Thanks to our excellent speakers, we are fortunate in this issue of ESPE News to have
insights into several of the talks you will be able to enjoy at ESPE 2021 Online. On page 6, Ali Abbara and Waljit Dhillo review our
understanding of kisspeptin’s role in puberty, with exciting potential developments in its therapeutic and diagnostic use. Meanwhile, on page 7, Peter Kühnen examines the melanocortin
4 receptor (MC4R) agonist setmelanotide as a treatment option in rare obesity syndromes. He explains the capacity of MC4R agonists to activate
different downstream signalling cascades (‘biased signalling’) and therefore elicit a range of effects. Supporting transgender/gender diverse youth
remains a complex and topical area of healthcare. Stephen Rosenthal discusses the associated issues, which he will address in his forthcoming presentation (page 8).
You can find out more about ESPE 2021
Online at www.eurospe.org/espe2021online.
As always, your contributions will form a central part of the meeting, so please make sure to submit your abstracts by 10 May 2021.
On page 4, we are extremely pleased to have contributions from colleagues in India about their lives in the time of COVID. Researchers
Anuradha Khadilkar and Vandana Jain reflect on the pandemic’s impact on their work with patients and other aspects of their research and daily
lives.The rest of the issue is bursting with the opportunities and support available to you from
ESPE. These extend from grants and committee vacancies to the prospect of future events such as ESPE Schools and the postponed ESPE Science
Symposium. Read on to learn more!We thank all this issue’s contributors for writing for us at such a busy and stressful time.
We wish them, you, and all your families and friends, health and peace in the coming months.
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Translators needed! Could you translate ESPE’s patient information? We are seeking help from ESPE members to translate ESPE patient information booklets into Dutch, French, German and Spanish. The booklets were all reviewed and updated in 2019 by the ESPE Clinical Practice Committee and are currently available in English, at two readability levels. They are a useful resource for clinicians to share with patients, and we want to make them available to as many patients, parents and carers as possible. Find out more at www.eurospe.org/news/item/14203/ Could-you-translate-ESPE’s-patient-information
Visiting Professorship of Rare Diseases The Visiting Professorship provides up to €15 000 to enable mid-career paediatric endocrinologists to make multiple short visits to other centres for collaboration and scientific renewal. Up to four grants are available in 2021. Apply by 15 January 2021 www.eurospe.org/grants-awards/grants/ visiting-professorship IFCAH-ESPE Grants ESPE is pleased to support IFCAH (the International Fund for Congenital Adrenal Hyperplasia). This private fundraising organisation promotes academic research, to improve understanding and management of CAH. ESPE-IFCAH Grants totalling €350 000 will be available in 2021, with selected research projects receiving up to €150 000. Submit letters of intent by 15 January 2021 Find out more at www.eurospe.org/grants-awards/ grants/ifcah-espe-grant Early Career Scientific Development Grant This grant normally finances a short visit to an external institution or a visit by an outside expert to your home institution. While COVID related travel restrictions are in place, it can also be used for a research period of up to 3 months at your home institution. Apply by 31 January 2021 See www.eurospe.org/grants-awards/grants/ early-career-scientific-development-grant ESPE Research Unit Grant This grant supports collaborative high quality research in paediatric endocrinology, for both physicians and scientists. One grant of €100 000 is available to ESPE members and their co-investigators. International collaboration is encouraged. Preliminary application deadline 15 February 2021 Find out more at www.eurospe.org/grants-awards/ grants/research-uni
2021 ESPE Awards We welcome your nominations for the 2021 ESPE Awards. These celebrate and recognise the achievements of ESPE members at all stages of their research and clinical careers, wherever they are in the world.ESPE Award Winners 2020 We congratulate our 2020 ESPE Award winners for their dedication and achievement in the field. Due to the postponement of ESPE Liverpool, we presented the Young Investigator Awards and Hormone Research in Paediatrics Prizes during ESPE Connect Online in November 2020. We will make presentations to our other 2020 award winners, either virtually or in person,
in 2021 Learn more about our winners here www.eurospe.org/2020-award-winners
ESPE Liverpool With the COVID-19 global pandemic still at the forefront of everyone’s minds, the ESPE Liverpool Programme Organising Committee is maintaining a close eye on preparations for next year’s ESPE Annual Meeting. While it is still our hope to be together again in person next May, we understand that this may not be possible, and are investigating all potential options for delivering a safe ESPE Meeting in 2021. It is still our intention for a physical event to take place in Liverpool next year, but we are preparing for all eventualities. For the latest information see www.eurospe.org/espe-liverpool
ESPE COVID-19 hub ESPE has a regularly updated web page dedicated to information related to coronavirus and its impact on paediatric endocrinology. You will find links to ESPE’s own guidance, material from patient support groups, third party published research and ways in which you can contribute to ongoing studies.
