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循环血浆纤维连接蛋白影响小鼠组织胰岛素敏感性、脂肪细胞分化和脂肪组织的转录谱。

Circulating plasma fibronectin affects tissue insulin sensitivity, adipocyte differentiation, and transcriptional landscape of adipose tissue in mice.

机构信息

Faculty of Dental Medicine and Oral Health Sciences (Biomedical Sciences), McGill University, Montreal, Quebec, Canada.

Department of Anatomy and Cell Biology, Faculty of Medicine and Health Sciences, McGill University, Montreal, Quebec, Canada.

出版信息

Physiol Rep. 2024 Jul;12(14):e16152. doi: 10.14814/phy2.16152.

DOI:10.14814/phy2.16152
PMID:39054559
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11272447/
Abstract

Plasma fibronectin (pFN) is a hepatocyte-derived circulating extracellular matrix protein that affects cell morphology, adipogenesis, and insulin signaling of adipocytes in vitro. In this study, we show pFN accrual to adipose tissue and its contribution to tissue homeostasis in mice. Hepatocyte-specific conditional Fn1 knockout mice (Fn1-/-ALB) show a decrease in adipose tissue FN levels and enhanced insulin sensitivity of subcutaneous (inguinal), visceral (epididymal) adipose tissue on a normal diet. Diet-induced obesity model of the Fn1-/-ALB mouse showed normal weight gain and whole-body fat mass, and normal adipose tissue depot volumes and unaltered circulating leptin and adiponectin levels. However, Fn1-/-ALB adipose depots showed significant alterations in adipocyte size and gene expression profiles. The inguinal adipose tissue on a normal diet, which had alterations in fatty acid metabolism and thermogenesis suggesting browning. The presence of increased beige adipocyte markers Ucp1 and Prdm16 supported this. In the inguinal fat, the obesogenic diet resulted in downregulation of the browning markers and changes in gene expression reflecting development, morphogenesis, and mesenchymal stem cell maintenance. Epididymal adipose tissue showed alterations in developmental and stem cell gene expression on both diets. The data suggests a role for pFN in adipose tissue insulin sensitivity and cell profiles.

摘要

血浆纤维连接蛋白 (pFN) 是一种肝细胞衍生的循环细胞外基质蛋白，可影响体外脂肪细胞的细胞形态、脂肪生成和胰岛素信号转导。在这项研究中，我们展示了 pFN 在小鼠脂肪组织中的积累及其对组织稳态的贡献。肝细胞特异性条件性 Fn1 敲除小鼠 (Fn1-/-ALB) 显示脂肪组织 FN 水平降低，并且在正常饮食下，皮下（腹股沟）和内脏（附睾）脂肪组织的胰岛素敏感性增强。Fn1-/-ALB 小鼠的饮食诱导肥胖模型显示体重正常增加，全身脂肪质量正常，脂肪组织储存量正常，循环瘦素和脂联素水平不变。然而，Fn1-/-ALB 脂肪组织中的脂肪细胞大小和基因表达谱发生了显著改变。正常饮食下的腹股沟脂肪组织出现脂肪酸代谢和产热的改变，提示棕色化。增加的 beige 脂肪细胞标志物 Ucp1 和 Prdm16 的存在支持了这一点。在腹股沟脂肪组织中，肥胖饮食导致 Browning 标志物下调，以及反映发育、形态发生和间充质干细胞维持的基因表达变化。在两种饮食下，附睾脂肪组织均显示出发育和干细胞基因表达的改变。数据表明 pFN 在脂肪组织胰岛素敏感性和细胞表型中起作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/d8e9b1ca5558/PHY2-12-e16152-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/1856e54590d2/PHY2-12-e16152-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/371275680804/PHY2-12-e16152-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/4df724c7e8e7/PHY2-12-e16152-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/b938dc4de0f0/PHY2-12-e16152-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/36892e3aafd2/PHY2-12-e16152-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/4ac5b2059c0e/PHY2-12-e16152-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/4b414ab8c333/PHY2-12-e16152-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/e35b26d9d008/PHY2-12-e16152-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/d8e9b1ca5558/PHY2-12-e16152-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/1856e54590d2/PHY2-12-e16152-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/371275680804/PHY2-12-e16152-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/4df724c7e8e7/PHY2-12-e16152-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/b938dc4de0f0/PHY2-12-e16152-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/36892e3aafd2/PHY2-12-e16152-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/4ac5b2059c0e/PHY2-12-e16152-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/4b414ab8c333/PHY2-12-e16152-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/e35b26d9d008/PHY2-12-e16152-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/97f3/11272447/d8e9b1ca5558/PHY2-12-e16152-g004.jpg

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