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Obesity is currently the most prevalent chronic childhood disease in Western countries. It is one of the most frequent consultations in general pediatrics and is even more common in pediatric endocrinology. As might be predicted, the prevalence of obesity-associated comorbidities is also increasing in children and adolescents. It is widely accepted...
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... Pediatric obesity has become one of the major global health challenges of our time (1). Obesity is a complex, multifactorial disease that is caused by a chronic imbalance between energy intake and expenditure (2). Early-onset severe obesity (defined (3) as an age-and sex-specific BMI corresponding to an adult BMI of ≥35 kg/m 2 with onset before age 5 years) can be caused by underlying medical conditions (4). ...
Background
Pediatric obesity is a multifactorial disease which can be caused by underlying medical disorders arising from disruptions in the hypothalamic leptin-melanocortin pathway, which regulates satiety and energy expenditure.AimTo investigate and compare resting energy expenditure (REE) and body composition characteristics of children and adolescents with severe obesity with or without underlying medical causes.Methods
This prospective observational study included pediatric patients who underwent an extensive diagnostic workup in our academic centre that evaluated endocrine, non-syndromic and syndromic genetic, hypothalamic, and medication-induced causes of obesity. REE was assessed by indirect calorimetry; body composition by air displacement plethysmography. The ratio between measured REE (mREE) and predicted REE (Schofield equations), REE%, was calculated, with decreased mREE defined as REE% ≤90% and elevated mREE ≥110%. Additionally, the influence of fat-free-mass (FFM) on mREE was evaluated using multiple linear regression.ResultsWe included 292 patients (146 [50%] with body composition measurements), of which 218 (75%) patients had multifactorial obesity and 74 (25%) an underlying medical cause: non-syndromic and syndromic genetic (n= 29 and 28, respectively), hypothalamic (n= 10), and medication-induced (n= 7) obesity. Mean age was 10.8 ± 4.3 years, 59% were female, mean BMI SDS was 3.8 ± 1.1, indicating severe obesity. Mean REE% was higher in children with non-syndromic genetic obesity (107.4% ± 12.7) and lower in children with hypothalamic obesity (87.6% ± 14.2) compared to multifactorial obesity (100.5% ± 12.6, both p<0.01). In 9 children with pseudohypoparathyroidism type 1a, mean REE% was similar (100.4 ± 5.1). Across all patients, mREE was decreased in 60 (21%) patients and elevated in 69 (24%) patients. After adjustment for FFM, mREE did not differ between patients within each of the subgroups of underlying medical causes compared to multifactorial obesity (all p>0.05).Conclusions
In this cohort of children with severe obesity due to various etiologies, large inter-individual differences in mREE were found. Consistent with previous studies, almost half of patients had decreased or elevated mREE. This knowledge is important for patient-tailored treatment, e.g. personalized dietary and physical activity interventions and consideration of pharmacotherapy affecting central energy expenditure regulation in children with decreased mREE.
... [7] The pathophysiologic mechanisms of the underlying medical conditions causing obesity are widely varied, leading to the suggestion to talk about "different diseases causing obesity" or "obesities". [8] Establishing an underlying diagnosis can give insight into the clinical course of the obesity, and lead to tailored monitoring and treatment. [9] In addition, it ends the diagnostic odyssey and can reduce the stigma that patients are confronted with. ...
... [10,11] Since pharmacological treatment for patients with genetic defects affecting the leptin-melanocortin pathway (the hypothalamic system that controls appetite and energy expenditure) [11] is currently being evaluated in clinical trials, identifying these diseases becomes even more relevant. [8,12] It is difficult to assess which patients should be evaluated for underlying causes. The current international clinical practice guideline for the evaluation and treatment of pediatric patients with obesity was published in 2017 by the Endocrine Society (ES). ...
Background
Underlying medical causes of obesity (endocrine disorders, genetic obesity disorders, cerebral or medication-induced obesities) are thought to be rare. Even in specialized pediatric endocrinology clinics, low diagnostic yield is reported, but evidence is limited. Identifying these causes is vital for patient-tailored treatment.Objectives
To present the results of a systematic diagnostic workup in children and adolescents referred to a specialized pediatric obesity center.Methods
This is a prospective observational study. Prevalence of underlying medical causes was determined after a multidisciplinary, systematic diagnostic workup including growth charts analysis, extensive biochemical and hormonal assessment and genetic testing in all patients.ResultsThe diagnostic workup was completed in n = 282 patients. Median age was 10.8 years (IQR 7.7-14.1); median BMI +3.7SDS (IQR +3.3-+4.3). In 54 (19%) patients, a singular underlying medical cause was identified: in 37 patients genetic obesity, in 8 patients cerebral and in 9 patients medication-induced obesities. In total, thirteen different genetic obesity disorders were diagnosed. Obesity onset
... genetic forms); 2) continuous and/or rapid weight gain associated with reduced height velocity or short stature; 3) delayed cognitive development; 4) dismorphic features; and 5) use of drugs inducing hyperphagia (i.e. corticosteroids, sodium valproate, risperidone, phenothiazines, ciproeptadine) [13]. ...
