Endocrine developmentPub Date : 2017-01-01Epub Date: 2017-08-15DOI: 10.1159/000475733
Allison C Sylvetsky, Ellen M Conway, Sheetal Malhotra, Kristina I Rother
{"title":"Development of Sweet Taste Perception: Implications for Artificial Sweetener Use.","authors":"Allison C Sylvetsky, Ellen M Conway, Sheetal Malhotra, Kristina I Rother","doi":"10.1159/000475733","DOIUrl":"https://doi.org/10.1159/000475733","url":null,"abstract":"<p><p>Humans have an innate liking for sweetness, which may have an evolutionary basis. Sweetness typically signals the presence of calories and nutrients and thus, universal liking for sweet taste once served to support survival. In the modern food supply, however, sweetness is often delivered via added sugars and sweeteners devoid of other beneficial nutrients. Nonnutritive sweeteners (NNS) provide sweetness with no or few calories, and therefore may offer a potential strategy to maintain food and beverage palatability, while reducing the caloric content. Despite marked increases in NNS use, their metabolic and health effects are not well-characterized, and particularly little is known about their effects when exposure starts early in life. Herein, we critically review existing data on NNS exposure in utero, during lactation, and throughout childhood and adolescence with respect to taste preferences, weight trajectory, and development of chronic disease. We specifically focus on potential mechanisms through which sweetness exposure during early development may affect key metabolic outcomes.</p>","PeriodicalId":72906,"journal":{"name":"Endocrine development","volume":"32 ","pages":"87-99"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000475733","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35327353","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}
Endocrine developmentPub Date : 2017-01-01Epub Date: 2017-08-15DOI: 10.1159/000475726
Martin Wabitsch
{"title":"Gastrointestinal Hormones Induced the Birth of Endocrinology.","authors":"Martin Wabitsch","doi":"10.1159/000475726","DOIUrl":"https://doi.org/10.1159/000475726","url":null,"abstract":"<p><p>The physiological studies by British physiologists William Maddock Bayliss and Ernest Henry Starling, at the beginning of the last century, demonstrated the existence of specific messenger molecules (hormones) circulating in the blood that regulate the organ function and physiological mechanisms. These findings led to the concept of endocrinology. The first 2 hormones were secretin, discovered in 1902, and gastrin, discovered in 1905. Both hormones that have been described are produced in the gut. This chapter summarizes the history around the discovery of these 2 hormones, which is perceived as the birth of endocrinology. It is noteworthy that after the discovery of these 2 gastrointestinal hormones, many other hormones were detected outside the gut, and thereafter gut hormones faded from both the clinical and scientific spotlight. Only recently, the clinical importance of the gut as the body's largest endocrine organ producing a large variety of hormones has been realized. Gastrointestinal hormones are essential regulators of metabolism, growth, development and behavior and are therefore the focus of a modern pediatric endocrinologist.</p>","PeriodicalId":72906,"journal":{"name":"Endocrine development","volume":"32 ","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000475726","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35327357","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}
Endocrine developmentPub Date : 2017-01-01Epub Date: 2017-08-15DOI: 10.1159/000475735
Martin Wabitsch
{"title":"Gastrointestinal Endocrinology in Bariatric Surgery.","authors":"Martin Wabitsch","doi":"10.1159/000475735","DOIUrl":"https://doi.org/10.1159/000475735","url":null,"abstract":"<p><p>The long-lasting weight-reducing effect of bariatric surgical procedures cannot simply be explained by the malabsorption of nutrients and the subsequent energy deficit due to this malabsorption. Clinical studies have shown that the reorganization of the anatomy of the gut and the subsequent alterations of gastrointestinal physiology have a large impact on the secretion and function of gastrointestinal hormones, which regulate hunger and satiety. These changes have been named the BRAVE effect: <under>b</under>ile flow alteration, <under>r</under>eduction of gastric size, <under>a</under>natomical gut rearrangement and altered flow of nutrients, <under>v</under>agal manipulation, and <under>e</under>nteric gut modulation. In addition, the metabolic improvements, for example, increased insulin secretion and improved glucose sensitivity after bariatric surgery cannot simply be explained by the weight loss achieved by the operation. Several metabolic improvements occur directly after bariatric surgery even before significant weight loss has occurred. Clinical studies revealed that the altered gastrointestinal physiology and the postoperative profile of gastrointestinal hormones are responsible for these metabolic alterations. Further insights into the changes of gastrointestinal hormone profiles before and after bariatric surgery may open new ways to prevent the surgical procedure and probably obtain equivalent results by nutraceuticals.