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Diet induced obesity is independent of metabolic endotoxemia, Tlr4 signalling and hypothalamic inflammation

ChEBI2018-10-23 更新2026-07-12 收录

儿童肥胖代谢

免疫代谢交叉研究

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-MTAB-6929 数据链接链接失效反馈

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资源简介：

Diet induced obesity is independent of metabolic endotoxemia, Tlr4 signalling and hypothalamic inflammation

应用场景：

创建时间：

2018-10-23

儿童肥胖代谢

细胞信号通路

Toll-like receptors/Interleukin-1 receptor (IL-1R) signaling plays an important role in High-fat diet (HFD)-induced adipose tissue dysfunction contributing to obesity-associated metabolic syndromes. H

NIAID Data Ecosystem90

Mus musculus Genome sequencing and assembly

单细胞转录组学

儿童肥胖代谢

Single-cell transcriptomics reveals myeloid-specific PRMT1 deletion-mediated obesity remission and distinct spatiotemporal distributions of cell types in epididymal adipose tissue in a high-fat diet

NIAID Data Ecosystem50

DataSheet_1_The effects of neurogranin knockdown on SERCA pump efficiency in soleus muscles of female mice fed a high fat diet.docx

肌肉钙离子转运调控

儿童肥胖代谢

The sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA) pump is responsible for the transport of Ca2+ from the cytosol into the sarcoplasmic reticulum at the expense of ATP, making it a regulator of both

NIAID Data Ecosystem30

Direct Evidence of Brown Adipocytes in Different Fat Depots in Children

棕色脂肪组织

儿童肥胖代谢

Recent studies suggested the persistence of brown adipocytes in adult humans, as opposed to being exclusively present in infancy. In this study, we investigated the presence of brown-like adipocytes i

NIAID Data Ecosystem60

Circulating incretin levels and microbiome in non-diabetic morbidly obese patients.. Circulating incretin levels and microbiome in non-diabetic morbidly obese patients

儿童肥胖代谢

微生物组

GLP-1 and GLP-2 (GLPs) are intestinal hormones with a key role in the homeostatic regulation of glucose metabolism and food intake. Their secretion by intestinal cells in response to food ingestion is

NIAID Data Ecosystem40

Diet induced obesity is independent of metabolic endotoxemia, Tlr4 signalling and hypothalamic inflammation

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