Apolipoprotein C-III is linked to the insulin resistance and beta-cell dysfunction that are present in rheumatoid arthritis
Candelaria Martín‐González, Tomás Martín-Folgueras, Juan Carlos Quevedo-Abeledo, Antonia de Vera-González, Alejandra González‐Delgado, Laura de Armas‐Rillo, Miguel Á. González‐Gay, Iván Ferraz‐Amaro
Abstract
BACKGROUND: Insulin resistance and beta-cell dysfunction are manifestations of rheumatoid arthritis (RA). Apolipoprotein C-III (ApoC3) has been associated with such insulin resistance and beta-cell dysfunction in the general population. Our purpose was to study whether ApoC3 is also related to the insulin resistance and beta-cell dysfunction that are present in patients with RA. METHODS: Three hundred thirty-eight non-diabetic patients with RA who had a glycemia 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 with those molecules and indices adjusting for classic factors associated with insulin resistance that included glucocorticoids. RESULTS: ApoC3 was related to significant higher levels of circulating insulin (beta coef. 0.37 [95%CI 0.01-0.73] µU/ml, p = 0.044) and C-peptide (beta coef. 0.13 [95%CI 0.05-0.22] ng/ml, p = 0.003), and higher insulin resistance -HOMA2-IR- (beta coef. 0.05 [95%CI 0.00-0.09], p = 0.041) and beta-cell dysfunction -HOMA2-%B- (beta coef. 2.94 [95%CI 0.07-5.80], p = 0.044) indices. This was found after a fully multivariable analysis that included, among others, prednisone intake and the classic factors associated with carbohydrate metabolism such as triglycerides, waist circumference, and obesity. CONCLUSION: ApoC3, insulin resistance, and beta-cell dysfunction are independently associated in patients RA.