</p>","PeriodicalId":72906,"journal":{"name":"Endocrine development","volume":"32 ","pages":"124-138"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000475735","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35327355","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":"Diabetes and Cancer.","authors":"S. Holden","doi":"10.1159/000439410","DOIUrl":"https://doi.org/10.1159/000439410","url":null,"abstract":"Diabetes and cancer are common conditions, affecting 384 million and 33 million people worldwide, respectively. Therefore, there is great potential for overlap, with people with diabetes also developing cancer and vice versa. However, people with diabetes may be at increased risk of developing cancer when compared with the general population. This is due to both shared risk factors associated with the two diseases and the metabolic derangements associated with diabetes, such as hyperglycaemia, insulin resistance, hyperinsulinaemia and oxidative stress. Glucose-lowering therapies may influence the risk of cancer in people with type 2 diabetes due to these therapies' effects on risk factors that are common to both conditions, including hyperglycaemia and obesity, as well as effects that are specific to the class of drug or drugs. Drugs that reduce circulating insulin levels, such as metformin, may reduce cancer risk, and drugs that increase circulating insulin levels, including exogenous insulin and insulin secretagogues, may increase cancer risk. The influence of glucose-lowering therapies on cancer risk may become an important consideration when selecting glucose-lowering therapies to treat people with type 2 diabetes and a high risk of cancer occurrence or recurrence.","PeriodicalId":72906,"journal":{"name":"Endocrine development","volume":"31 1","pages":"135-45"},"PeriodicalIF":0.0,"publicationDate":"2016-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000439410","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64906200","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":"Hypertension and Diabetic Nephropathy.","authors":"Jeppe Skov, J. Christiansen, P. Poulsen","doi":"10.1159/000439393","DOIUrl":"https://doi.org/10.1159/000439393","url":null,"abstract":"Diabetic nephropathy (DN) is a major complication of both type 1 and type 2 diabetes. DN is the most common cause of end-stage renal disease, and it markedly enhances the risk of cardiovascular events. An elevated urinary albumin excretion rate, increased blood pressure (BP), and a continual loss of renal function are characteristics of DN. Screening for microalbuminuria is central to diabetes care, and antihypertensive agents are used for the primary prevention and treatment of DN. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers play central roles and have protective properties beyond their BP-lowering effects. BP control in relation to DN is the main focus of this review, but tight control of the glucose level is equally important. There is an unmet need for new treatment options, and while a few promising candidates exist, their roles in clinical practice have not yet been determined.","PeriodicalId":72906,"journal":{"name":"Endocrine development","volume":"31 1","pages":"97-107"},"PeriodicalIF":0.0,"publicationDate":"2016-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000439393","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64905745","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":"Long-Acting Growth Hormone: An Update.","authors":"P. Saenger, Jorge Mejia-Corletto","doi":"10.1159/000439333","DOIUrl":"https://doi.org/10.1159/000439333","url":null,"abstract":"After the introduction of recombinant human growth hormone (rhGH) in 1985, a myriad of children and adults have benefited from its growth-promoting and metabolic effects. Nowadays, current therapeutic regimens rely on daily subcutaneous GH injections that could be burdensome and inconvenient to pediatric patients. As expected with any long-term parenteral pharmacological treatment, these daily regimens may promote nonadherence, poor compliance, treatment abandonment and/or suboptimal clinical outcomes. In order to improve patient and caregiver acceptance of proposed regimens, simplified dosing schedules could potentially aid in reducing poor compliance and maximize the therapeutic end results. Long-acting GH formulations have been designed and perfected over the last two decades, and currently there are several formulations in advanced stages of research as a reasonable attempt to improve patient's adherence to GH treatment. A long-acting GH preparation allowing for reduced injection frequency is likely to improve treatment adherence and to decrease the distress and inconvenience associated with daily injections. This review presents an update about the status of current and recent efforts that have enabled the formulation of sustained-release, long-acting rhGH as it has been longed for many years in the pediatric endocrinology field.","PeriodicalId":72906,"journal":{"name":"Endocrine development","volume":"30 1","pages":"79-97"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000439333","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64904274","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":"Aromatase Inhibitors in the Treatment of Short Stature.","authors":"M. Hero","doi":"10.1159/000439338","DOIUrl":"https://doi.org/10.1159/000439338","url":null,"abstract":"Reports published in the 1990s of men with estrogen deficiency caused by defective aromatase or estrogen resistance due to a defective estrogen receptor α confirmed the crucial role of estrogen in bone maturation, closure of the epiphyses and cessation of statural growth. Based on these findings, it became reasonable to postulate that selective inhibition of estrogen synthesis with aromatase inhibitors could increase adult height by delaying bone maturation and prolonging the period of growth in males. To date, aromatase inhibitors have been employed in rare pediatric conditions associated with sex steroid excess, and in randomized controlled trials involving boys with short stature and/or constitutional delay of puberty. Findings from these randomized trials suggest that potent aromatase inhibitors increase predicted height, but final adult height data are scarce. Moreover, several safety issues remain inadequately studied. In this paper, published findings on the use of aromatase inhibitors in growth indications are reviewed with emphasis on treatment efficacy and safety.","PeriodicalId":72906,"journal":{"name":"Endocrine