<i>Rhinacanthin C</i> Ameliorates Insulin Resistance and Lipid Accumulation in NAFLD Mice via the AMPK/SIRT1 and SREBP‐1c/FAS/ACC Signaling Pathways

Gong, Zhiqiang; Han, Shuang; Li, Chenlin; Meng, Tianxiu; Yu, Hao; Liu, Xianfu; Huang, Yanhong; Yang, Lifang

doi:10.1155/2023/6603522

Cited by 13 publications

(4 citation statements)

References 38 publications

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“…SREBP-1c mainly regulates genes related to triglyceride and fatty acid synthesis, such as ACC and SCD1 [49]. Recent studies have shown that SREBP-1c can also inhibit the transcription of insulin receptor substrate-2 (IRS-2), thereby exacerbating insulin resistance; this suggested that it might have a negative regulatory effect on insulin signaling [50,51]. ChREBPα is a transcription factor in the glucose signaling pathway, which plays an important role in regulating glucose metabolism [52], fat metabolism, and fat deposition in mammals [53].…”

Section: Discussionmentioning

confidence: 99%

Physalis alkekengi L. Calyx Extract Alleviates Glycolipid Metabolic Disturbance and Inflammation by Modulating Gut Microbiota, Fecal Metabolites, and Glycolipid Metabolism Gene Expression in Obese Mice

et al. 2023

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Physalis alkekengi L. calyx (PC) extract can relieve insulin resistance and has glycemic and anti-inflammatory effects; however, the potential mechanisms related to gut microbiota and metabolites remain elusive. This study aimed to understand how PC regulates gut microbiota and metabolites to exert anti-obesogenic effects and relieve insulin resistance. In this study, a high-fat high-fructose (HFHF)-diet-induced obesity C57BL/6J male mice model with glycolipid metabolism dysfunction was established, which was supplemented with the aqueous extract of PC daily for 10 weeks. The results showed that the PC supplementation could effectively cure the abnormal lipid metabolism and maintain glucose metabolism homeostasis by regulating the expression of adipose metabolic genes and glucose metabolism genes in the liver, thereby effectively alleviating the inflammatory response. PC treatment also increased the contents of fecal short-chain fatty acids (SCFAs), especially butyric acid. PC extract could restore the HFHF-disrupted diversity of gut microbiota by significantly increasing the relative abundance of Lactobacillus and decreasing those of Romboutsia, Candidatus_Saccharimonas, and Clostridium_sensu_stricto_1. The negative effects of the HFHF diet were ameliorated by PC by regulating multiple metabolic pathways, such as lipid metabolism (linoleic acid metabolism, alpha-linolenic acid metabolism, and sphingolipid metabolism) and amino acid metabolism (histidine and tryptophan metabolism). Correlation analysis showed that among the obesity parameters, gut microbiota and metabolites are directly and closely related. To sum up, this study suggested that PC treatment exhibited therapeutic effects by regulating the gut microbiota, fecal metabolites, and gene expression in the liver to improve glucose metabolism, modulate adiposity, and reduce inflammation.

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Section: Discussionmentioning

confidence: 99%

Physalis alkekengi L. Calyx Extract Alleviates Glycolipid Metabolic Disturbance and Inflammation by Modulating Gut Microbiota, Fecal Metabolites, and Glycolipid Metabolism Gene Expression in Obese Mice

et al. 2023

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“…Rhinacanthin decreases adipogenic marker expression, including that of PPARγ, C/EBPα, and aP2, by phosphorylating AMPKα. Moreover, it suppresses adipogenesis by deactivating SREBP-1c, acetyl-CoA carboxylase, Fas cell surface death receptor, and stearoyl-Coenzyme A desaturase 1 [ 40 ]. AMPKα activation is widely recognized to inhibit C/EBPα, C/EBPβ, and PPARγ expression during adipogenesis.…”

Section: Discussionmentioning

confidence: 99%

Anti-Obesity Effect of Lactobacillus acidophilus DS0079 (YBS1) by Inhibition of Adipocyte Differentiation through Regulation of p38 MAPK/PPARγ Signaling

