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GLP1 targets lncRNA Gas5 in diabetic adipocytes
Author(s) -
Lui Ashley,
Kraja Gearta,
Rupani Rea,
Bader Deena,
Patel Niketa
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.476.14
Subject(s) - gas5 , metformin , insulin , endocrinology , type 2 diabetes , downregulation and upregulation , medicine , diabetes mellitus , receptor , glucagon like peptide 1 , insulin receptor , population , pharmacology , chemistry , insulin resistance , biochemistry , gene , long non coding rna , environmental health
Diabetes type 2 affects 10% of the US population whereas 80% of patients affected are insulin resistant. We previously showed that lncRNA Gas5 was downregulated in the serum of T2DM patients. Here we sought to investigate the underlying molecular mechanisms of Gas5. Our data shows that Gas5 is down regulated in type II diabetic adipocytes and their secretome. Depletion of Gas5 in non‐diabetic adipocytes resulted in decreased glucose uptake. Using an unbiased diabetes transcriptomics screen, we demonstrated that this reduction of Gas5 resulted in a decrease of both insulin receptors A and B. Glucagon‐Like Peptide‐1 mimetics are new therapeutics available for diabetic patients and have recently been seen as the leading treatment for patients who are no longer responsive to metformin. Our data has shown treatment with GLP‐1 in adipocytes results in an increase in Gas5 resulting in an increase in glucose uptake. Gas5 has been recognized as a biomarker for T2DM, but this is the first time it has been studied mechanistically in adipocytes and researched as a therapeutic target. Support or Funding Information VAMR This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .