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Non‐alcoholic fatty liver disease (NAFLD) has become an important health problem in the world. Natural products, with anti‐inflammatory properties, are potential candidates for alleviating NAFLD. Metformin (MET) and chlorogenic acid (CGA) have been reported to be effective in the improvement of NAFLD. Here, we aimed to evaluate the efficacy of MET and CGA combination in ameliorating NAFLD in high‐fat diet (HFD) fed mice. Fifty C57BL/6 male mice were divided into two groups, one fed a standard chow diet (n = 10) and the other was fed an HFD (n = 40) for 10 weeks. Animals in the HFD group were then randomly divided into a four groups (HFD, HFD + MET (0.25%), HFD + CGA (0.02%) and HFD + MET + CGA (0.25 + 0.02%). MET and CGA combination decreases fasting blood glucose and improves glucose intolerance. Decreased hepatic triglyceride level was associated with lower expression levels of fatty acid synthase and sterol regulatory element‐binding protein‐1c in MET+CGA treated mice. MET and CGA combination treatment resulted in the polarization of macrophages to the M2 phenotype, reduction of the expression of pro‐inflammatory cytokines (TNF‐α, IL‐1β and IL‐6), and decreasing protein level of NF‐kB p65. It was found that the lowering effect of combined MET and CGA on the expression of gluconeogenic genes was accompanied by increasing phosphorylation of glycogen synthase kinase 3β. Treatment of HFD mice with the combination of MET and CGA was found to be more effective at alleviating inflammation and lipid accumulation by increasing phosphorylation of AMP‐activated protein kinase. In conclusion, these findings suggest that the MET + CGA combination might exert therapeutic effects against NAFLD.

Background: Recent studies point toward the possible regulatory roles of two lncRNAs; metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and taurine upregulated gene 1 (TUG1) in the pathogenesis of obesity-related disorders and regulation of lipogenesis and adipogenesis. In an attempt to understand the molecules involved in human obesity pathogenesis, we aimed to evaluate the expression of MALAT1 and TUG1 in visceral adipose tissues (VAT) and subcutaneous adipose tissues (SAT) of obese women, as compared to normal-weight women. The mRNA expression of possible target genes including peroxisome proliferator-activated receptor gamma (PPARγ), PPARγ coactivator-1 alpha (PGC1α), sterol regulatory element-binding protein-1c (SREBP-1c), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC) which are involved in adipogenesis and lipogenesis were also examined. Methods: This study was conducted on 20 obese [body mass index (BMI) ≥ 30 kg/m 2] female participants and 19 normal-weight (BMI < 25 kg/m 2) female participants. Real-time PCR was performed to investigate the mRNA expression of the above-mentioned genes in VAT and SAT from all participants. Results: The results showed lower mRNA levels of TUG1 in both the VAT and SAT of obese women, compared to normal-weight women. Furthermore, TUG1 expression in SAT positively correlated with BMI, waist circumference (WC), hip circumference, HOMA-IR, and insulin levels, eGFR value, creatinine levels, and hs-CRP in all participants independent of age and HOMA-IR. However, VAT mRNA expression of TUG1 had a positive correlation with obesity indices and HOMA-IR and insulin levels in the whole population. Moreover, SAT mRNA level of TUG1 was positively correlated with SAT gene expression of PGC1α, SREBP-1c, FAS, and ACC independent of age and HOMA-IR. Although mRNA expression of MALAT1 did not differ between two groups for any tissue, it was positively correlated with SAT mRNA levels of SREBP-1c, PPARγ, and their targets; FAS and ACC, as well as with VAT mRNA levels of PGC1α. Conclusions: It seems likely that TUG1 with distinct expression pattern in VAT and SAT are involved in the regulation of lipogenic and adipogenic genes and obesity-related parameters. However, more studies are necessary to establish this concept.

Ample evidence highlights the potential benefits of polyphenols in health status especially in obesity‐related metabolic disorders such as insulin resistance, type 2 diabetes, and cardiovascular diseases. Mechanistically, due to the key role of “Metainflammation” in the pathomechanism of metabolic disorders, recently much focus has been placed on the properties of polyphenols in obesity‐related morbidities. This narrative review summarizes the current knowledge on the role of polyphenols, including genistein, chlorogenic acid, ellagic acid, caffeic acid, and silymarin in inflammatory responses pertinent to metabolic disorders and discusses the implications of this evidence for future directions. This review provides evidence that the aforementioned polyphenols benefit health status in metabolic disorders via direct and indirect regulation of a variety of target proteins involved in inflammatory signaling pathways. However, due to limitations of the in vitro and in vivo studies and also the lack of long‐term human clinical trials studies, further high‐quality investigations are required to firmly establish the clinical efficacy of the polyphenols for the prevention and management of metabolic disorders.

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