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胰岛素抵抗、糖尿病前期、代谢综合征:每位儿科医生都应该了解什么?

Insulin Resistance, Prediabetes, Metabolic Syndrome: What Should Every Pediatrician Know?

作者信息

Ighbariya Ahmad, Weiss Ram

机构信息

Ruth Rappaport Children's Hospital, Clinic of Pediatrics, Haifa, Israel.

出版信息

J Clin Res Pediatr Endocrinol. 2017 Dec 30;9(Suppl 2):49-57. doi: 10.4274/jcrpe.2017.S005. Epub 2017 Dec 27.

DOI:10.4274/jcrpe.2017.S005
PMID:29280741
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5790325/
Abstract

The Metabolic syndrome describes a clustering of typical cardiovascular risk factors. The syndrome is also known as "Insulin Resistance syndrome" as a substantial part of the pathophysiology is driven by resistance to the metabolic effects of insulin. The major cause of insulin resistance in childhood is a typical lipid partitioning pattern characterized by increased deposition of lipids within insulin responsive tissues, such as the liver and skeletal muscle and within the viscera. This lipid deposition pattern is also associated with infiltration of intra-abdominal tissues with cells of the immune system, inducing systemic, low-grade inflammation typically observed in insulin resistant obese children and adolescents. Several clues derived from a careful history and physical examination, along with a basic laboratory workup, provide clues in regards to risk stratification in obese children.

摘要

代谢综合征描述了一组典型的心血管危险因素。该综合征也被称为“胰岛素抵抗综合征”,因为其病理生理学的很大一部分是由对胰岛素代谢作用的抵抗所驱动的。儿童期胰岛素抵抗的主要原因是一种典型的脂质分布模式,其特征是脂质在胰岛素反应性组织(如肝脏、骨骼肌和内脏)内的沉积增加。这种脂质沉积模式还与免疫系统细胞浸润腹内组织有关,从而引发通常在胰岛素抵抗的肥胖儿童和青少年中观察到的全身性、低度炎症。通过仔细的病史和体格检查以及基本的实验室检查得出的一些线索,为肥胖儿童的风险分层提供了线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e53c/5790325/bdfe65bd4685/JCRPE-09-49-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e53c/5790325/bdfe65bd4685/JCRPE-09-49-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e53c/5790325/bdfe65bd4685/JCRPE-09-49-g4.jpg

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Effects of Dietary Fructose Restriction on Liver Fat, De Novo Lipogenesis, and Insulin Kinetics in Children With Obesity.
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Front Nutr. 2024 Dec 11;11:1475111. doi: 10.3389/fnut.2024.1475111. eCollection 2024.
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