Although the exact mechanism linking obesity to type 2 diabetes (T2D) remains unknown, accumulating evidence suggests that low-grade chronic metabolic inflammation or ‘metainflammation’ plays a pivotal role. Adipose tissue is the primary site of meta-inflammation, and overproduction of pro-inflammatory cytokines in this tissue affects other organs such as the liver, skeletal muscle, pancreas, and brain. This leads to the development of insulin resistance and metabolic irregularities in these tissues. Therefore, strategies targeting metainflammation could be effective in treating T2D and related metabolic traits. Resveratrol, a polyphenol, is suggested to possess anti-inflammatory and immunomodulatory activities. The anti-inflammatory effect of resveratrol is mediated through several mechanisms including the suppression of nuclear factor kB (NF-kB), down-regulation of extracellular signal-regulated kinase (ERK)/p38 mitogen-activated protein kinase (MAPK) signaling, suppression of toll-like receptor (TLR)-mediated pathway; inhibition of NLR family pyrin domain containing 3 (NLRP3) inflammasome activation, reduction of reactive oxygen species (ROS) generation, suppression of immune cell infiltration into tissues; and inhibition of pro-inflammatory cytokines production. This review will examine the evidence on the role of resveratrol in modulating inflammation in various organs affected by obesity such as liver, skeletal muscle, kidney, heart and brain.

Adipose tissue is recognized as an endocrine organ that influences the health status of other tissues by releasing various adipokines. Chemerin is one such adipokine, and its serum level exhibits a positive correlation with the amount of fat tissue and obesity. Certain genetic polymorphisms of chemerin, namely rs17173608, rs1799983, rs693, rs4721, and rs3735167, are known to be associated with diseases such as diabetes, gestational diabetes mellitus (GDM), obesity, insulin resistance (IR), cardiovascular diseases, metabolic syndrome (MetS), end stage renal disease (ESRD), polycystic ovary syndrome (PCOS), and rheumatoid arthritis (RA). Existing data suggest that chemerin is also associated with inflammatory diseases. This review focuses on the association between the genetic variants or polymorphisms of chemerin and some pathological states.

Objectives: The effectiveness of Scrophularia striata in controlling infections and promoting wound healing has been reported. This study aimed to investigate the antioxidant properties of the methanol extract from Scrophularia striata.
Methods: Scrophularia striata, a perennial wild plant found in various temperate and tropical areas of Iran, underwent a methanol extraction process to obtain its active compounds. The antioxidant property of the methanol extract of Scrophularia striata was evaluated by quantifying the total antioxidant level, determining the total phenol content, and conducting DPPH radical scavenging assays.
Results: As the extraction concentrations of Scrophularia striata increase, both the total antioxidant level and total phenol content rise dramatically. With the progression of time and increase in plant extract concentrations, the efficacy of DPPH radical scavenging also shows a corresponding enhancement. Moreover, the IC50% value of Scrophularia striata for DPPH radical scavenging consistently decreases over the observation period.
Conclusion: The data suggest that Scrophularia striata possesses antioxidant properties. The presence of flavonoids and phenolic compounds in Scrophularia striata highlights its potential to alleviate various disorders by modulating oxidative stress levels.

Objectives: The aim of this study is to compare three distinct bone markers in metabolically healthy and unhealthy obese and non-obese subjects, according to various metabolic health criteria.
Methods: The study enrolled a total of 35 subjects, including 11 healthy normal-weight and 23 obese subjects. Based on HOMA-Beta, all participants were divided into three groups: normal weight (HOM-Beta<100%, n=11), obese (HOMA-Beta <100%, n=12), and obese (HOMA-Beta>100%, n=12). The serum levels of osteocalcin, procollagen I amino-terminal propeptide (P1NP), and beta-cross Laps as bone turnover markers, as well as serum levels of 25 (OH) vitamin D3, and PTH were analyzed.
Results: Significant differences were observed in BMI, age, 25(OH)D3, FBS, Insulin, HOMAIR, and HOMA-Beta among the groups. Analysis of bone markers revealed that the serum levels of Beta-cross Laps, P1NP, and osteocalcin were significantly different among all studied groups categorized by the HOMA-Beta model. In this context, circulating levels of osteocalcin and Betacross Laps in the normal weight group (HOMA-Beta<100%) were significantly higher than the obese group (HOMA-Beta <100%). In obese patients with HOMA-Beta <100%, Beta-cross Laps and P1NP levels were lower compared to the obese group with HOMA-Beta >100%.
Conclusion: The data suggests that HOMA-Beta, as an index of β-cell function, can be used in part of metabolically healthy obese (MHO) criteria and bone remodeling is altered in the context of metabolically healthy obesity.

