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遗传性、下丘脑性、药物诱导性或多因素严重肥胖儿童和青少年的静息能量消耗和身体成分。

Resting Energy Expenditure and Body Composition in Children and Adolescents With Genetic, Hypothalamic, Medication-Induced or Multifactorial Severe Obesity.

机构信息

Dept. of Pediatrics, div. of Endocrinology, Erasmus MC-Sophia Children's Hospital, University Medical Center Rotterdam, Rotterdam, Netherlands.

Obesity Center CGG, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands.

出版信息

Front Endocrinol (Lausanne). 2022 Jul 11;13:862817. doi: 10.3389/fendo.2022.862817. eCollection 2022.

DOI:10.3389/fendo.2022.862817
PMID:35898454
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9309560/
Abstract

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.

AIM

To 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.

RESULTS

We 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.

摘要

背景

小儿肥胖是一种多因素疾病,可能由下丘脑瘦素-黑素皮质素途径紊乱引起的潜在医学疾病引起,该途径调节饱腹感和能量消耗。

目的

研究和比较有或无潜在医学病因的严重肥胖儿童和青少年的静息能量消耗 (REE) 和身体成分特征。

方法

本前瞻性观察研究纳入了在我们的学术中心接受广泛诊断评估的儿科患者,该评估评估了肥胖的内分泌、非综合征和综合征遗传、下丘脑和药物引起的原因。通过间接量热法评估 REE;通过空气置换体积描记法评估身体成分。计算实测 REE (mREE)与预测 REE (Schofield 方程)之间的比值,REE%,定义为 mREE%≤90%为低 REE,mREE%≥110%为高 REE。此外,使用多元线性回归评估无脂肪质量 (FFM) 对 mREE 的影响。

结果

我们纳入了 292 名患者(146 名[50%]进行了身体成分测量),其中 218 名(75%)患者为多因素肥胖,74 名(25%)有潜在的医学病因:非综合征和综合征遗传(分别为 29 名和 28 名)、下丘脑(10 名)和药物引起的肥胖(7 名)。平均年龄为 10.8±4.3 岁,59%为女性,平均 BMI SDS 为 3.8±1.1,表明严重肥胖。与多因素肥胖(100.5%±12.6)相比,非综合征遗传肥胖的儿童 REE%(107.4%±12.7)较高,而下丘脑肥胖的儿童 REE%(87.6%±14.2)较低(均 p<0.01)。在 9 名假性甲状旁腺功能减退症 1a 型患者中,平均 REE%相似(100.4±5.1)。在所有患者中,60 名(21%)患者的 mREE 降低,69 名(24%)患者的 mREE 升高。调整 FFM 后,与多因素肥胖相比,各亚组潜在病因患者之间的 mREE 无差异(均 p>0.05)。

结论

在本队列中,由于各种病因导致严重肥胖的儿童中,mREE 存在较大的个体间差异。与先前的研究一致,几乎一半的患者的 mREE 降低或升高。这一知识对于个体化治疗非常重要,例如针对降低 mREE 的儿童的个性化饮食和体力活动干预以及考虑影响中枢能量消耗调节的药物治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c416/9309560/f4a266627d72/fendo-13-862817-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c416/9309560/7df9ed69d2d0/fendo-13-862817-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c416/9309560/7f07f5fd872b/fendo-13-862817-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c416/9309560/f4a266627d72/fendo-13-862817-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c416/9309560/7df9ed69d2d0/fendo-13-862817-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c416/9309560/7f07f5fd872b/fendo-13-862817-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c416/9309560/f4a266627d72/fendo-13-862817-g003.jpg

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