Breast feeding, obesity, and asthma association: clinical and molecular views.

Q2 Medicine
Naghmeh Kian, Alireza Bagheri, Fardis Salmanpour, Afsaneh Soltani, Zahra Mohajer, Noosha Samieefar, Behzad Barekatain, Roya Kelishadi
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引用次数: 1

Abstract

Asthma is a chronic condition that affects children worldwide. Accumulating number of studies reported that the prevalence of pediatric obesity and asthma might be altered through breastfeeding. It has been proposed that Leptin, which exists in human milk, is oppositely associated with weight increase in newborns. It may also influence peripheral immune system by promoting TH1 responses and suppressing TH2 cytokines. Leptin influences body weight and immune responses through complex signaling pathways at molecular level. Although previous studies provide explanations for the protective role of breastfeeding against both obesity and asthma, other factors such as duration of breastfeeding, parental, and prenatal factors may confound this relationship which requires further research.

Abstract Image

母乳喂养、肥胖和哮喘的关联:临床和分子观点。
哮喘是一种影响全世界儿童的慢性疾病。越来越多的研究报告称,母乳喂养可能会改变儿童肥胖和哮喘的患病率。有人提出,母乳中存在的瘦素与新生儿体重增加相反。它还可能通过促进TH1反应和抑制TH2细胞因子来影响外周免疫系统。瘦素通过分子水平上复杂的信号通路影响体重和免疫反应。尽管先前的研究解释了母乳喂养对肥胖和哮喘的保护作用,但母乳喂养的持续时间、父母和产前因素等其他因素可能会混淆这种关系,需要进一步研究。
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来源期刊
Clinical and Molecular Allergy
Clinical and Molecular Allergy Medicine-Immunology and Allergy
CiteScore
8.20
自引率
0.00%
发文量
11
审稿时长
13 weeks
期刊介绍: Clinical and Molecular Allergy is an open access, peer-reviewed, online journal that publishes research on human allergic and immunodeficient disease (immune deficiency not related to HIV infection/AIDS). The scope of the journal encompasses all aspects of the clinical, genetic, molecular and inflammatory aspects of allergic-respiratory (Type 1 hypersensitivity) and non-AIDS immunodeficiency disorders. However, studies of allergic/hypersensitive aspects of HIV infection/AIDS or drug desensitization protocols in AIDS are acceptable. At the basic science level, this includes original work and reviews on the genetic and molecular mechanisms underlying the inflammatory response.
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