The aim is to assess metabolic disturbance in early rheumatoid arthritis patients and its relation to the clinical characteristics of patients. Forty recently diagnosed untreated rheumatoid arthritis (RA) patients with disease duration less than 1 year (group I) along with age- and sex-matched forty healthy volunteers who served as controls (group II) were studied. Disease activity score was used to assess disease activity. Blood pressure, BMI, glucose, insulin and complete lipid profile, visfatin, and adiponectin were measured. Insulin resistance (IR) was estimated by the homeostasis model assessment for insulin resistance (HOMA-IR). Beta-cell function was estimated by the homeostasis model assessment (HOMA-B). Also, rheumatoid factor, anticyclic citrullinated peptide antibodies were measured. Group I had significantly higher fasting insulin, HOMA-(IR, B), visfatin, lipid profile (except HDL), and lower adiponectin versus group II (p = 0.000). There were significant positive correlations between visfatin and the following biochemical parameters: insulin, HOMA-IR, HOMA-B, cholesterol, triglycerides, LDL-C (p = 0.05, 0.029, 0.005, 0.001, 0.002, 0.045, respectively). Also, the disease activity score was positively correlated with visfatin (p = 0.003). Meanwhile, there were significant negative correlations between adiponectin and the following biochemical parameters: insulin, HOMA-IR, HOMA-B, cholesterol, triglycerides, LDL-C, visfatin (p = 0.031, 0.023, 0.001, 0.000, 0.000, 0.016, 0.000, respectively). Also, the disease activity score was negatively correlated with adiponectin (p = 0.001). The findings of the present study showed that recently diagnosed untreated RA patients are characterized by a severe metabolic disturbance state that is driven primarily by disease activity.

Non-alcoholic fatty liver disease (NAFLD) is related to metabolic syndrome via insulin resistance, where preventing disease progression is crucial in the management process. The study included 240 NAFLD patients with type 2 diabetes who were randomly allocated into empagliflozin 25 mg (EMPA group), ursodeoxycholic acid 250 mg (UDCA group), or the control group (placebo). The study outcomes included: changes in liver fat content (LFC; %) (utilizing the Dixon-based MRI-PDFF approach), liver enzymes, lipid and glycemic profiles, FIB-4 index, and non-alcoholic fatty liver score (NFS). All endpoints were assessed at baseline and after 6 months. EMPA outperformed UDCA and placebo in decreasing LFC (−8.73% vs. −5.71% vs. −1.99%; p < 0.0001). In post-treatment ultrasound images and MRI-PDFF calculations, more patients had normal fatty liver grade (no steatosis or LFC < 6.5%) with EMPA compared to UDCA. EMPA and UDCA showed significant regression in the FIB-4 index (−0.34 vs. −0.55; p = 0.011) and NFS scores (−1.00 vs. −1.11; p = 0.392), respectively. UDCA achieved higher reductions in insulin resistance than EMPA (p = 0.03); however, only EMPA significantly increased beta-cell function (54.20; p = 0.03). When exploring the differences between the two drugs, EMPA was better in decreasing LFC (%), while UDCA achieved higher reductions in liver fibrosis scores. Both showed a similar safety profile in managing liver steatosis.

Background and objectives Nesfatin-1 as a potent anorexigenic peptide is secreted by pancreatic β cells. Conflicting data are available about its level among diabetic patients. Our study aimed to assess nesfatin-1 levels in newly diagnosed drug-naïve diabetic and pre-diabetic patients and its association with cardio-metabolic risk and insulin resistance (IR). This case-control study included drug-naive patients with DMT2 (group 1, n = 30) and pre-diabetes (group 2, n = 30) in addition to healthy subjects (group 3, n = 28). Anthropometric and routine biochemical assessments were performed. Serum nesfatin-1and plasma insulin levels were assessed by ELISA methods. Homeostatic model for assessment of IR (HOMA-IR) was calculated. Results Serum nesfatin-1 was significantly lower in diabetic and pre-diabetic compared to healthy subjects (3.89 ± 1.1 ng/dl and 7.47 ± 1.22 ng/dl versus 15.39 ± 3.53 respectively, p < 0.001). Also diabetic patients had statistically significant lower nesfatin-1 levels than pre-diabetic patients (p < 0.001) Roc curve analysis identified cut-off values of ≤ 9 ng/dl and ≤ 5.5 ng/dl with an AUC of 0.94 and 0.97, sensitivity of 96.7 and 100%, and specificity of 93.3% and 96.7% for diagnosis of pre-diabetes and diabetes respectively. Using bivariate analysis, nesfatin-1 was negatively correlated with glycemic parameters (fasting and 2 h postprandial blood sugar, HBA1c), IR parameters (fasting insulin and HOMA-IR) and atherogenic lipid profile (triglyceride, cholesterol, and LDL-c); and positively correlated to HDL-c in both diabetic and pre-diabetic but not in healthy. Conclusion Nesfatin-1 is an excellent predictor for pre-diabetes and DMT2. It is associated with favorable glucose and lipid metabolism probably via insulin signaling pathway.

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