Cell death and inflammation during obesity: "Know my methods, WAT(son)"

Obesity is a state of low-grade chronic inflammation that causes multiple metabolic diseases. During obesity, signalling via cytokines of the TNF family mediate cell death and inflammation within the adipose tissue, eventually resulting in lipid spill-over, glucotoxicity and insulin resistance. Thes...

Full description

Saved in:
Bibliographic Details
Published in:Cell death and differentiation Vol. 30; no. 2; pp. 279 - 292
Main Authors: Hildebrandt, Ximena, Ibrahim, Mohamed, Peltzer, Nieves
Format: Journal Article
Language:English
Published: England Nature Publishing Group 01.02.2023
Subjects:
Adipocytes
Adipose tissue
Adipose Tissue - metabolism
Apoptosis
Body fat
Cell Death
Cytokines
Diabetes
Energy
Energy balance
Gene expression
Genomics
Glucose
Glucose tolerance
Homeostasis
Humans
Hyperplasia
Inflammation
Inflammation - metabolism
Insulin
Insulin Resistance
Intolerance
Kinases
Lipids
Metabolic disorders
Metabolic syndrome
Nuclear Family
Obesity
Obesity - metabolism
ISSN:1350-9047, 1476-5403, 1476-5403
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Obesity is a state of low-grade chronic inflammation that causes multiple metabolic diseases. During obesity, signalling via cytokines of the TNF family mediate cell death and inflammation within the adipose tissue, eventually resulting in lipid spill-over, glucotoxicity and insulin resistance. These events ultimately lead to ectopic lipid deposition, glucose intolerance and other metabolic complications with life-threatening consequences. Here we review the literature on how inflammatory responses affect metabolic processes such as energy homeostasis and insulin signalling. This review mainly focuses on the role of cell death in the adipose tissue as a key player in metabolic inflammation.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ObjectType-Review-3
content type line 23
ISSN:1350-9047
1476-5403
1476-5403
DOI:10.1038/s41418-022-01062-4