Suppr超能文献

高脂肪饮食诱导的肥胖和年龄影响小鼠脂肪组织中的端粒庇护复合物和端粒酶基因表达。

High-fat diet induced obesity and age influence the telomere shelterin complex and telomerase gene expression in mouse adipose tissue.

机构信息

Department of Health and Human Physiological Sciences, Skidmore College, Saratoga Springs, NY, USA.

Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA.

出版信息

Physiol Rep. 2020 Jun;8(11):e14461. doi: 10.14814/phy2.14461.

Abstract

Obesity and aging are linked to inflammation and increased risk of chronic disease. Telomeres are the endcaps of chromosomes that are regulated by telomerase, the enzyme that elongates telomeres, as well as a protein complex known as shelterin. Telomere dysfunction is associated with inflammation, aging, and disease. However, the effect of high-fat diet (HFD) induced obesity and advancing age on the shelterin complex and telomerase in adipose tissue is unknown. The present study investigated the effects of obesity and aging on C57BL/6J mice adipose tissue mRNA expression of shelterin complex genes. Young (YG) mice (3 mo) were randomly assigned to be fed either a high-fat diet (YG + HFD; 60% kcal from fat) or a low-fat diet (YG + LFD; 10% kcal from fat). A subset of mice were aged until 16 months. Body weight and epididymal white adipose tissue (EWAT) weight increased with age or a HFD. There was a trend for increased Terf2 expression, as expression was increased in HFD + YG by ~47% and aged mice by ~80%. Pot1b expression was increased in aged mice by ~35%-60% compared to YG, independent of diet. mTert, the gene that codes for the catalytic subunit of telomerase, was significantly elevated in aged mice. Changes in telomere associated gene expression was accompanied by changes in expression of inflammatory markers Mcp1 and Tnfα. These findings suggest obesity and age impact expression of shelterin complex and telomerase related genes in adipose, perhaps altering telomere function in adipose tissue thereby increasing inflammation and risk of chronic disease.

摘要

肥胖和衰老与炎症和慢性疾病风险增加有关。端粒是染色体的末端帽,由端粒酶调节,端粒酶是延长端粒的酶,以及一种称为庇护体的蛋白质复合物。端粒功能障碍与炎症、衰老和疾病有关。然而,高脂肪饮食(HFD)诱导的肥胖和年龄增长对脂肪组织中的庇护体复合物和端粒酶的影响尚不清楚。本研究调查了肥胖和衰老对 C57BL/6J 小鼠脂肪组织庇护体复合物基因 mRNA 表达的影响。年轻(YG)小鼠(3 个月)被随机分配给予高脂肪饮食(YG+HFD;60%的卡路里来自脂肪)或低脂肪饮食(YG+LFD;10%的卡路里来自脂肪)。一部分小鼠被饲养至 16 个月。体重和附睾白色脂肪组织(EWAT)重量随年龄或 HFD 而增加。Terf2 的表达有增加的趋势,HFD+YG 组的表达增加了约 47%,老年小鼠增加了约 80%。与 YG 相比,Pot1b 的表达在老年小鼠中增加了约 35%-60%,与饮食无关。编码端粒酶催化亚基的 mTert 基因在老年小鼠中显著升高。与端粒相关基因表达的变化伴随着炎症标志物 Mcp1 和 Tnfα 表达的变化。这些发现表明,肥胖和年龄会影响脂肪组织中庇护体复合物和端粒酶相关基因的表达,这可能改变脂肪组织中端粒的功能,从而增加炎症和慢性疾病的风险。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa86/7280005/96276f366ded/PHY2-8-e14461-g001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验