The open endocrinology journal最新文献

{"title":"Current Knowledge on Growth Hormone and Insulin-Like Growth Factors and their Role in the Central Nervous System: Growth Hormone in Down Syndrome","authors":"Å. Myrelid","doi":"10.2174/1874216501206010103","DOIUrl":"https://doi.org/10.2174/1874216501206010103","url":null,"abstract":"Down syndrome (DS) is a chromosomal disorder associated with short stature and psychomotor delay. Growth hormone (GH) and insulin-like growth factor I (IGF-I) are of interest in DS as the pronounced growth retardation coincides in time when GH becomes essential for growth. Simultaneously mean intelligence quotient (IQ) decreases markedly. There is no evidence of a general GH deficiency in children with DS, but suboptimal endogenous production of GH and selective deficiency of IGF-I have been demonstrated. GH and IGF-I are important brain growth promoting factors. IGF receptors are present in brain cells from foetuses with DS, but there is no information as to whether disturbances of intracerebral GH binding or IGF-I production may contribute to the brain dysfunction in DS. GH therapy normalized growth velocity and improved fine motor performance in young children with DS, but the limited therapy was followed by a marked \"catch-down\" growth and lacked effect on final height. In adolescents with DS treatment with GH during early childhood show some positive late effects, where subjects previously treated had greater head circumference and improved performance regarding cognitive function and motor skills. Few studies have addressed the effect of GH in Down syndrome. Nevertheless, GH has been designated beneficial effects on cognition, energy, mood and behaviour through extensive studies in several other conditions and it is not unlikely that GH may have similar effects in DS. It should be emphasised that even small changes in psychomotor attainment may be of substantial importance in a developmentally delayed population.","PeriodicalId":88751,"journal":{"name":"The open endocrinology journal","volume":"6 1","pages":"103-109"},"PeriodicalIF":0.0,"publicationDate":"2012-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68057217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial - Current Knowledge on Growth Hormone and Insulin-Like GrowthFactors and their Role in the Central Nervous System","authors":"F. Nyberg","doi":"10.2174/1874216501206010001","DOIUrl":"https://doi.org/10.2174/1874216501206010001","url":null,"abstract":"GH mediates most of its effects by releasing insulin-like growth factor-1 (IGF-1) through stimulation of GH receptors (GHR), in particular in the liver. Both GH and IGF-1 are shown to cross the blood-brain barrier (BBB) and affect specific targets for these hormones in the brain. The discovery of GH and IGF-1 receptors in the CNS and their distribution in brain areas associated with the functional anatomy of behavioral effects induced by activation of the somatotrophic axis (GH/IGF-1 axis) has brought up new aspects on the mechanisms underlying beneficial effects seen for the two hormones.","PeriodicalId":88751,"journal":{"name":"The open endocrinology journal","volume":"6 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2012-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68057485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The GH/IGF-1-Axis in Psychopathological Functions","authors":"M. Auer, C. Sievers, H. Schneider, G. Stalla","doi":"10.2174/1874216501206010062","DOIUrl":"https://doi.org/10.2174/1874216501206010062","url":null,"abstract":"Alterations of the somatotropic system as seen in Growth Hormone Deficiency (GHD) or acromegaly can lead to a variety of mental and physical impairments. Especially the prevalence of psychiatric disorders is elevated and cognitive function is impaired. These changes are paralleled by disturbances of the macroscopic brain tissue architecture and may persist despite achievement of biochemical control. On the other hand strong alterations in GH-secretion and impaired regulatory response to exogenous stimulation have been described in a variety of studies investigating the somatotropic feedback-loop in mood disorders. This reciprocal relationship indicates certain effects of this hormone system in the modulation of neuronal function and an involvement in the pathogenesis of psychiatric disorders.","PeriodicalId":88751,"journal":{"name":"The open endocrinology journal","volume":"6 