development","volume":"30 1","pages":"130-40"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000439338","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64905219","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":"Normal Variation in Pubertal Timing: Genetic Determinants in Relation to Growth and Adiposity.","authors":"R. Willemsen, D. Dunger","doi":"10.1159/000438957","DOIUrl":"https://doi.org/10.1159/000438957","url":null,"abstract":"In humans, there is a considerable variation in age of onset of puberty. Twin studies have indicated that pubertal timing is a highly heritable trait. Recently, a few rare genetic causes of precocious puberty have been reported as well as genetic mutations associated with isolated hypogonadotropic hypogonadism. Genome-wide association (GWA) studies have helped to explore the genetic determinants of the normal variation in pubertal timing, but have been able to explain only 2.7% of the variance in age at menarche, highlighting the involvement of multiple genes with small effect sizes. These studies indicate an overlap of genes involved in pubertal timing and adiposity, and epidemiological data suggest the existence of a pathway of early infancy weight gain, increased height gain in childhood, earlier pubertal timing and increased adiposity in adulthood. This chapter summarises the data from GWA and epidemiological studies on the normal variation in pubertal timing in relation to growth and adiposity. We discuss putative mechanisms linking early life events to pubertal timing, potential short-term and life-course consequences of earlier pubertal timing, and the impact of these data on clinical management of pubertal disorders.","PeriodicalId":72906,"journal":{"name":"Endocrine development","volume":"29 1","pages":"17-35"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000438957","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64900355","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":"Nutritional and Pubertal Disorders.","authors":"M. Teresa Mu�oz-Calvo, Jes�s Argente","doi":"10.1159/000438884","DOIUrl":"https://doi.org/10.1159/000438884","url":null,"abstract":"Caloric-protein malnutrition can slow growth and cause pubertal delay. This chapter focuses on endocrine abnormalities and pubertal alterations in patients with eating disorders, childhood obesity, the female athlete triad and children cancer survivors. Patients with anorexia nervosa (AN) exhibit multiple endocrine abnormalities, including isolated hypogonadotropic hypogonadism. The delay in pubertal development and reduction in growth seen in AN patients may be a direct result of malnutrition. Appropriate psychiatric, nutritional and hormonal therapy is necessary. It is suggested that obesity during childhood can accelerate pubertal onset and these children usually exhibit accelerated linear growth during puberty. In girls the relationship between childhood obesity and early pubertal onset could be related to their insulin resistance and/or hyperinsulinemia. The female athlete triad is often observed in physically active girls and women in whom low energy availability with or without disordered eating, menstrual dysfunction and low bone mineral density can be present. In prepubertal girls excess exercise can cause delayed menarche with no effects on adult height, while in postpubertal females it results in menstrual cycle irregularities. The consequences of childhood cancer depend on the type of cancer, its location, the age at which the disease was diagnosed, the dose of radiotherapy, and the type and dose of chemotherapy.","PeriodicalId":72906,"journal":{"name":"Endocrine development","volume":"29 1","pages":"153-73"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000438884","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64898875","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":"Novel Therapeutic Approaches in Diabetes.","authors":"B. Gallwitz","doi":"10.1159/000439372","DOIUrl":"https://doi.org/10.1159/000439372","url":null,"abstract":"This chapter deals with novel therapeutic approaches, predominantly for type 2 diabetes. Incretin-based therapies utilize the effects of glucagon-like peptide-1 (GLP-1), which stimulates insulin and inhibits glucagon secretion in a glucose-dependent manner. Incretin-based therapies comprise injectable GLP-1 receptor agonists and orally active dipeptidyl peptidase-IV inhibitors. Both have a low hypoglycaemia risk. GLP-1 receptor agonists (exenatide, liraglutide, lixisenatide, dulaglutide, albiglutide) reduce glycated haemoglobin levels more effectively than oral antidiabetic agents do and lead to weight loss as well as a slight decrease in systolic blood pressure. The most common side effects are nausea and fullness, especially during the start of therapy. Dipeptidyl peptidase-IV inhibitors (alogliptin, linagliptin, saxagliptin, sitagliptin, vildagliptin) are not inferior to sulfonylureas, causing significantly less hypoglycaemia and not inducing weight gain. Specific adverse effects have not been discovered yet, and cardiovascular safety has been demonstrated in respective studies. Sodium-glucose transporter-2 inhibitors (dapagliflozin, canagliflozin, empagliflozin) were introduced recently. They block the tubular reabsorption of glucose in the kidney and represent an insulin-independent mode of action, with low hypoglycaemia risk and allowing weight loss. The most common side effects are genital and urinary tract infections. Other novel drugs in development (G-protein-coupled receptor agonists, interleukin-1 antagonists) are also described.","PeriodicalId":72906,"journal":{"name":"Endocrine development","volume":"31 1","pages":"43-56"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000439372","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64905606","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}
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