Yearbook of Paediatric Endocrinology 2020 This valuable reference tool provides a collection of abstracts summarising the highlights of publications in paediatric endocrinology from the past year. The latest Yearbook of Paediatric Endocrinology, edited by Ken Ong and Ze’ev Hochberg, is now freely available online. See www.espeyearbook.org Yearbook of Paediatric Endocrinology 2020 Editors Ken Ong Ze’ev Hochberg ESPE e-Learning Supporting this issue’s theme: • ‘Molecular-genetic evaluation in childhood obesity’ is a chapter within Obesity in General Content. It includes descriptions of three problem-solving cases. • ‘Obesity in a resource-limited setting’ can be found within Obesity under Resource Limited Countries. It is provided in five languages (English, French, Spanish, Chinese and Swahili). In addition: The following problem-solving cases have been added in General Content: • ‘A case of infantile hypercalcaemia with unusual findings’ and ‘A young boy with abnormal gait’ under Calcium and Bone Metabolism. • ‘Addison’s disease with ptosis of the eyes’ under Multiple Endocrine Deficits. • ‘Ryan, a neonate with a low blood sugar’ under Pituitary. See www.espe-elearning.org. Registration is free of charge.
Bringing you recent highlights from the world of research
New consensus guidelines on pseudohypoparathyroidism (PHP) cover the initial presentation, clinical features and genetic heterogeneity, and have an algorithm for genetic diagnosis. The statement was written by the European Network on Pseudohypoparathyroidism (Euro-PHPnet), which was funded by an ESPE grant. Major features include: parathyroid hormone (PTH) resistance and/or ectopic ossifications and/or early-onset (before 2 years of age) obesity associated with thyrotrophin resistance and/or Albright‘s hereditary osteodystrophy. Minor features include: unexplained primary hypothyroidism, hypercalcitoninaemia, hypogonadism, growth hormone (GH) deficiency, cognitive impairment, hearing impairment, craniosynostosis and neurosurgical features, tooth ankylosis, oligodontia, cataract and/or central nervous system calcifications, sleep apnoea, ear infections, asthma and restricted fetal growth. The guidelines cover management of PTH resistance and hypocalcaemia, which is more problematic during rapid growth, ectopic ossification, skeletal abnormalities, growth and GH deficiency, obesity and metabolic syndrome, and cognitive aspects of PHP, as well as other hormone resistances. They emphasise the need for a life-long multidisciplinary approach with appropriate genetic evaluation. The paucity of strong evidence based data is highlighted. There is a need for registries to collect the longitudinal data, which is key to development of disease
This study examined a cohort comprising 24 232 patients from eight European countries in the SAGhE (Safety and Appropriateness of Growth Hormone Treatments in Europe) Consortium, who were treated with recombinant human growth hormone (r-hGH) during childhood. There were more than 400 000 patient-years of follow-up for the cohort. The authors stated that ‘In low risk patients with isolated GH deficiency or idiopathic short stature, all-cause mortality was not significantly increased (SMR 1.1, 95% CI 0.9–1.3). In children born small for gestational age, all-cause mortality was significantly increased when analysed for all countries (SMR 1.5, CI 1.1–1.9), but this result was driven by the French subcohort. In patients at moderate or high risk, mortality was increased (SMR 3.8, CI 3.3–4.4 and SMR 17.1, CI 15.6–18.7, respectively).’ Mortality was not associated with mean daily or cumulative doses of r-hGH. The authors concluded that all-cause mortality was associated with underlying diagnosis. This is the largest long term mortality follow-up study to date for children treated with r-hGH. One major limitation of the study was the lack of control group
