Coffee Restores Expression of lncRNAs Involved in Steatosis and Fibrosis in a Mouse Model of NAFLD
Background and aim: Coffee intake exerts protective effects against non-alcoholic fatty liver disease (NAFLD), although without fully cleared mechanisms. In this study we aimed to assess whether coffee consumption may influence the expression of long non-coding RNAs (lncRNAs) in the liver. Methods:...
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MDPI AG
2021-08-01
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| Series: | Nutrients |
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| Online Access: | https://www.mdpi.com/2072-6643/13/9/2952 |
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| author | Stefania Di Mauro Federico Salomone Alessandra Scamporrino Agnese Filippello Filomena Morisco Maria Guido Vincenzo Lembo Valentina Cossiga Rosaria Maria Pipitone Stefania Grimaudo Roberta Malaguarnera Francesco Purrello Salvatore Piro |
| author_facet | Stefania Di Mauro Federico Salomone Alessandra Scamporrino Agnese Filippello Filomena Morisco Maria Guido Vincenzo Lembo Valentina Cossiga Rosaria Maria Pipitone Stefania Grimaudo Roberta Malaguarnera Francesco Purrello Salvatore Piro |
| author_sort | Stefania Di Mauro |
| collection | DOAJ |
| description | Background and aim: Coffee intake exerts protective effects against non-alcoholic fatty liver disease (NAFLD), although without fully cleared mechanisms. In this study we aimed to assess whether coffee consumption may influence the expression of long non-coding RNAs (lncRNAs) in the liver. Methods: C57BL/6J mice were fed a 12-week standard diet (SD), high-fat diet (HFD) or HFD plus decaffeinated coffee solution (HFD + coffee). Expression of specific lncRNAs involved in NAFLD was analyzed by real-time PCR. For the most differentially expressed lncRNAs, the analysis was also extended to their mRNA targets. Results: Decaffeinated coffee intake reduced body weight gain, prevented NAFLD, lowered hyperglycemia and hypercholesterolemia. NAFLD was associated with lower hepatic expression of Gm16551, a lncRNA inhibiting <i>de novo</i> lipogenesis, and higher expression of H19, a lncRNA promoting fibrogenesis. Coffee intake restored Gm16551 to levels observed in lean mice and downregulated gene expression of its targets acetyl coenzyme A carboxylase 1 and stearoyl coenzyme A desaturase 1. Furthermore, coffee consumption markedly decreased hepatic expression of H19 and of its target gene collagen alpha-1(I) chain; consistently, in mice fed HFD + coffee liver expression of αSMA protein returned to levels of mice fed SD. Expression of lncRNA involved in circadian clock such as fatty liver-related lncRNA 1 (FLRL1) and fatty liver-related lncRNA 2 (FLRL2) were upregulated by HFD and were also modulated by coffee intake. Conclusion. Hepatoprotective effects of coffee may be depending on the modulation of lncRNAs involved in key pathways of NAFLD onset and progression. |
| first_indexed | 2024-03-10T07:21:44Z |
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| institution | Directory Open Access Journal |
| issn | 2072-6643 |
| language | English |
| last_indexed | 2024-03-10T07:21:44Z |
| publishDate | 2021-08-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Nutrients |
| spelling | doaj.art-edd9ddf2879c4f5d8373ef3b13b7518b2023-11-22T14:34:58ZengMDPI AGNutrients2072-66432021-08-01139295210.3390/nu13092952Coffee Restores Expression of lncRNAs Involved in Steatosis and Fibrosis in a Mouse Model of NAFLDStefania Di Mauro0Federico Salomone1Alessandra Scamporrino2Agnese Filippello3Filomena Morisco4Maria Guido5Vincenzo Lembo6Valentina Cossiga7Rosaria Maria Pipitone8Stefania Grimaudo9Roberta Malaguarnera10Francesco Purrello11Salvatore Piro12Department of Clinical and Experimental Medicine, University of Catania, 95122 Catania, ItalyDivision of Gastroenterology, Ospedale di Acireale, Azienda Sanitaria Provinciale di Catania, 