also discussed.
Angiotensin-converting enzyme 2, angiotensin-(1–7) and Mas: new players of the renin–angiotensin system
Tập 216 Số 2 - Trang R1-R17 - 2013
Robson A.S. Santos, Anderson J. Ferreira, Thiago Verano‐Braga, Michael Bäder
Angiotensin (Ang)-(1–7) is now recognized as a biologically active component of the renin–angiotensin system (RAS). Ang-(1–7) appears to play a central role in the RAS because it exerts a vast array of actions, many of them opposite to those attributed to the main effector peptide of the RAS, Ang II. The discovery of the Ang-converting enzyme (ACE) homolog ACE2 brought to light an important metabolic pathway responsible for Ang-(1–7) synthesis. This enzyme can form Ang-(1–7) from Ang II or less efficiently through hydrolysis of Ang I to Ang-(1–9) with subsequent Ang-(1–7) formation by ACE. In addition, it is now well established that the G protein-coupled receptor Mas is a functional binding site for Ang-(1–7). Thus, the axis formed by ACE2/Ang-(1–7)/Mas appears to represent an endogenous counterregulatory pathway within the RAS, the actions of which are in opposition to the vasoconstrictor/proliferative arm of the RAS consisting of ACE, Ang II, and AT1receptor. In this brief review, we will discuss recent findings related to the biological role of the ACE2/Ang-(1–7)/Mas arm in the cardiovascular and renal systems, as well as in metabolism. In addition, we will highlight the potential interactions of Ang-(1–7) and Mas with AT1and AT2receptors.
Development of a microtitre plate enzyme immunoassay for the determination of progesterone
Tập 101 Số 1 - Trang 41-49 - 1984
Coralie Munro, G. H. Stabenfeldt
ABSTRACT A rapid, solid-phase microtitre plate enzyme immunoassay (EIA) for progesterone is described using progesterone 3-O-carboxymethyloxime–horseradish peroxidase as the label and an antiserum raised in rabbits to a progesterone 11α-hemisuccinyl–bovine serum albumin immunogen. A competitive reaction was used with a reaction time of 2 h. Antibody-bound and free steroid were separated in a simple washing step of the antibody-adsorbed well surface. 2,2′-Azino-di-(3-ethylbenzthiazoline sulphonic acid) diammonium salt was used as the substrate with a reaction time of 1 h. A lower limit of sensitivity of 0·25 pg/well was obtained with the response being linear (logit/log) through 1000 pg/well. Results obtained by EIA and radioimmunoassay in several species gave excellent agreement (r = 0·98). This assay system allows accurate determination of progesterone in plasma with good specificity, precision and accuracy, and is suitable for the rapid assessment of luteal function and reproductive status in both clinical and research situations in a wide variety of species. J. Endocr. (1984) 101, 41–49
Fibroblast growth factor-23 regulates parathyroid hormone and 1α-hydroxylase expression in cultured bovine parathyroid cells
Tập 195 Số 1 - Trang 125-131 - 2007
Tijana Krajisnik, Peyman Björklund, Richard Marsell, Östen Ljunggren, Göran Åkerström, Kenneth B. Jonsson, Gunnar Westin, Tobias E. Larsson
Fibroblast growth factor-23 (FGF23) is a circulating factor that decreases serum levels of inorganic phosphate (Pi) as well as 1,25-dihydroxyvitamin D3. Recent studies also suggest a correlation between serum levels of FGF23 and parathyroid hormone (PTH) in patients with chronic kidney disease. It is, however, unknown whether FGF23 directly modulates PTH expression, or whether the correlation is secondary to abnormalities in Pi and vitamin D metabolism. The objective of the current study was therefore to elucidate possible direct effects of FGF23 on bovine parathyroid cells in vitro. Treatment of parathyroid cells with a stabilized form of recombinant FGF23 (FGF23(R176Q)) induced a rise in early response gene-1 mRNA transcripts, a marker of FGF23 signaling. FGF23(R176Q) potently and dose-dependently decreased the PTH mRNA level within 12 h. In agreement, FGF23(R176Q) also decreased PTH secretion into conditioned media. In contrast, FGF23(R176Q) dose-dependently increased 1α-hydroxylase expression within 3 h. FGF23 (R176Q) did not affect cell viability nor induce apoptosis, whereas a small but significant increase in cell proliferation was found. We conclude that FGF23 is a negative regulator of PTH mRNA expression and secretion in vitro. Our data suggest that FGF23 may be a physiologically relevant regulator of PTH. This defines a novel function of FGF23 in addition to the previously established roles in controlling vitamin D and Pi metabolism.