Elder et al. tested six nasal formulations of synacthen in dexamethasone-suppressed healthy volunteers and compared the plasma cortisol levels following the nasal and i.v. formulations. They found one of the formulations (Nasacthin003, 500µg) to demonstrate an equivalent plasma cortisol response to 250μg i.v. synacthen at 60min. Furthermore, it was well tolerated: in 70 doses administered to 22 adults and 24 children, only minor adverse events were described. Paired blood and saliva samples for plasma cortisol and salivary cortisol and cortisone were analysed. The salivary cortisol and cortisone responses in children were similar following administration of Nasacthin003 and i.v. synacthen, but slightly lower in adults. The authors conclude that this test could represent a non invasive alternative to the i.v. synacthen test that would offer the potential for cost savings and a reduced healthcare burden for patients
There is no doubt about the importance of the redox cofactor couple NADH/NAD+ for cellular energy metabolism. Less is known, however, about the causality of changes in NADH/NAD+. Does an altered NADH/NAD+ ratio cause changes in energy metabolism or is it a consequence of metabolic changes? To answer this question, Goodman et al. used a bacterial NAD oxidase that selectively lowers NADH/NAD+ in the cytosol. Circulating α-hydroxybutyrate (αHB), previously linked to insulin resistance and mitochondrial disease, was identified as directly depending on hepatic NADH/NAD+. The strongest genetic determinant in a genetic association study for circulating αHB levels was single nucleotide polymorphisms in the GCKR gene. This encodes glucokinase regulatory protein, which sequesters glucokinase and attenuates hepatic glycolytic flux. The authors found that glucokinase regulatory protein directly influences free cytosolic NADH/NAD+ in the liver. They conclude that increased hepatic NADH/NAD+ or reductive stress is an effector of GCKR, linking genetic variation in GCKR to several metabolic traits, such as circulating triglycerides and fibroblast growth factor 21 levels.
Thomas Reinehr considers the implications for health and
society of obesity amongst adolescents, along with potential
Adolescent obesity carries an immense burden of disease, and results in premature death by several mechanisms (see Table). The classic cardiovascular risk factors associated with obesity (e.g. hypertension, dyslipidaemia and type 2 diabetes mellitus) lead to disease and early death.1 Furthermore, adolescent obesity is associated with many life-limiting types of cancer 10−20 years later, replacing smoking as the leading modifiable cause for cancer.2 However, obesity in adolescence has major implications not only for the affected adolescents but also for society. It is associated with a range of social problems, including difficulties securing an apprenticeship or a job, or finding a partner. Adolescents with obesity are also at increased risk of having children with obesity later in life. Costly consequences All these consequences lead to high costs for the healthcare system. It is clear that obesity in adolescence is associated with increased healthcare use (direct cost). There is an estimated cost per year of approximately US$1400 per additional BMI (body mass index) unit.3 The difference in direct and indirect costs between adults who were normal weight and those who were obese as adolescents has been estimated at ~€9000 annually. Indirect costs are incurred owing to productivity losses, including sick-leave days, long term incapacity, early retirement and premature death. Additionally, adolescents with obesity might be less able to contribute to financing our social system when they are adults, since they are likely to have problems in securing employment. Treatment options Today, we have no approved, effective drugs for adolescents with obesity. In the near future, we will probably not be able
to develop such drugs. Body weight is not regulated by one system and is therefore difficult to modify. Additionally, the regulation of body weight interferes with many other cerebral functions. Centrally active drugs for weight loss, such as rimonabant, have been rejected from the market owing to severe adverse effects such as depression and suicide. Peripherally active drugs in the pipeline focus on gastrointestinal hormones, sympathetic nervous system activity and adipocyte hormones. However, most changes in adipokines and gastrointestinal hormones normalise with weight loss and are characterised by receptor down regulation (as demonstrated for leptin), limiting the effect of such drugs.4 Efficient treatment options are available that have been proven in randomised controlled trials, such as lifestyle interventions for