000			03138nam a22003737a 4500
008			240723s20242024 xxu||||| |||| 00| 0 eng d
022			_a2472-1972
024			_abvad179 [pii]
024			_aPMC10853002 [pmc]
040			_aOvid MEDLINE(R)
099			_a38333889
245			_aGAD65Abs Are Not Associated With Beta-Cell Dysfunction in Patients With T2D in the GRADE Study.
251			_aJournal of the Endocrine Society. 8(3):bvad179, 2024 Jan 16.
252			_aJ. endocr. soc.. 8(3):bvad179, 2024 Jan 16.
253			_aJournal of the Endocrine Society
260			_c2024
260			_p2024 Jan 16
260			_fFY2024
265			_sepublish
265			_tPubMed-not-MEDLINE
520			_aConclusion: Evidence for islet autoimmunity in the pathophysiology of T2D beta-cell dysfunction is growing, but T1D-associated autoantibodies may not accurately reflect the nature of their autoimmune process. Copyright © The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society.
520			_aContext: Autoantibodies directed against the 65-kilodalton isoform of glutamic acid decarboxylase (GAD65Abs) are markers of autoimmune type 1 diabetes (T1D) but are also present in patients with Latent Autoimmune Diabetes of Adults and autoimmune neuromuscular diseases, and also in healthy individuals. Phenotypic differences between these conditions are reflected in epitope-specific GAD65Abs and anti-idiotypic antibodies (anti-Id) against GAD65Abs. We previously reported that 7.8% of T2D patients in the GRADE study have GAD65Abs but found that GAD65Ab positivity was not correlated with beta-cell function, glycated hemoglobin (HbA1c), or fasting glucose levels.
520			_aContext: In this study, we aimed to better characterize islet autoantibodies in this T2D cohort. This is an ancillary study to NCT01794143.
520			_aMethods: We stringently defined GAD65Ab positivity with a competition assay, analyzed GAD65Ab-specific epitopes, and measured GAD65Ab-specific anti-Id in serum.
520			_aResults: Competition assays confirmed that 5.9% of the patients were GAD65Ab positive, but beta-cell function was not associated with GAD65Ab positivity, GAD65Ab epitope specificity or GAD65Ab-specific anti-Id. GAD65-related autoantibody responses in GRADE T2D patients resemble profiles in healthy individuals (low GAD65Ab titers, presence of a single autoantibody, lack of a distinct epitope pattern, and presence of anti-Id to diabetes-associated GAD65Ab). In this T2D cohort, GAD65Ab positivity is likely unrelated to the pathogenesis of beta-cell dysfunction.
546			_aEnglish
650			_zAutomated
651			_aMedStar Good Samaritan Hospital
657			_aJournal Article
700			_aPark, Jean Y _bMGSH
790			_aHampe CS, Shojaie A, Brooks-Worrell B, Dibay S, Utzschneider K, Kahn SE, Larkin ME, Johnson ML, Younes N, Rasouli N, Desouza C, Cohen RM, Park JY, Florez HJ, Valencia WM, Stempel R, Palmer JP, Balasubramanyam A
856			_uhttps://dx.doi.org/10.1210/jendso/bvad179 _zhttps://dx.doi.org/10.1210/jendso/bvad179
942			_cART _dArticle
999			_c14258 _d14258