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Beta-cell function is disrupted in patients with systemic lupus erythematosus

Abstract: Objectives: To investigate how markers of beta-cell secretion (proinsulin-processing metabolites) are expressed in SLE patients and their potential relation to features associated with the disease such as activity or damage. Methods: One hundred and forty-four SLE patients and 69 nondiabetic sex- and age-matched controls were assessed. Beta-cell secretion molecules, as measured by insulin, split and intact proinsulins, and C-peptide levels were analysed in both groups. Multiple regression analysis was performed to compare proinsulin propeptides between groups and to explore the interrelations with SLE features. Analyses were adjusted for glucocorticoid intake and for insulin resistance classic risk factors. Results: Fully multivariable analysis demonstrated that regardless of glucocorticoid use, SLE patients exhibited higher levels of split proinsulin. Likewise, the split proinsulin-to-insulin ratio was upregulated in patients with SLE undergoing glucocorticoid therapy [beta coeficient 0.19 (95% Confidence Interval 0.07, 0.30), P = 0.002] or not [beta coef. 0.09 (95% CI: 0.01, 0.17), P = 0.025]. Similar results were found for the intact proinsulin-to-insulin ratio, although differences were only statistically significant for patients taking glucocorticoids [beta coef. 0.08 (95% CI: 0.03, 0.12), P = 0.001]. SLE damage score was associated with higher serum levels of intact [beta coef. 0.51 (95% CI 0.17, 0.86) pmol/l, P = 0.004] and split proinsulins [beta coef. 1.65 (95% CI 0.24, 3.06) pmol/l, P = 0.022] after multivariable analysis, including disease duration and prednisone use. Conclusion: Among patients with SLE, proinsulin-processing metabolites, a marker of beta-cell disruption, are upregulated compared with matched controls. This disproportionate hyperproinsulinemia can be explained by the damage produced by the disease and occurs independently of prednisone use.

Otras publicaciones de la misma revista o congreso con autores/as de la Universidad de Cantabria

 Fuente: Rheumatology (Oxford) . 2021 Aug 2;60(8):3826-3833

Editorial: Oxford University Press

 Año de publicación: 2021

Nº de páginas: 8

Tipo de publicación: Artículo de Revista

 DOI: 10.1093/rheumatology/keaa874

ISSN: 1462-0324,1462-0332

Url de la publicación: https://www.doi.org/10.1093/rheumatology/keaa874

Autoría

GARCÍA-DORTA, ALICIA

QUEVEDO-ABELEDO, JUAN CARLOS

RUA-FIGUEROA, ÍÑIGO

DE VERA-GONZÁLEZ, ANTONIA M

GONZÁLEZ-DELGADO, ALEJANDRA

MEDINA-VEGA, LILIAN

GONZÁLEZ-RIVERO, AGUSTÍN F

FRANCISCO-HERNÁNDEZ, FELIX