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Apolipoprotein C3 and beta-cell dysfunction are linked in patients with systemic lupus erythematosus
C. Martín-González1, C. Ferrer-Moure2, J.C. Quevedo-Abeledo3, M.Á. González-Gay4, I. Ferraz-Amaro5
- Division of Internal Medicine, Hospital Universitario de Canarias, Tenerife, and Department of Internal Medicine, University of La Laguna (ULL), Tenerife, Spain.
- Division of Central Laboratory, Hospital Universitario de Canarias, Tenerife, Spain.
- Division of Rheumatology, Hospital Doctor Negrín, Las Palmas de Gran Canaria, Spain.
- Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases; Division of Rheumatology, Hospital Universitario Marqués de Valdecilla, Universidad de Cantabria, Santander, Spain; and Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa. miguelaggay@hotmail.com
- Department of Internal Medicine, University of La Laguna (ULL), Tenerife, and Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain. iferrazamaro@hotmail.com
CER15222
2022 Vol.40, N°11
PI 2032, PF 2037
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PMID: 34936546 [PubMed]
Received: 07/10/2021
Accepted : 15/11/2021
In Press: 22/12/2021
Published: 04/11/2022
Abstract
OBJECTIVES:
Systemic lupus erythematosus (SLE) has been associated with insulin resistance and beta-cell dysfunction. Apolipoprotein C3 (ApoC3) is a component of very low-density lipoproteins. Since ApoC3 has been linked to beta-cell impairment in the general population, in this study we aimed to discover if this lipoprotein is related to glucose homeostasis disturbance in patients with SLE.
METHODS:
One hundred and forty non diabetic patients with SLE who had a glycaemia lower than 110 mg/dl were recruited. Insulin, C-peptide, and ApoC3 were assessed. Insulin resistance and beta-cell function were calculated using the Homeostasis Model Assessment (HOMA2) indices. A multivariable regression analysis was performed to study the relationship of ApoC3 to those molecules and indices adjusting for classical factors associated with insulin resistance that included glucocorticoids.
RESULTS:
In the multivariable regression analysis that included prednisone intake, a significant relation of ApoC3 to C-peptide was found (beta coef. 0.27 [95%CI 0.03–0.51) ng/ml, p=0.030). Similarly, ApoCa3 was associated with higher degree of beta-cell dysfunction (HOMA2-%B) although in this case statistical significance was not achieved (beta coef. 8 [95%CI–1-18], p=0.086). This relationship was not found with serum insulin levels or IR indices. Furthermore, in the univariable analysis, but not after multivariable adjustment, the disease damage score was found to significantly mediate the effect of ApoC3 on circulating C-peptide. and HOMA2-%B.
CONCLUSIONS:
Beta-cell dysfunction and ApoC3 are linked in patients with SLE.