Objectives: The aim of this study was to evaluate the effect of silymarin on liver enzyme levels and serum lipid profiles in patients with Non-Alcoholic Fatty Liver Disease (NAFLD), the most common chronic liver disease worldwide.
Methods: This randomized double-blinded clinical trial included 80 NAFLD patients referred to the gastrointestinal clinic of Kowsar Hospital in Semnan. Forty of these patients were supplemented with 150 mg of silymarin twice a day for two months, while the other 40 received a placebo. Both groups were advised to follow a hypertriglyceridemia correction and lifestyle modification. Evaluation of serum lipid profiles and liver enzymes in both groups were performed at the baseline and after two months.
Results: The results showed that silymarin use significantly reduced ALT (U/L) (58.72±32.16 vs 42.2 ± 20.2, p = 0.003) and AST (U/L) (36.62± 13.46 vs 30.3 ± 9.7, p = 0.036) levels compared with the placebo group. Additionally, a statistically significant reducing effect of silymarin on triglycerides (mg/dL) (189.5 ± 65.5 vs 164.6 ± 91.3, p = 0.026), total cholesterol (mg/dL) (192.8 ± 40.3 vs 174.07± 34.5, p = 0.027), and LDL-cholesterol (mg/dL) (114.6±33.9 vs 95.6± 26.5, p = 0.012) levels was found, with no significant statistical difference for HDL-C (mg/dL) (41.5 ± 6.8 vs 43.5± 9.2, p = 0.44).
Conclusion: Silymarin, at a dose of 150 mg twice daily, significantly reduced liver enzymes and some lipid markers in patients with NAFLD, suggesting that this compound could be a novel therapy for NAFLD.

Objectives: The endothelium constitutes a significant part of the vasculature. Oxidative stress, an imbalance between the generation of reactive oxygen species (ROS) and the antioxidant defense system, contributes to the impairment of endothelial function. ROS regulate several signaling pathways, such as transforming growth factor β (TGF-β) and nuclear factor kappa B (NF-κB). This study aimed to investigate the effects of curcumin, a polyphenol with antioxidant properties, on these two molecules in endothelial cells treated with hydrogen peroxide (H2O2).
Methods: Cultured Bovine aortic endothelial cells (BAECs) were treated with different concentrations of H2O2 (20 µM, 40 µM, and 200μM) for 1 and 24 hours in the absence and presence of curcumin. TGF-β expression was detected by quantitative real-time PCR analysis, and phosphorylation of NF-κB-p65 was examined by western blot.
Results: H2O2 up-regulates TGF-β mRNA expression and induces the phosphorylation of the p65 subunit of NF-kB in a dose-dependent manner in BAECs. Curcumin inhibited both H2O2-stimulated TGF-β expression and phosphorylation of NF-κB-p65 in these cells.
Conclusion: The findings demonstrate that curcumin reduces TGF-β mRNA expression and inhibits NFκB-p65 phosphorylation in endothelial cells.

Objectives: It has been reported that Metformin (MET), Resveratrol (RSV), and Quercetin (QRS) possess anti-lipogenic effects. This study aimed to investigate the combined effects of these compounds on lipid accumulation in HepG2 cells treated with high glucose (HG).
Methods: HepG2 cells were treated with HG (33 mM), and different concentrations of MET, QRS, and RSV. The cytotoxic effects of these compounds were determined by an MTT assay. Changes in total lipid content and triglyceride (TG) levels were measured using Oil Red O staining and a triglyceride assay kit, respectively. The expression of fatty acid synthetase (FAS) and sterol regulatory element-binding protein 1c (SREBP-1c) was evaluated by quantitative real-time PCR.
Results: MET at doses 1, 2, and 5 mM, QRS at doses 5, 10, and 20 µM, and RSV at doses 25 and 50 µM could decrease total lipid content and triglyceride levels in HepG2 cells. The EC50 (half maximal effective concentration) from Oil red O staining results were MET: 1.786 mM, QRS: 8.132 μM, and RSV: 10.9 μM. The combination of MET (mM), QRS (µM), and RSV (µM) at ratios of (2:20:50), (1:10:25), and (0.5:5:10), could reduce lipogenesis greater than that observed with each of the individual compounds of MET, QRS, or RSV or the double combinations of MET+QRS or MET+RSV. In addition, combined treatment of MET (0.5mM), QRS (5 µM), and RSV (10 µM) was able to decrease SREBP-1c and FAS genes expression in HG-treated cells.
Conclusion: The combination of MET, QRS, and RSV could inhibit lipid accumulation in HepG2 cells by reducing total lipid content, triglyceride levels, and the expression of the genes involved in lipogenesis.