adolescents with obesity and bariatric surgery for adolescents with severe obesity. However, these interventions fail frequently in clinical practice, as most adolescents with obesity do not seek medical care.5 Identifying barriers to treatment is urgently needed. Adherence to treatment Even if we can develop an ideal lifestyle intervention or drug to treat obesity and motivate adolescents, we will have to solve an additional major problem: treatment outcome clearly depends on treatment adherence. Adolescent patients are characterised by low treatment adherence because of their unique developmental, psychosocial and lifestyle issues.6 Adherence generally drops after the first months of therapy. Maintaining adherence to a chronic lifestyle treatment is difficult, as the short term burden of lifestyle change is often more apparent than the long term benefits of therapy. Poor adherence could also be a result of poor education, psychological and emotional problems, or social problems, frequently observed in obese adolescents. Non adherence to treatment also suggests that contact with healthcare professionals has been inadequate. Useful techniques to improve treatment adherence are positive attitude of therapists by avoidance of blaming, focusing on strengths and not on failures, allowing patients to express their concerns and supporting self efficacy as well as using an empathic and non-directive communication style. However, these are time- and staff-consuming and require special education, so it is unsurprising that they are not comprehensively available. Involving peer groups in interventions and use of new media seem promising, but their effectiveness has not been studied in detail. Since adolescent obesity leads to reduced quality of life, many social problems, premature death and immense costs, we must identify and overcome treatment barriers and optimise approaches, even if our current attempts frequently fail. Thomas Reinehr Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany
Members of the EuRRECa Project Team and Rare Obesity Study Group discuss the registries’ uses
By creating a secure, virtual environment for multicentre collaboration, registries allow pooling of data for research and are particularly useful for studying conditions that are rare or have a low prevalence. The endocrine community has a long record of using rare disease registries. A mapping exercise 4 years ago showed that a cross-border registry existed in Europe for about 75% of rare endocrine conditions.1 However, it also highlighted the gaps that existed in coverage of rare endocrine conditions, as well as in awareness of existing registries. The case for the EuRRECa (European Registries for Rare Endocrine Conditions) project was built on these findings. EuRRECa The EuRRECa project (www.eurreca.net) is funded by the EU’s 3rd Health Programme. It launched in 2018 with the primary aim of maximising the opportunity for patients, healthcare professionals and researchers to participate in and use high quality registries. The project includes an e-reporting registry and a core registry that collects a common dataset and clinician- and patient-reported outcomes. EuRRECa works closely with Endo-ERN, ESPE and the European Society of Endocrinology (ESE). The platforms it has developed have also been recently adopted by ERN-BOND (the ERN on Rare Bone Diseases; www.ernbond.eu) and its related registry, EuRR-Bone (www.eurr-bone.com). More recently, EuRRECa also started working with the ESE Rare Disease Committee to map and quantify COVID-19-related morbidity in people with rare endocrine conditions. e-REC e-Reporting of Rare Conditions (e-REC) is an electronic reporting platform designed to allow a better understanding of the occurrence of a wide range of rare endocrine conditions. The platform is open to all centres that work within a clinical or research network. With approximately 5000 new encounters reported by 50 centres from 20 countries since July 2018, the e-REC platform is quickly showing its acceptability within its current user community. For selected conditions, e-REC notification can also be followed by a short secondary survey (www.eurreca.net/ secondary-surveys) that collects clinical data for quality assurance and to understand the clinical presentation of the reported condition.
