Suppr超能文献

急性分子机制对肠系膜脂肪组织中的进食和膳食成分的反应。

Acute molecular mechanisms responsive to feeding and meal constitution in mesenteric adipose tissue.

机构信息

Functional Genomics Laboratory, Department of Anatomy and Physiology, Molecular Endocrinology and Oncology Research Center, Laval University Medical Center, Laval University, Québec, Quebec, Canada.

出版信息

Obesity (Silver Spring). 2010 Feb;18(2):410-3. doi: 10.1038/oby.2009.257. Epub 2009 Aug 20.

Abstract

To identify the acute effects of feeding on mesenteric fat, we have performed a transcriptomic study in the mesenteric adipose tissue after low-fat (LF) and high-fat (HF) meal ingestion. After fasting, one group of mice was killed and the others were fed ad libitum with HF or LF meal, and killed 3 h after the ingestion. Serial analysis of gene expression (SAGE) was performed, generating approximately 150,000 tags/sample. The results were confirmed using quantitative real-time PCR (qRT-PCR). Transcripts involved in lipid biosynthesis were upregulated only by LF meal, whereas intracellular lipid catabolism was repressed by feeding. Apoptotic genes were downregulated, whereas antiapoptosis and proteolysis were upregulated by feeding. The expression levels of genes coding for adiponectin and ribosomal proteins were decreased by HF meal, as well as transcripts involved in mRNA processing, cytoskeleton, and extracellular matrix. Several other fat-responsive genes were identified, including diverse uncharacterized transcripts. These results revealed that mesenteric adipose tissue transcriptome was responsive to food intake and was affected differently according to meal constitution. The identification of uncharacterized transcripts regulated by LF and HF meals is a first step toward further understanding the early mechanisms of diet-induced obesity as well as discovering new therapeutic targets for obesity-related diseases.

摘要

为了研究进食对肠系膜脂肪的急性影响,我们在进食低脂(LF)和高脂(HF)餐后对肠系膜脂肪组织进行了转录组学研究。禁食后,一组小鼠被处死,其余小鼠自由进食 HF 或 LF 餐,并在进食后 3 小时处死。进行了基因表达序列分析(SAGE),每个样本生成约 150,000 个标签。使用定量实时 PCR(qRT-PCR)对结果进行了验证。仅 LF 餐可上调参与脂质生物合成的转录物,而进食则抑制细胞内脂质分解。凋亡基因下调,而进食可上调抗凋亡和蛋白水解。HF 餐还可下调编码脂联素和核糖体蛋白的基因以及涉及 mRNA 处理、细胞骨架和细胞外基质的转录物的表达水平。还鉴定了其他一些脂肪反应基因,包括各种未鉴定的转录物。这些结果表明,肠系膜脂肪组织的转录组对食物摄入有反应,并且根据膳食组成而受到不同的影响。鉴定 LF 和 HF 餐调节的未鉴定转录物是进一步了解饮食诱导肥胖的早期机制以及发现肥胖相关疾病新的治疗靶点的第一步。

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