Lee,

Iqbal,

Lee

et al. 2024

J. Microbiol. Biotechnol.

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Obesity is spawned by an inequality between the portion of energy consumed and the quantity of energy expended. Disease entities such as cardiovascular disease, arteriosclerosis, hypertension, and cancer, which are correlated with obesity, influence society and the economy. Suppression of adipogenesis, the process of white adipocyte generation, remains a promising approach for treating obesity. Oil Red O staining was used to differentiate 3T3-L1 cells for screening 20 distinct Lactobacillus species. Among these, Lactobacillus acidophilus DS0079, referred to as YBS1, was selected for further study. YBS1 therapy decreased 3T3-L1 cell development. Triglyceride accumulation and mRNA expression of the primary adipogenic marker, peroxisome proliferator-activated receptor gamma (PPARγ), including its downstream target genes, adipocyte fatty acid binding protein 4 and adiponectin, were almost eliminated. YBS1 inhibited adipocyte differentiation at the early stage (days 0–2), but no significant difference was noted between the mid-stage (days 2–4) and late-stage (days 4–6) development. YBS1 stimulated the activation of p38 mitogen-activated protein kinase (p38 MAPK) during the early stages of adipogenesis; however, this effect was eliminated by the SB203580 inhibitor. The data showed that YBS1 administration inhibited the initial development of adipocytes via stimulation of the p38 MAPK signaling pathway, which in turn controlled PPARγ expression. In summary, YBS1 has potential efficacy as an anti-obesity supplement and requires further exploration.

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“…PPAR-α has been demonstrated to be involved in fatty acid metabolism in various tissues, including the liver, and the activation of PPAR-α leads to significant improvements in hepatic steatosis and inflammation in NAFLD [66]. SREBP-1c can increase the expression levels of lipogenic genes such as FAS and ACC, which enhances the synthesis of fatty acids and accelerates the accumulation of TG [67]. The upregulation of SREBP-1c, along with its downstream genes including FAS and ACC, as well as the downregulation of PPAR-α, are recognized as the interfering factors contributing to the development of hepatic steatosis [68].…”

Section: Discussionmentioning

confidence: 99%

Maternal Folic Acid Supplementation during Pregnancy Prevents Hepatic Steatosis in Male Offspring of Rat Dams Fed High-Fat Diet, Which Is Associated with the Regulation of Gut Microbiota

Zhang,

Wang,

Zhang

et al. 2023

Nutrients

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Maternal dietary patterns during pregnancy have been demonstrated to impact the structure of the gut microbiota in offspring, altering their susceptibility to diseases. This study is designed to elucidate whether the impact of folic acid supplementation during pregnancy on hepatic steatosis in male offspring of rat dams exposed to a high-fat diet (HFD) is related to gut–liver axis homeostasis. In this study, female rats were administered a HFD and simultaneously supplemented with 5 mg/kg folic acid throughout their pregnancy. Histopathological examination showed that folic acid supplementation effectively ameliorated hepatic lipid accumulation and inflammatory infiltrate in male offspring subjected to a maternal HFD. Maternal folic acid supplementation reduced the abundance of Desulfobacterota and the Firmicutes/Bacteroidota (F/B) ratio in male offspring. The expression of tight junction proteins in the colon was significantly upregulated, and the serum LPS level was significantly reduced. Furthermore, there was a notable reduction in the hepatic expression of the TLR4/NF-κB signaling pathway and subsequent inflammatory mediators. Spearman’s correlation analysis revealed significant associations between hepatic inflammation-related indices and several gut microbiota, particularly Desulfobacterota and Lactobacillus. With a reduction in hepatic inflammation, the expression of PPAR-α was upregulated, and the expression of SREBP-1c and its downstream lipid metabolism-related genes was downregulated. In summary, folic acid supplementation during pregnancy modulates gut microbiota and enhances intestinal barrier integrity in male offspring of HFD dams. This helps reduce the LPS leakage and suppress the expression of TLR4/NF-κB pathway in the liver, thereby improving lipid metabolism disorders, and alleviating hepatic steatosis.

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Rhinacanthin C Ameliorates Insulin Resistance and Lipid Accumulation in NAFLD Mice via the AMPK/SIRT1 and SREBP‐1c/FAS/ACC Signaling Pathways

Cited by 13 publications

References 38 publications

Physalis alkekengi L. Calyx Extract Alleviates Glycolipid Metabolic Disturbance and Inflammation by Modulating Gut Microbiota, Fecal Metabolites, and Glycolipid Metabolism Gene Expression in Obese Mice

Physalis alkekengi L. Calyx Extract Alleviates Glycolipid Metabolic Disturbance and Inflammation by Modulating Gut Microbiota, Fecal Metabolites, and Glycolipid Metabolism Gene Expression in Obese Mice

Anti-Obesity Effect of Lactobacillus acidophilus DS0079 (YBS1) by Inhibition of Adipocyte Differentiation through Regulation of p38 MAPK/PPARγ Signaling

Maternal Folic Acid Supplementation during Pregnancy Prevents Hepatic Steatosis in Male Offspring of Rat Dams Fed High-Fat Diet, Which Is Associated with the Regulation of Gut Microbiota

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