As e-REC and its related secondary surveys do not collect any personally identifiable information, the ethics and information governance approvals granted to this platform allow users to participate without obtaining patient consent. All data collected by e-REC are only shared with investigators following approval by EuRRECa’s Data Access Committee (DAC) (www.eurreca.net/data-access committee). Core Registry The EuRRECa Core Registry has been operational since June 2019 and is approved for collection of data that are gathered during routine clinical care, which may be shared with approved users to perform or develop new studies. The Core Registry does not collect names, addresses and local hospital numbers, but does collect date of birth. Patients can also alter their preferences, including consent; they can access their own information and can complete generic or condition-specific outcomes. Given the potential to collect a greater amount of information, including some which is personally identifiable, participation in the EuRRECa Core Registry requires patient consent. Patient consent also allows the transfer of data to other disease registries that are approved and recognised as affiliates by EuRRECa. Like e-REC, EuRRECa’s Core Registry is available for use by any endocrine centre, and data supply for research requires approval by the DAC. Rare obesity syndromes Between July 2018 and June 2020 inclusive, 13 centres from 8 countries who have opted to report on rare obesity syndromes on the e-REC platform have reported 47 new cases of Prader−Willi syndrome and Prader−Willi-like syndrome, and 21 cases of other forms of rare obesity syndrome, in children less than 18 years of age. A further 16 cases of Prader−Willi syndrome and Prader−Willi-like syndrome and 2 cases of other forms of rare obesity syndrome have been also been reported at these centres in adults. A study group has formed to look at the initial presentation of these cases through an e-REC secondary survey. This group is also assisting the EuRRECa project by advising on the more detailed disease classification for rare obesity syndromes that are being included in the EuRRECa Core Registry. You can see this classification at www.eurreca.net/data-elements. In summary EuRRECa’s registry platforms are gaining wide acceptability. e-REC is ideally suited for surveillance and feasibility studies; it is agile, versatile and responsive to the needs of the endocrine community. Please participate in EuRRECa activities and use the data to improve the quality of research and healthcare in rare conditions. S Faisal Ahmed, Salma R Ali, Jillian Bryce and I Netchine EuRRECa Project Team Erica LT van den Akker, Hoong W Gan and M Guftar Shaikh EuRRECa Rare Obesity Study Grou
Tom Fleming explains how many diseases can be traced back to an adverse environment at conception, leading to altered embryonic development.
It is commonly thought that the origin of non communicable disease in later life lies either in our unhealthy adult lifestyle or in inheriting a defective parental gene. However, disease risk can be traced back to gestation and, for example, the quality of nutrition provided by mothers. Thus, lower birthweight across the normal range increases cardiometabolic disease susceptibility in adulthood. This concept is known as the developmental origins of health and disease (DOHaD).1 We can now pinpoint the time around conception as possibly the most critical window for environment to influence development and health over a lifetime. This was seen, for example, in the descendants of the Dutch Hunger Winter of the Second World War.2,3 Periconception The period around conception, or periconception (PC), broadly covers the final maturation of male and female gametes, fertilisation and early development of the embryo up to implantation into the endometrium: a few weeks in our lives. Whilst PC is recognised for its reproductive importance and establishment of a viable embryo, it is also when external stimuli can modulate this progression, with enduring consequences. Diverse conditions across mammalian species, including humans, such as poor or over-rich maternal diet or alcohol consumption, similar lifestyle factors in fathers, and the altered in vitro environment experienced by assisted reproduction treatments (ARTs), can all affect PC in a DOHaD context. Adverse environments can change the developmental programme, altering growth, metabolism, gene expression and physiology with remarkable long term outcomes, leading to increased cardiovascular and metabolic syndrome risks and neurological ill-health in adulthood.2−4 Maternal obesity effects Mechanistic understanding of this phenomenon has come largely from controlled animal models, but is supported by evidence from clinical studies. Adverse programming may derive by means of early perturbations to reproductive tissues. Thus, fatty acids and hyperglycaemic metabolites accumulate within ovarian follicular fluid as a result of maternal obesity and high fat diet. These rich nutrients seep into the oocyte and persist in the early embryo, causing metabolic oxidative stress and reducing mitochondrial function and energy production.5,6 Whilst maternal obesity is known to reduce fertility, these cellular consequences also change the metabolic homeostasis of the fetus and offspring, altering the growth trajectory and conferring increased adiposity risk in offspring.7
