Fig 1: Ridge trace curve of the association between Ln UACR, OC, and the clinical parameters. (A–C) y = Ln UACR as dependent variables in all (A), male (B), and post-menopausal female (C) patients, and x1–x7 = OC, ADPN, P1NP, ß-CTx, Ln HbA1c, Ln miR-154-5p, and CTGF as the independent variables, respectively; (D–F) y = OC as dependent variables in all (D), male (E), and post-menopausal female (F) patients, and x1–x7 = Ln UACR, ADPN, P1NP, ß-CTx, Ln HbA1c, Ln miR-154-5p, and CTGF as the independent variables, respectively. UACR, urinary albumin excretion rate; HbA1c, glycated hemoglobin A1c; ADPN, adiponectin; P1NP, procollagen type 1 N-terminal propeptide; ß-CTx, ß-C-terminal telopeptide of type I collagen; CTGF, connective tissue growth factor; OC, osteocalcin.
Fig 2: Scatter dot plots between OC and (A) Ln UACR, (B) Ln HbA1c, (C) ADPN, (D) P1NP, (E) ß-CTx, (F) CTGF, (G) Ln miR-154-5p. UACR, urinary albumin excretion rate; HbA1c, glycated hemoglobin A1c; ADPN, adiponectin; P1NP, procollagen type 1 N-terminal propeptide; ß-CTx, ß-C-terminal telopeptide of type I collagen; CTGF, connective tissue growth factor; OC, osteocalcin.
Fig 3: Scatter dot plots between Ln UACR and (A) Ln miR-154-5p, (B) Ln HbA1c, (C) ADPN, (D) P1NP, (E) ß-CTx, (F) CTGF, (G) OC. UACR, urinary albumin excretion rate; HbA1c, glycated hemoglobin A1c; ADPN, adiponectin; P1NP, procollagen type 1 N-terminal propeptide; ß-CTx, ß-C-terminal telopeptide of type I collagen; CTGF, connective tissue growth factor; OC, osteocalcin.
Fig 4: Scatter dot plots between Ln miR-154-5p and (A) Ln UACR, (B) Ln HbA1c, (C) ADPN, (D) P1NP, (E) ß-CTx, (F) CTGF, (G) OC. UACR, urinary albumin excretion rate; HbA1c, glycated hemoglobin A1c; ADPN, adiponectin; P1NP, procollagen type 1 N-terminal propeptide; ß-CTx, ß-C-terminal telopeptide of type I collagen; CTGF, connective tissue growth factor; OC, osteocalcin.
Fig 5: Effect of biological drugs. Insulin resistance influence in the therapy response(A) ? DAS28 in insulin resistance RA patients compared with insulin sensitivity RA patients after six months of treatment with biologicals (n = 67).(B) HOMA-IR levels at baseline in responders and non-responder RA patients (n = 67).(C) Insulin levels at baseline in responder and non-responder RA patients (n = 67).(D) Glucose levels at baseline in responder and non-responder RA patients (n = 123).(E) Visfatin levels at baseline in responder and non-responder RA patients (n = 123).(F) Vaspin levels at baseline in responder and non-responder RA patients (n = 123).(G) Effect of anti-CD20 therapy on the ACPAs titers and the adipocytokine profile after six months of treatment (n = 56).(H) Effect of anti-TNF-a therapy on the ACPAs titers and the adipocytokine profile after six months of treatment (n = 45).(I) Effect of the anti-IL6R therapy on the ACPAs titers and the adipocytokine profile after six months of treatment (n = 22). DAS28: disease activity score 28; HOMA-IR: homeostatic model assessment-insulin resistance; IR: insulin resistance; IS: insulin sensitivity; ns: non-significant; ACPAs: anti-bodies to citrullinated protein antigens; Resp: responder; TNF-a: tumor necrosis factor alpha: IL: interleukin; IL-6R: interleukin 6 receptor; CD: cluster differentiation; ADIPOQ: adiponectin. Significance was determined by t-test or Mann–Whitney rank-sum test for unpaired groups. t-test or Wilcoxon matched-pairs signed rank test were used for paired groups. *Significant differences vs baseline, p < 0.05. **Significant differences vs baseline, p < 0.01. ***Significant differences vs baseline, p < 0.001. Data are represented as mean ± SEM.
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