Adipose HuR protects against diet-induced obesity and insulin resistance.

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 (HuRAKO) mice. As compared with control mice, HuRAKO 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 HuRAKO 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.

• Authors: Jingyuan Li, Li Gong, Shaozhuang Liu, Yujie Zhang, Chunmei Zhang, Mi Tian, Huixia Lu, Peili Bu, Jianmin Yang, Changhan Ouyang, Xiuxin Jiang, Jiliang Wu, Yun Zhang, Qing Min, Cheng Zhang, Wencheng Zhang
• Journal: Nature communications (Nat Commun) Vol. 10 Issue 1 Pg. 2375 (05 30 2019) ISSN: 2041-1723 [Electronic] England
• PMID: 31147543 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• ELAV-Like Protein 1
• ELAVL1 protein, human
• Elavl1 protein, mouse
• Lipase
• PNPLA2 protein, mouse

Topics

• Adipocytes (pathology)
• Adipose Tissue (immunology, metabolism)
• Adipose Tissue, White (immunology, metabolism)
• Animals
• Cell Enlargement
• Diet, High-Fat
• ELAV-Like Protein 1 (genetics, metabolism)
• Fatty Liver (genetics, metabolism, pathology)
• Glucose Intolerance (genetics, metabolism)
• Humans
• Hypercholesterolemia (genetics, metabolism)
• Hypertrophy
• Inflammation (immunology)
• Insulin Resistance (genetics)
• Lipase (genetics, metabolism)
• Metabolic Syndrome (genetics, metabolism)
• Mice
• Mice, Knockout
• Obesity (genetics, metabolism)
• Protein Biosynthesis
• RNA Stability (genetics)
• Subcutaneous Fat (metabolism)