Maternal undernutrition The PC environment can also induce an adaptive capacity in the embryo to optimise development dependent upon maternal nutrition. Such a strategy permits morphogenesis over the duration of pregnancy to be co-ordinated by local conditions. The converse of obesity, that of maternal protein restriction (a status more commonplace in evolution), acts accordingly. Thus, maternal protein deprivation reduces amino acid availability systemically but also within the uterine lumen, where early developing embryos are bathed before implantation. Here, the embryo has sensing mechanisms to detect selected amino acid levels. It responds to deficiency by activating signalling pathways, driving compensatory processes to form a more efficient placenta and yolk sac, thereby protecting nutrient supply from the mother.9 Health problems materialise if maternal nutrition changes in later pregnancy, causing early adaptations to become unnecessary, resulting in overgrowth, adiposity and increased adult disease risk.2,3 Importance of epigenetics PC programming of an individual’s phenotype requires a ‘biological memory’ of the early environment to persist across the lifespan. This is achieved through the global epigenetic restructuring that occurs soon after fertilisation, and concurrent with the activation of the new embryonic genome. DNA demethylation of paternally and maternally inherited alleles occurs during cleavage of the zygote. It is followed by remethylation of the genome, to co-ordinate the developmental programme, after blastocyst formation and during differentiation of embryonic and extra-embryonic lineages.10 Disturbance or compensatory modification of this delicate process has been demonstrated in response to several PC DOHaD models, leading to persistent (lifetime) change in the pattern and extent of gene expression. One illustration is the relative level of methylation of the rDNA genes, which inversely regulates transcription of rRNA for ribosome biogenesis, to fine-tune protein translation and growth. Here, PC maternal protein restriction activates this epigenetic mechanism to optimise growth across somatic tissues through to adulthood.11 Clinical implications There are significant clinical implications to consider in this field. An ART randomised controlled trial has shown human birthweight varies dependent upon the selection of embryo culture medium some 9 months earlier.12 Children conceived by ART also demonstrate increased cardiometabolic health risks and altered epigenetic status during their life, compared with the naturally conceived population.2,3 Similar datasets using fertile animal models indicate these outcomes are not caused by patient infertility. Clearly, pregnancy needs to be approached with a healthy lifestyle not just for reproductive success but for the well-being of the next generation − no pressure there then. Tom P Fleming School of Biological Sciences, University of Southampton, Southampton, UK
Data from the ESPE Obesity Working Group’s Insulin Resistance Survey were presented at ESPE 2019, in a session entitled ‘Insulin resistance in obese youth: from pathogenic aspects to practical considerations’. The results are currently under review for publication. Here, the Group discusses the background to its work.
The problem of paediatric obesity The obesity epidemic has become one of the most important public health issues of modern times. The prevalence of overweight and obesity has increased globally from 32 million in 1990 to 41 million in 2016.1 The World Obesity Federation (2019) predicted that the number of children aged 5−19 years with obesity in 2030 will be 254 million worldwide.2 Individuals who have obesity during their childhood have a three times higher risk of mortality in early adulthood compared with the general population3 and a 20-fold increased risk of developing type 2 diabetes mellitus (T2DM) before the age of 30.4 T2DM in the young is a devastating disease, with high morbidity and mortality.5,6 Thus, the paediatric obesity epidemic will place a substantial burden on society in the future, contributing to increased morbidity and mortality in adulthood.7 Insulin sensitivity and obesity-related comorbidities Impaired insulin sensitivity appears to be the cornerstone of multiple obesity-related comorbidities that are usually seen in metabolic syndrome clusters, such as dyslipidaemia, hypertension, dysglycaemia, hepatic steatosis and subclinical inflammation, in both adults8 and children.9 It is well known that impaired insulin sensitivity predisposes to an increased risk of developing T2DM and cardiovascular disease,10 and a link between insulin resistance, impaired adipocytokine concentrations and clinical symptoms in obese children has been well documented.11,12 In adolescents and young adults with T2DM, diabetic nephropathy is more prevalent than among matched individuals with type 1 diabetes mellitus, despite lower glycosylated haemoglobin, which may indicate that insulin resistance also directly affects the development of diabetes comorbidities.13 Evaluation of insulin resistance Because of the importance of the assessment of insulin resistance, multiple studies have been conducted in order to ascertain the best determinant of insulin sensitivity. For quantification of whole body insulin sensitivity, the euglycemic hyperinsulinaemic clamp technique has been advocated as the ‘gold standard’.14 Many surrogate