The Italian Consensus Position Statement on Diagnosis, Treatment and Prevention of Obesity in Children and Adolescents integrates and updates the previous guidelines to deliver an evidence based approach to the disease. The following areas were reviewed: (1) obesity definition and causes of secondary obesity; (2) physical and psychosocial comorbidities; (3) treatment and care settings; (4) prevention.
The main novelties deriving from the Italian experience lie in the definition, screening of the cardiometabolic and hepatic risk factors and the endorsement of a staged approach to treatment. The evidence based efficacy of behavioral intervention versus pharmacological or surgical treatments is reported. Lastly, the prevention by promoting healthful diet, physical activity, sleep pattern, and environment is strongly recommended since the intrauterine phase.
Electronic supplementary material
The online version of this article (10.1186/s13052-018-0525-6) contains supplementary material, which is available to authorized users.
... Etiology of childhood obesity is multifactorial and includes genetic, neuroendocrine, metabolic, psychological, environmental and socio-cultural factors. Constitutional obesity and mental retardation cooccur in several multiple congenital syndromes, including Prader-Willi (PWS), Bardet-Biedl, Cohen, Albright hereditary osteodystrophy, and Borjeson-Forssman-Lehmann syndrome as well as some rare disorders [6]. Bariatric surgery seems to offer, as in adult population, excellent result in adolescents, gaining progressive consensus in the scientific communities [7][8][9][10]. ...
Introduction:
Childhood obesity is an emerging health problem. Surgical treatment of obese adolescents, particularly those affected by congenital syndrome, represents a controversial issue. The aim of this multicenter study was to retrospectively assess the results of laparoscopic sleeve gastrectomy (LSG) in a cohort of adolescents affected by morbid obesity, with or without congenital syndromes.
Materials and methods:
Forty-one obese (BMI 49 ± 6 kg/m(2)) adolescents with mean age of 16 ± 3 years (58.5% with previous intragastric balloon failure), and subjected to LSG, were retrospectively evaluated for complications rate, % excess weight loss (%EWL), and inhibition of co-morbidities after 2 years of follow-up.
Results:
All the operations were completed laparoscopically and no intra-operative complications were recorded. No mortality was recorded while peri- or post-operative complications only occurred in two patients (4.9%). The EWL% at 6, 12, and 24 months were 42.3, 58.3, and 59.4, respectively. %EWL was comparable (p = 0.7) between non-syndromic and syndromic obese adolescents at 24 months. Conversely patients with previous intragastric balloon surgery had a significant lower EWL (%) at 24 month (p < 0.01). Moreover, at the same time point, co-morbidity resolution rate was 78.2% while improvement rate was 57.6%. Specifically, remission rate of type 2 diabetes (T2DM), hypertension and obstructive sleep apnea (OSA) were 71, 75 and 61%, respectively.
Conclusion:
LSG is advantageous in the treatment of morbidly obese juveniles concerning safety, weight loss and co-morbidity control and at same time presenting, a possible effective therapeutic option for patients affected by congenital syndrome.
Childhood obesity has emerged worldwide, as one of the most important medical and public health problems. The prevalence of obesity has progressively increased during the past 30 years in developed countries including the United States and most European countries. The term obesity refers to an excess of body fat. The body mass index (BMI), is the most widely accepted clinical standard measure of overweight and obesity for children 2 years and older. Childhood obesity is the consequence of an interaction among a complex set of factors that are related to genetics and the environment. It is associated with comorbidities affecting almost every system in the body, including the endocrine, gastrointestinal, pulmonary, cardiovascular, and musculoskeletal systems. The prevention of pediatric obesity by promoting healthy diets, physical activity, and environment should be a primary goal. Several behavioral and pharmacotherapy studies reported modest success. Pharmacotherapy and/or bariatric surgery should be considered in adolescents if there has been no response to structured weight management.
Background:
Development of obesity and its comorbidities is not only the result of excess energy intake, but also of dietary composition. Understanding how hypothalamic metabolic circuits interpret nutritional signals is fundamental to advance towards effective dietary interventions.
Objective:
We aimed to determine the metabolic response to diets enriched in specific fatty acids.
Methods:
Male mice received a diet enriched in unsaturated fatty acids (UOLF) or saturated fatty acids (SOLF) for 8 weeks.
Results:
UOLF and SOLF mice gained more weight and adiposity, but with no difference between these two groups. Circulating leptin levels increased on both fatty acid-enriched diet, but were higher in UOLF mice, as were leptin mRNA levels in visceral adipose tissue. In contrast, serum non-esterified fatty acid levels only rose in SOLF mice. Hypothalamic mRNA levels of NPY decreased and of POMC increased in both UOLF and SOLF mice, but only SOLF mice showed signs of hypothalamic astrogliosis and affectation of central fatty acid metabolism. Exogenous leptin activated STAT3 in the hypothalamus of all groups, but the activation of AKT and mTOR and the decrease in AMPK activation in observed in controls and UOLF mice was not found in SOLF mice.
Conclusions:
Diets rich in fatty acids increase body weight and adiposity even if energy intake is not increased, while increased intake of saturated and unsaturated fatty acids differentially modify metabolic parameters that could underlie more long-term comorbidities. Thus, more understanding of how specific nutrients affect metabolism, weight gain, and obesity associated complications is necessary.