1","pages":"62-67"},"PeriodicalIF":0.0,"publicationDate":"2012-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68057168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence of Daytime Variation of Asymmetric Dimethylarginine: An Intervention Study with Rosiglitazon in Type 2 Diabetes","authors":"M. Carlsson, T. Lindström, F. Nystrom, I. Nilsson, L. Brudin, P. Wanby","doi":"10.2174/1874216501105010014","DOIUrl":"https://doi.org/10.2174/1874216501105010014","url":null,"abstract":"Background: Asymmetric dimethylarginine (ADMA) has in some, but not all studies been associated with insulin resistance (IR). We wanted to challenge the hypothesis that plasma ADMA levels are associated with IR in an intervention study using an insulin sensitizing drug. Another aim of the study was to study daytime ADMA variation and if food intake influence ADMA concentration. Methods: Nine patients with diet treated type 2 diabetes were investigated with daytime profiles of ADMA (8 am-5 pm) before and during treatment with rosiglitazone for 8 weeks. A control group matched for age and sex underwent a similar investigation at baseline. Results: After treatment with rosiglitazone, ADMA (0.63- 0.64 � mmol/L; p=0.26) and homocysteine (10.3 -10.6 � mol/L; p=0.61) concentrations did not change. Postprandial (10 am - 5 pm) ADMA concentrations were 10% higher than fasting morning levels (p=0.006) and this difference was similar for controls and diabetes patients both pre and post treatment with rosiglitazone. Conclusions: Treatment with rosiglitazone aiming to improve insulin sensitivity did not affect ADMA concentration in type 2 diabetes patients. The ADMA daytime variation and the relation to food intake appear to be a novel finding and should be considered in future studies.","PeriodicalId":88751,"journal":{"name":"The open endocrinology journal","volume":"13 1","pages":"14-18"},"PeriodicalIF":0.0,"publicationDate":"2011-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68057411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Subclinic Hypothyroidism on a Basic Primary Healthcare Area","authors":"María del Carmen Neipp López, P. López, J. Montes, J. S. Albero, Ángel Celada Rodríguez, A. Gálvez","doi":"10.2174/1874216501105010008","DOIUrl":"https://doi.org/10.2174/1874216501105010008","url":null,"abstract":"Objective: Assess the prevalence of subclinical hypothyroidism in the general population of an urban health area and describe the main clinical and socio-demographic characteristics of patients with subclinical hypothyroidism. Method: A retrospective descriptive observational study. We reviewed case histories from June 2005 to July 2007. We analysed the following variables: General data: age and gender. Family background: thyroid pathology and other diseases. Personal background: cardiovascular, lung, autoimmunity, gynaeco-obsetric alterations, diabetes, hypertension (HT), dyslipidaemia, obesity, alterations of psychiatric haemotologic pathology, other laboratory data: TSH levels, free T4 levels, presence of antiperoxidase antibodies, total and partial cholesterol levels. Results: The prevalence of our sample of 100 patients enrolled in 8 months was 3.8% with a mean of 4.2% ± 1.3 SD in the general population aged over 14 years, of whom 79 were women and 21 were men. The; 13% were associated with type 2 diabetes mellitus, 23% with HT and 40% with dyslipidaemia. Being overweight or obese revealed a mean of 23%, TSH level in 6.92 � U/ml, range from 4,5 to 18,75� U/ml, while the mean free T4 was 1.16 ± 0.16 ng/ml. Conclusions: The prevalence of subclinical hypothyroidism was 3.8%. It was more frequent in women of a mean age of 46 years. Gynaecologic alternations were reported for 17% of females. The incidence of cardiovascular risk factors was relatively high: 13% with DM, 23% with HBP, 40% with dyslipidaemia and 23% with obesity. There are no common guidelines for subclinical hypothyroidism management. Therefore, the implementation and promotion of action guidelines are required in Primary Health Care.","PeriodicalId":88751,"journal":{"name":"The open endocrinology journal","volume":"5 1","pages":"8-13"},"PeriodicalIF":0.0,"publicationDate":"2011-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68057392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Calcium-Sensing Receptor is Upregulated in Post Myocardial Infarct Hearts and Downregulates ANP Expression in Rat Cardiac Myocytes but is Not Expressed in Rat Cardiac Fibroblasts In Vitro","authors":"R. Jabbari, Sanela