measurements have since been proposed and have found favour, based on practicality and convenience.15−19 One of the most popular measurements is the homeostatic model assessment of insulin resistance (HOMA-IR), which is particularly useful in adults and children.20 Despite this, criticism of the validity of such techniques for the measurement of insulin resistance in children persists.21,22 The Insulin Resistance in Children Consensus Conference Group (2010) concluded that the assessment of insulin resistance in children, its risk factors and the effective strategy for prevention are unknown.23 Furthermore, routine insulin measurement was not recommended by the Endocrine Society when evaluating children or adolescents for obesity.24 However, insulin secretion is affected well before blood glucose concentrations are within the range of prediabetes and diabetes. It is well established that abnormal β-cell function and peripheral insulin resistance are associated with elevated 2-h glucose levels, even within the normal glucose tolerance range, without meeting the criteria for impaired glucose tolerance and impaired fasting glucose.25 Whilst elevated 2-h blood glucose is a strong predictor for the development of T2DM in adults,26 it appears to be less so in paediatric cohorts.27,28 Fasting levels of insulin greater than 15μIU/ml, or insulin peak (post-oral glucose tolerance test, OGTT) levels of more than 150μIU/ml and/or more than 75μIU/ml at 120min of OGTT, are suggestive of insulin resistance in adults.29 Whilst other reference values can be found in the literature, they are not entirely applicable to children. Some age- and sex-specific reference values of insulin, glucose, glycosylated haemoglobin and HOMA-IR for prepubertal children were presented by the IDEFICS (Identification and Prevention of Dietary- and Lifestyle-induced Health Effects in Children and Infants) consortium.30 However, the fact that laboratories use different assays to assess insulin concentrations makes the assessment more challenging. Ethnicity, pubertal development and family history contribute to insulin sensitivity in children.27 However, despite evidence of strong genetic predisposition to the particular insulin sensitivity patterns31 and T2DM,32,33 it is difficult to explain why the incidence of T2DM and prediabetes varies so much between countries with the same ethnicity and epigenetic impact.27,34 ESPE Obesity Working Group activities The ESPE Obesity Working Group initiated the Insulin Resistance Survey to understand how the diagnosis of hyperinsulinaemia and insulin resistance is made in different hospitals in several countries, and what the cut offs for hyperinsulinemia and insulin resistance are for local practice (manuscript in revision). We thank all survey participants. It was revealed that there is no exact standard for evaluation of insulin resistance and OGTT in EU or non-EU centres. We welcome further support of our Working Group activities. You can contact us via tatyana.chaychenko@ gmail.com.
ESPE Connect Online in November attracted more than 5000 attendees from over 120 countries across its 9 days. The virtual content proved hugely popular amongst all of you who joined us; we thank you for taking part
Attendees enjoyed 12 symposia on a wide range of topics, with live Q&A sessions. There were also plenty of Hot Topic, ‘How Do I…?’ and Yearbook sessions, as well as 2 Personal Opinion Future Research talks and 6 diverse industry-sponsored satellite symposia. The Hot Topic sessions included 2 from the winners of the Hormone Research in Paediatrics Prizes, and there were also presentations by the 2 Young Investigator Award recipients. We are grateful to the delegates, speakers, Programme Organising Committee and corporate sponsors who helped to make ESPE Connect Online 2020 a resounding success. We hope you all found the scientific content as insightful and inspiring as we did. Don’t forget Registered delegates can access all of the presentations free of charge until November 2021. This means you can revisit the talks you found useful or catch up on sessions you might have missed, at a time that suits you. What’s more, you can still download the official ESPE Connect Online app from Google Play or the Apple Store, so you can make the most of all the scientific content on-the-go
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