| Increased Susceptibility to Metabolic Syndrome in Adult Offspring of Angiotensin Type 1 Receptor Autoantibody-Positive Rats. | |
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MedLine Citation:
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PMID: 22304458 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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<b><i>Aims:</b></i> Abnormal fetal and early postnatal growth is closely associated with adult-onset metabolic syndrome (MetS). However, the underlying etiological factors remain complex. Presence of the autoantibody against angiotensin II type 1 receptor (AT1-Ab), a known risk factor for preeclampsia, may create a suboptimal intrauterine fetal environment. The current study investigated whether middle-aged offspring of AT1-Ab-positive mothers were prone to metabolic disorder development. <b><i>Results:</b></i> AT1-Abs were detected in placental trophoblastic cells, capillary endothelium, and milk of pregnant rats actively immunized with the second extracellular loop of the AT1 receptor. AT1-Abs in newborn rats induced vasoconstriction, increased intracellular free Ca<sup>2+</sup> <i>in vitro</i>, and were undetectable 7 weeks later. Immunized group offspring exhibited increased weight variability and insulin resistance at 40 weeks age under normal diet, evidenced by elevated fasting serum insulin and homeostasis model assessment (HOMA) score compared to the vehicle control. To further observe metabolic alterations, offspring were given a high-sugar diet (containing 20% sucrose) 40-48 weeks postnatal. The fasting plasma glucose in immunized group offspring was markedly increased. Concomitantly, these offspring manifested increased visceral adipose tissue, increased fatty liver, increased triglycerides, decreased high-density lipoprotein cholesterol, and decreased adiponectin levels, indicative of metabolic syndrome. <b><i>Innovation:</b></i> AT1-Abs could transfer from mother to offspring via the placenta and milk. Moreover, offspring of AT1-Ab-positive mother were more vulnerable to metabolic syndrome development in middle age. <b><i>Conclusion:</b></i> AT1-Ab-positivity of mothers during pregnancy is a previously unrecognized "silent" risk factor for MetS development in their offspring. |
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Authors:
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Suli Zhang; Xi Zhang; Lihong Yang; Zi Yan; Li Yan; Jue Tian; Xiaoyu Li; Li Song; Li Wang; Xiaoli Yang; Ronghua Zheng; Waynebond Lau; Xin-Liang Ma; Huirong Liu |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-2-5 |
Journal Detail:
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Title: Antioxidants & redox signaling Volume: - ISSN: 1557-7716 ISO Abbreviation: - Publication Date: 2012 Feb |
Date Detail:
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Created Date: 2012-2-6 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100888899 Medline TA: Antioxid Redox Signal Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Shanxi Medical University, Department of Physiology, Taiyuan, Shanxi , China; sueney716@gmail.com. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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