Smajilovic, N. Chattopadhyay, S. Haunsø, J. Tfelt‐Hansen","doi":"10.2174/1874216501105010001","DOIUrl":"https://doi.org/10.2174/1874216501105010001","url":null,"abstract":"Recently, several reports demonstrated functional expression of calcium-sensing receptor (CaSR) in the heart. Initial reports found the CaSR to be present in the cardiomyocytes, in contrast a recent report have found the CaSR to be present in sheep fibroblasts of the heart. The calcimimetic drug AMG 073 is a pharmacological (allosteric) modulator of CaSR that is in clinical use for the treatment of hyperparathyroidism. Here, we show that CaSR mRNA levels were up- regulated in the hearts from rats having myocardial infarction (MI) compared to sham operated rats. Furthermore, we found that in rat cardiomyocytes AMG 073 in the presence of extracellular Ca 2+ decreased mRNA levels of atrial natriuretic pre-pro peptide (pre-pro-ANP), which is a marker for cardiac hypertrophy. Surprisingly, CaSR mRNA was not detectable in rat neonatal ventricular fibroblasts (RNVF) by reverse transcriptase PCR. Yet, extracellular calcium exerts a biphasic response in DNA synthesis of RNVFs and AMG 073 seems to suppress DNA synthesis in RNVFs. In addition, calcium and calcimimetic activate MEK/ERK signalling in RNVFs that appears to be independent of CaSR activation. From these results it appears that an additional calcium-sensing mechanism may exist in RNVF. Our findings may be of importance in regards to a potential protective role of calcium and perhaps CaSR against cardiac hypertrophy.","PeriodicalId":88751,"journal":{"name":"The open endocrinology journal","volume":"5 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2011-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68057367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial - Regulation of Postnatal β Cell Mass","authors":"M. Gannon","doi":"10.2174/1874216501004010009","DOIUrl":"https://doi.org/10.2174/1874216501004010009","url":null,"abstract":"Pancreatic cells are responsible for producing all of the insulin required by an organism to maintain glucose homeostasis. Defects in the development, maintenance, or expansion of cell mass can result in diabetes. Current treatments for diabetes primarily focus on replacing insulin (Types 1 and 2 diabetes) and improving cell function (Type 2 diabetes only). However, increasing a patient's own cell mass or preventing cell loss could improve or cure their condition. Currently, efforts are ongoing in several laboratories to differentiate cells from precursor populations and to expand cells in vitro to generate an unlimited supply for transplantation. Theoretically, the same could be done in vivo to regenerate and/or expand a patient's existing cell population. Thus, it is important to understand the molecular regulation of cell mass development, survival, and expansion. cell mass is increased by cell neogenesis (differentiation from precursor cells), cell proliferation, and cell hypertrophy (increased cell size), while cell mass is decreased by cell death and atrophy (decreased cell size). Although it was once thought that cell number did not expand after birth, prevailing evidence now shows that new cells can form throughout life in both rodent models and humans. The primary mechanism by which new cells form during adulthood in the mouse is via proliferation rather than neogenesis, although this is less clear in humans. A reduced cell population at birth may result in fewer cells available to enter the cell cycle later in life, and therefore a reduction in adult cell mass expansion leading to diabetes with age. Under normal circumstances during adulthood, cells are a slowly-renewing population, with steady low levels of proliferation and apoptosis, although cell proliferation normally declines with age. In addition to maintaining cell mass under normal circumstances, an organism must also be able to alter its cell mass in accordance with its requirements for insulin. In states of insulin resistance, such as pregnancy and obesity, cell mass is known to increase, and when compensatory cell mass expansion is inadequate, diabetes ensues. Inherent defects that render cells more susceptible to apoptosis, would also result in a negative balance in cell mass, and could contribute to diabetes risk. This special issue of The Open Endocrinology Journal focuses on our current understanding of the genetics and signaling pathways that augment cell mass and enhance cell survival postnatally. Each of the articles in this issue provides an in-depth review of a different facet of cell …","PeriodicalId":88751,"journal":{"name":"The open endocrinology journal","volume":"4 1","pages":"9-10"},"PeriodicalIF":0.0,"publicationDate":"2010-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68057242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TSC1/TSC2 Signaling in Pancreatic β-Cells","authors":"C. Cras-Méneur, L. Elghazi, Bo Ye, M. Blandino-Rosano, Ernesto Bernal-MiIzrachi","doi":"10.2174/1874216501004010033","DOIUrl":"https://doi.org/10.2174/1874216501004010033","url":null,"abstract":"The Tuberous Sclerosis complex (TSC) integrates metabolic and growth signals. Recent data demonstrate that this pathway is a major player in regulation of metabolism and energy balance. In this review, we will focus on the role of TSC in modulation of -cell mass and function.","PeriodicalId":88751,"journal":{"name":"The open endocrinology journal","volume":"4 1","pages":"33-39"},"PeriodicalIF":0.0,"publicationDate":"2010-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68057269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Control of β -Cell Mass Homeostasis","authors":"M. M. Soundarapandian, Maria L. Nieves, R. Pasquier, Ulrika Bergstrom, M. Atkinson, B. Tyrberg","doi":"10.2174/1874216501004010011","DOIUrl":"https://doi.org/10.2174/1874216501004010011","url":null,"abstract":"Control of  -cell function and mass is tightly linked to glucose homeostasis. Failing  -cells inevitably lead to diabetes. Recently, several contradictory studies have been published arguing against or in favor of various mechanisms controlling  -cell mass regulation. Here we review the literature on control of adult  -cell mass and aim to reconcile thereby the contradictions. We discuss the role of � -cell proliferation and neogenesis, both in mice and man. We also discuss the influence of genetic predisposition on  -cell mass control. We conclude that  -cell generation in the adult human and mouse likely depends on many paths to assure sufficient numbers of  -cells at any given time, thereby balancing mechanisms for negative regulation of  -cell numbers. A simple model with only one pathway does not fit the current literature.","PeriodicalId":88751,"journal":{"name":"The open endocrinology journal","volume":"4 1","pages":"11-22"},"PeriodicalIF":0.0,"publicationDate":"2010-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68057254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glucose Mediated Regulation of Beta Cell Proliferation","authors":"A. García-Ocaña, Laura C. Alonso","doi":"10.2174/1874216501004010055","DOIUrl":"https://doi.org/10.2174/1874216501004010055","url":null,"abstract":"The pancreatic beta cell, as the sole source of circulating insulin, is indispensible for normal glucose metabolism. All forms of diabetes are characterized by insufficient insulin to meet metabolic needs, and inadequate beta cell mass is present in most forms of diabetes. Beta cell regenerative therapies provide one potential avenue for the prevention or cure of diabetes. Study of the pathways and mechanisms involved in endogenous beta cell proliferation can provide important clues to how regeneration occurs. Glucose is one important regulator of beta cell replication. Here we review the published literature investigating the effect of glucose on beta cell proliferation, and then describe the data supporting various known mechanisms of action. First, in vitro studies on fetal and adult beta cells from rodents and humans are reviewed. Next, we review evidence that circulating blood glucose regulates beta cell proliferation in living animals. These studies encompass a variety of in vivo models, including dietary manipulation, partial pancreatectomy, intravenous infusion of glucose, islet transplantation, and studies on diabetic hyperglycemia. Finally, mechanistic studies, both in vitro and in vivo, point to several different mitogenic pathways activated by glucose. Especially prominent are insulin signaling pathway members, glucose metabolism, and glucose impact on signaling by other growth factors. Multiple unanswered questions remain, and are highlighted throughout. With today's technologies we can now address questions first raised in the early 1900s, and hopefully develop new approaches to assuage the devastation of clinical diabetes.","PeriodicalId":88751,"journal":{"name":"The open endocrinology journal","volume":"2 1","pages":"55-65"},"PeriodicalIF":0.0,"publicationDate":"2010-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68057306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}