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The complement system is linked to insulin resistance in patients with systemic lupus erythematosus
M. García-González1, F. Gómez-Bernal2, J.C. Quevedo-Abeledo3, Y. Fernández-Cladera4, A.F. González-Rivero5, R. López-Mejías6, F. Díaz-González7, M.Á. González-Gay8, I. Ferraz-Amaro9
- Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain.
- Division of Central Laboratory, Hospital Universitario de Canarias, Tenerife, Spain.
- Division of Rheumatology, Hospital Doctor Negrín, Las Palmas de Gran Canaria, Spain.
- Division of Central Laboratory, Hospital Universitario de Canarias, Tenerife, Spain.
- Division of Central Laboratory, Hospital Universitario de Canarias, Tenerife, Spain.
- Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain.
- Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, Spain.
- Division of Rheumatology, IIS-Fundación Jiménez Díaz, Madrid; University of Cantabria, IDIVAL, 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
- Division of Rheumatology, Hospital Universitario de Canarias, Tenerife, and Department of Internal Medicine, University of La Laguna (ULL), Tenerife, Spain. iferrazamaro@hotmail.com
CER16851
2024 Vol.42, N°1
PI 0115, PF 0121
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PMID: 37706313 [PubMed]
Received: 22/05/2023
Accepted : 10/07/2023
In Press: 06/09/2023
Published: 24/01/2024
Abstract
OBJECTIVES:
Systemic lupus erythematosus (SLE) patients more commonly have insulin resistance (IR) than control subjects. Recent studies have revealed that the complement (C) system is not only a mediator of the immune system but is also related to the pathogenesis of atherosclerosis in the general population. Given that the C alteration is a characteristic of SLE, in the present work we set out to analyse if there is a relationship between the C system and IR in patients with SLE.
METHODS:
New generation functional assays of the three pathways of the C system were performed in 225 non-diabetic patients with SLE. In addition, the serum levels of inactive (C1q, C2, C3, C4, factor D), activated (C3a) and regulators (C1 inhibitor and factor H) molecules of the C system were evaluated. Insulin and C-peptide serum levels were measured, and insulin resistance and indices of beta cell function were calculated using the homeostatic model assessment (HOMA). Metabolic syndrome criteria fulfillments were applied. Multivariable linear regression analysis was performed to assess the relationship between C system and IR indices and the presence of metabolic syndrome.
RESULTS:
After adjusting for covariates that included traditional cardiovascular risk factors associated with IR and prednisone, serum C3a and factor H levels were positively related to higher levels of the HOMA2-IR index. Besides, in the multivariable analysis, after adjustment for covariates, serum levels of C1q and C3 associated with a higher odds ratio for the presence of metabolic syndrome.
CONCLUSIONS:
IR and metabolic syndrome are positively and independently related to higher serum levels of some serum C elements in patients with SLE with a predominant role of the alternative pathway elements.
