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Upregulated lncRNA HCG18 in Patients with Non-Alcoholic Fatty Liver Disease and Its Regulatory Effect on Insulin Resistance
PURPOSE: Non-alcoholic fatty liver disease (NAFLD) is a disease associated with genetic-environmental-metabolic stress, which severely damages the liver function of patients. This study aimed to explore the significance and probable functions of HCG18 in NAFLD. PATIENTS AND METHODS: The expression o...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8651094/ https://www.ncbi.nlm.nih.gov/pubmed/34887672 http://dx.doi.org/10.2147/DMSO.S333431 |
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author | Xia, Yu Zhang, Yanxia Wang, Huiyun |
author_facet | Xia, Yu Zhang, Yanxia Wang, Huiyun |
author_sort | Xia, Yu |
collection | PubMed |
description | PURPOSE: Non-alcoholic fatty liver disease (NAFLD) is a disease associated with genetic-environmental-metabolic stress, which severely damages the liver function of patients. This study aimed to explore the significance and probable functions of HCG18 in NAFLD. PATIENTS AND METHODS: The expression of HCG18 and miR-197-3p was tested by qRT-PCR. The clinical signification of HCG18 was provided by the ROC curve and Pearson correlation. The corresponding mechanism was punctuated by the luciferase reporter assay and HFD-managed mice. RESULTS: HCG18 expression was higher in the patients with NAFLD than in controls and in individuals with HOMA-IR score ≥2.5 than those with HOMA-IR score <2.5. HCG18 expression in NAFLD patients was related to BMI, HOMA-IR, ALT, FBG, TC, and TG. HCG18 showed satisfactory predictive accuracy in differentiating NAFLD patients and patients with HOMA-IR ≥2.5. Besides, HCG18 had protective impacts on blood glucose and fat deposition but not on body weight. MiR-197-3p is a direct gene of HCG18, and a reverse correlation was found between miR-197-3p and HCG18. Furthermore, miR-197-3p regulated the influence of HCG18 on insulin resistance and lipid accumulation. CONCLUSION: Increased levels of HCG18 might be an alternate indicator for NAFLD patients. The HCG18-miR-197-3p axis exerted effects on the progression of fat sedimentation and glucose disorder in NAFLD. |
format | Online Article Text |
id | pubmed-8651094 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-86510942021-12-08 Upregulated lncRNA HCG18 in Patients with Non-Alcoholic Fatty Liver Disease and Its Regulatory Effect on Insulin Resistance Xia, Yu Zhang, Yanxia Wang, Huiyun Diabetes Metab Syndr Obes Original Research PURPOSE: Non-alcoholic fatty liver disease (NAFLD) is a disease associated with genetic-environmental-metabolic stress, which severely damages the liver function of patients. This study aimed to explore the significance and probable functions of HCG18 in NAFLD. PATIENTS AND METHODS: The expression of HCG18 and miR-197-3p was tested by qRT-PCR. The clinical signification of HCG18 was provided by the ROC curve and Pearson correlation. The corresponding mechanism was punctuated by the luciferase reporter assay and HFD-managed mice. RESULTS: HCG18 expression was higher in the patients with NAFLD than in controls and in individuals with HOMA-IR score ≥2.5 than those with HOMA-IR score <2.5. HCG18 expression in NAFLD patients was related to BMI, HOMA-IR, ALT, FBG, TC, and TG. HCG18 showed satisfactory predictive accuracy in differentiating NAFLD patients and patients with HOMA-IR ≥2.5. Besides, HCG18 had protective impacts on blood glucose and fat deposition but not on body weight. MiR-197-3p is a direct gene of HCG18, and a reverse correlation was found between miR-197-3p and HCG18. Furthermore, miR-197-3p regulated the influence of HCG18 on insulin resistance and lipid accumulation. CONCLUSION: Increased levels of HCG18 might be an alternate indicator for NAFLD patients. The HCG18-miR-197-3p axis exerted effects on the progression of fat sedimentation and glucose disorder in NAFLD. Dove 2021-12-03 /pmc/articles/PMC8651094/ /pubmed/34887672 http://dx.doi.org/10.2147/DMSO.S333431 Text en © 2021 Xia et al. https://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (https://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Xia, Yu Zhang, Yanxia Wang, Huiyun Upregulated lncRNA HCG18 in Patients with Non-Alcoholic Fatty Liver Disease and Its Regulatory Effect on Insulin Resistance |
title | Upregulated lncRNA HCG18 in Patients with Non-Alcoholic Fatty Liver Disease and Its Regulatory Effect on Insulin Resistance |
title_full | Upregulated lncRNA HCG18 in Patients with Non-Alcoholic Fatty Liver Disease and Its Regulatory Effect on Insulin Resistance |
title_fullStr | Upregulated lncRNA HCG18 in Patients with Non-Alcoholic Fatty Liver Disease and Its Regulatory Effect on Insulin Resistance |
title_full_unstemmed | Upregulated lncRNA HCG18 in Patients with Non-Alcoholic Fatty Liver Disease and Its Regulatory Effect on Insulin Resistance |
title_short | Upregulated lncRNA HCG18 in Patients with Non-Alcoholic Fatty Liver Disease and Its Regulatory Effect on Insulin Resistance |
title_sort | upregulated lncrna hcg18 in patients with non-alcoholic fatty liver disease and its regulatory effect on insulin resistance |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8651094/ https://www.ncbi.nlm.nih.gov/pubmed/34887672 http://dx.doi.org/10.2147/DMSO.S333431 |
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