Adipose HuR protects against diet-induced obesity and insulin resistance.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 31147543.
- Also identified by DOI 10.1038/s41467-019-10348-0 and PMC identifier 6542850.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Human antigen R (HuR) is a member of the Hu family of RNA-binding proteins and is involved in many physiological processes. Obesity, as a worldwide healthcare problem, has attracted more and more attention. To investigate the role of adipose HuR, we generate adipose-specific HuR knockout (HuR<sup>AKO</sup>) mice. As compared with control mice, HuR<sup>AKO</sup> mice show obesity when induced with a high-fat diet, along with insulin resistance, glucose intolerance, hypercholesterolemia and increased inflammation in adipose tissue. The obesity of HuR<sup>AKO</sup> mice is attributed to adipocyte hypertrophy in white adipose tissue due to decreased expression of adipose triglyceride lipase (ATGL). HuR positively regulates ATGL expression by promoting the mRNA stability and translation of ATGL. Consistently, the expression of HuR in adipose tissue is reduced in obese humans. This study suggests that adipose HuR may be a critical regulator of ATGL expression and lipolysis and thereby controls obesity and metabolic syndrome.
Medical subject headings
- Adipose Tissue, White
- ELAV-Like Protein 1
- Glucose Intolerance
- Hypercholesterolemia
- Insulin Resistance
- Lipase
- Obesity