| Effects of macrophage-specific adiponectin expression on lipid metabolism in vivo. | |
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MedLine Citation:
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PMID: 21505149 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Epidemiological studies have associated low circulating levels of the adipokine adiponectin with multiple metabolic disorders, including metabolic syndrome, obesity, insulin resistance, type II diabetes, and cardiovascular disease. Recently, we reported that adiponectin selectively overexpressed in mouse macrophages can improve insulin sensitivity and protect against inflammation and atherosclerosis. To further investigate the role of adiponectin and macrophages on lipid and lipometabolism in vivo, we engineered the expression of adiponectin in mouse macrophages (Ad-TG mice) and examined effects on plasma lipoproteins and on the expression levels of genes involved in lipoprotein metabolism in tissues. Compared with the wild-type (WT) mice, Ad-TG mice exhibited significantly lower levels of plasma total cholesterol (-21%, P < 0.05) due to significantly decreased LDL (-34%, P < 0.05) and VLDL (-32%, P < 0.05) cholesterol concentrations together with a significant increase in HDL cholesterol (+41%, P < 0.05). Further studies investigating potential mechanisms responsible for the change in lipoprotein cholesterol profile revealed that adiponectin-producing macrophages altered expression of key genes in liver tissue, including apoA1, apoB, apoE, the LDL receptor, (P < 0.05), and ATP-binding cassette G1 (P < 0.01). In addition, Ad-TG mice also exhibited higher total and high-molecular-weight adipnection levels in plasma and increased expression of the anti-inflammatory cytokine IL-10 as well as a decrease in the proinflammatory cytokine IL-6 in adipose tissue. These results indicate that macrophages engineered to produce adiponectin can influence in vivo gene expression in adipose tissue in a manner that reduces inflammation and macrophage infiltration and in liver tissue in a manner that alters the circulating lipoprotein profile, resulting in a decrease in VLDL and LDL and an increase in HDL cholesterol. The data support further study addressing the use of genetically manipulated macrophages as a novel therapeutic approach for treatment of cardiometabolic disease. |
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Authors:
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Nanlan Luo; Xiangdong Wang; B Hong Chung; Mi-Hye Lee; Richard L Klein; W Timothy Garvey; Yuchang Fu |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. Date: 2011-04-19 |
Journal Detail:
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Title: American journal of physiology. Endocrinology and metabolism Volume: 301 ISSN: 1522-1555 ISO Abbreviation: Am. J. Physiol. Endocrinol. Metab. Publication Date: 2011 Jul |
Date Detail:
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Created Date: 2011-06-27 Completed Date: 2011-09-06 Revised Date: 2012-04-09 |
Medline Journal Info:
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Nlm Unique ID: 100901226 Medline TA: Am J Physiol Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: E180-6 Citation Subset: IM |
Affiliation:
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Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, Alabama 35294-0012, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adiponectin
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blood,
genetics,
metabolism Adipose Tissue / metabolism Animals Cells, Cultured Cytokines / blood, genetics, metabolism Gene Expression Regulation Glucose / metabolism Inflammation / genetics, metabolism, pathology Lipid Metabolism / genetics*, physiology Lipids / analysis, blood Lipoproteins / analysis, metabolism Liver / metabolism Macrophages, Peritoneal / metabolism*, physiology Mice Mice, Transgenic Organ Specificity / genetics |
| Grant Support | |
ID/Acronym/Agency:
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DK-038764/DK/NIDDK NIH HHS; DK-079626/DK/NIDDK NIH HHS; DK-083562/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Adiponectin; 0/Adipoq protein, mouse; 0/Cytokines; 0/Lipids; 0/Lipoproteins; 50-99-7/Glucose |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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