The intergenerational effects of fetal programming: non-genomic mechanisms for the inheritance of low birth weight and cardiovascular risk
Tập 180 Số 1 - Trang 1-16 - 2004
Amanda J. Drake, Brian R. Walker
Many epidemiological studies in diverse populations have demonstrated a link between low birth weight and subsequent disease. This evidence has given rise to the fetal origins hypothesis, which suggests that exposure of the fetus to an adverse environment in utero leads to permanent programming of tIssue function and a risk of cardiovascular disease. An alternative hypothesis is that low birth weight and adult cardiovascular disease are independent features of a genetic predisposition to cardiovascular disease. This review describes evidence that the programming phenomenon may not be limited to the first generation offspring. Results of human and animal studies identify intergenerational programmed effects on both birth weight and cardiovascular disease. This may represent a mechanism for the non-genetic inheritance of a predisposition to low birth weight and adverse cardiovascular risk across a number of generations.
A METHOD FOR THE DETERMINATION OF URINARY PREGNANEDIOL
Tập 12 Số 3 - Trang 209-219 - 1955
Arnold Klopper, Eileen A. Michie, J. B. Brown
SUMMARY A new chromatographic procedure for determining small amounts of pregnanediol in urine is described. The method involves (1) acid hydrolysis, (2) toluene extraction, (3) a new permanganate oxidation step, (4) chromatography on alumina columns, (5) acetylation, (6) further chromatography on alumina, and (7) colorimetry after developing a colour with sulphuric acid. The method is considered under the headings of specificity, sensitivity, accuracy and convenience. The significance of results obtained from male, proliferative phase female, and post-menopausal urine is discussed.
THE DESTRUCTIVE EFFECT OF CADMIUM ION ON TESTICULAR TISSUE AND ITS PREVENTION BY ZINC
Tập 15 Số 1 - Trang 56-63 - 1957
J Parízek
SUMMARY The subcutaneous administration of cadmium salts (cadmium chloride or lactate) to male rats and mice leads to acute destruction of the testes, with destruction of the seminiferous epithelium and interstitial tissue. These changes in turn evoke castration phenomena, but the atrophied accessory sex organs retain the ability to react to testosterone propionate. Within 20 days after the injection of cadmium, proliferation of fibroblasts in the interstitial spaces under the albuginea begins and is accompanied by an extensive formation of new blood vessels. Later, new Leydig cells appear; this is followed by a gradual return of the endocrine function of the testes. The spermatogenic epithelium of the seminiferous tubules, on the other hand, does not regenerate even 133 days after the injection of cadmium. The simultaneous administration of a large dose of zinc salts protects the testes completely against cadmium damage. The mechanism of interaction between these physico-chemically related metals and the theoretical and practical significance of these observations will be studied further.
Rapid non-genomic effects of corticosteroids and their role in the central stress response
Tập 209 Số 2 - Trang 153-167 - 2011
Femke Groeneweg, Henk Karst, E. R. de Kloet, Marian Joëls
In response to a stressful encounter, the brain activates a comprehensive stress system that engages the organism in an adaptive response to the threatening situation. This stress system acts on multiple peripheral tissues and feeds back to the brain; one of its key players is the family of corticosteroid hormones. Corticosteroids affect brain functioning through both delayed, genomic and rapid, non-genomic mechanisms. The latter mode of action has long been known, but it is only in recent years that the physiological basis in the brain is beginning to be unravelled. We now know that corticosteroids exert rapid, non-genomic effects on the excitability and activation of neurons in (amongst others) the hypothalamus, hippocampus, amygdala and prefrontal cortex. In addition, corticosteroids affect cognition, adaptive behaviour and neuroendocrine output within minutes. Knowledge on the identity of the receptors and secondary pathways mediating the non-genomic effects of corticosteroids on a cellular level is accumulating. Interestingly, in many cases, an essential role for the ‘classical’ mineralocorticoid and glucocorticoid receptors in a novel membrane-associated mechanism is found. Here, we systematically review the recent literature on non-genomic actions of corticosteroids on neuronal activity and functioning in selected limbic brain targets. Further, we discuss the relevance of these permissive effects for cognition and neuroendocrine control, and the integration of this novel mode of action into the complex balanced pattern of stress effects in the brain.