95024 Catania, ItalyDepartment of Clinical and Experimental Medicine, University of Catania, 95122 Catania, ItalyDepartment of Clinical and Experimental Medicine, University of Catania, 95122 Catania, ItalyDepartment of Clinical Medicine and Surgery, University of Naples “Federico II”, 80125 Naples, ItalyDepartment of Medicine, University of Padua, 35121 Padua, ItalyDepartment of Clinical Medicine and Surgery, University of Naples “Federico II”, 80125 Naples, ItalyDepartment of Clinical Medicine and Surgery, University of Naples “Federico II”, 80125 Naples, ItalyDepartment PROMISE, University of Palermo, 90128 Palermo, ItalyDepartment PROMISE, University of Palermo, 90128 Palermo, ItalyFaculty of Medicine and Surgery, “Kore” University of Enna, 94100 Enna, ItalyDepartment of Clinical and Experimental Medicine, University of Catania, 95122 Catania, ItalyDepartment of Clinical and Experimental Medicine, University of Catania, 95122 Catania, ItalyBackground and aim: Coffee intake exerts protective effects against non-alcoholic fatty liver disease (NAFLD), although without fully cleared mechanisms. In this study we aimed to assess whether coffee consumption may influence the expression of long non-coding RNAs (lncRNAs) in the liver. Methods: C57BL/6J mice were fed a 12-week standard diet (SD), high-fat diet (HFD) or HFD plus decaffeinated coffee solution (HFD + coffee). Expression of specific lncRNAs involved in NAFLD was analyzed by real-time PCR. For the most differentially expressed lncRNAs, the analysis was also extended to their mRNA targets. Results: Decaffeinated coffee intake reduced body weight gain, prevented NAFLD, lowered hyperglycemia and hypercholesterolemia. NAFLD was associated with lower hepatic expression of Gm16551, a lncRNA inhibiting <i>de novo</i> lipogenesis, and higher expression of H19, a lncRNA promoting fibrogenesis. Coffee intake restored Gm16551 to levels observed in lean mice and downregulated gene expression of its targets acetyl coenzyme A carboxylase 1 and stearoyl coenzyme A desaturase 1. Furthermore, coffee consumption markedly decreased hepatic expression of H19 and of its target gene collagen alpha-1(I) chain; consistently, in mice fed HFD + coffee liver expression of αSMA protein returned to levels of mice fed SD. Expression of lncRNA involved in circadian clock such as fatty liver-related lncRNA 1 (FLRL1) and fatty liver-related lncRNA 2 (FLRL2) were upregulated by HFD and were also modulated by coffee intake. Conclusion. Hepatoprotective effects of coffee may be depending on the modulation of lncRNAs involved in key pathways of NAFLD onset and progression.https://www.mdpi.com/2072-6643/13/9/2952NAFLDcoffeelncRNAGm16551H19 |
| spellingShingle | Stefania Di Mauro Federico Salomone Alessandra Scamporrino Agnese Filippello Filomena Morisco Maria Guido Vincenzo Lembo Valentina Cossiga Rosaria Maria Pipitone Stefania Grimaudo Roberta Malaguarnera Francesco Purrello Salvatore Piro Coffee Restores Expression of lncRNAs Involved in Steatosis and Fibrosis in a Mouse Model of NAFLD Nutrients NAFLD coffee lncRNA Gm16551 H19 |
| title | Coffee Restores Expression of lncRNAs Involved in Steatosis and Fibrosis in a Mouse Model of NAFLD |
| title_full | Coffee Restores Expression of lncRNAs Involved in Steatosis and Fibrosis in a Mouse Model of NAFLD |
| title_fullStr | Coffee Restores Expression of lncRNAs Involved in Steatosis and Fibrosis in a Mouse Model of NAFLD |
| title_full_unstemmed | Coffee Restores Expression of lncRNAs Involved in Steatosis and Fibrosis in a Mouse Model of NAFLD |
| title_short | Coffee Restores Expression of lncRNAs Involved in Steatosis and Fibrosis in a Mouse Model of NAFLD |
| title_sort | coffee restores expression of lncrnas involved in steatosis and fibrosis in a mouse model of nafld |
| topic | NAFLD coffee lncRNA Gm16551 H19 |
| url | https://www.mdpi.com/2072-6643/13/9/2952 |
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