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Potential of Hibiscus sabdariffa Linn. in managing FGF21 resistance in diet‐induced‐obesity rats via miR‐34a regulation
BACKGROUND: Obesity is a cause of FGF21 resistance, which affects the browning and thermogenesis process of the adipose tissue. Decreased receptor expression is influenced by miR‐34a, whose expression is increased in obesity. While FGF21‐based therapies have been widely investigated, the potential a...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8788974/ https://www.ncbi.nlm.nih.gov/pubmed/34687158 http://dx.doi.org/10.1002/vms3.653 |
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author | Kartinah, Neng Tine Komara, Nisa Noviati, Nuraini Diah Dewi, Syarifah Yolanda, Sophie Radhina, Afifa Heriyanto, Heriyanto Sianipar, Imelda Rosalyn |
author_facet | Kartinah, Neng Tine Komara, Nisa Noviati, Nuraini Diah Dewi, Syarifah Yolanda, Sophie Radhina, Afifa Heriyanto, Heriyanto Sianipar, Imelda Rosalyn |
author_sort | Kartinah, Neng Tine |
collection | PubMed |
description | BACKGROUND: Obesity is a cause of FGF21 resistance, which affects the browning and thermogenesis process of the adipose tissue. Decreased receptor expression is influenced by miR‐34a, whose expression is increased in obesity. While FGF21‐based therapies have been widely investigated, the potential activity of Hibiscus sabdariffa Linn. extract (HSE) against FGF21 resistance is unknown. OBJECTIVE: This study aims to determine the effects of HSE on the expression of miR‐34a and FGF21 receptors in white adipose tissue. METHODS: This experimental study used 24 male Sprague‐Dawley rats and divided into four groups: Control (N); diet‐induced‐obesity rats (DIO); DIO rats with HSE 200 mg/kgBW/day and DIO rats with HSE 400 mg/kgBW/day. Rats were fed a high‐fat diet for 17 weeks. HSE was administered daily for 5 weeks. The administration of HSE 400 mg/kgBW/day resulted in the equivalent expression of miR‐34a to that of the control (p > 0.05). RESULTS: FGFR1 receptor expression was also similar to controls (p > 0.05). Beta‐klotho expression was significantly lower than that of control (p < 0.05) but equivalent to that of DIO rats (p < 0.05). CONCLUSIONS: H. sabdariffa has the potential to reduce FGF21 resistance in DIO rats through the suppression of miR‐34a expression and an increase in the number of FGFR1 and beta‐klotho receptors in adipose tissue. |
format | Online Article Text |
id | pubmed-8788974 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-87889742022-02-01 Potential of Hibiscus sabdariffa Linn. in managing FGF21 resistance in diet‐induced‐obesity rats via miR‐34a regulation Kartinah, Neng Tine Komara, Nisa Noviati, Nuraini Diah Dewi, Syarifah Yolanda, Sophie Radhina, Afifa Heriyanto, Heriyanto Sianipar, Imelda Rosalyn Vet Med Sci RODENTS BACKGROUND: Obesity is a cause of FGF21 resistance, which affects the browning and thermogenesis process of the adipose tissue. Decreased receptor expression is influenced by miR‐34a, whose expression is increased in obesity. While FGF21‐based therapies have been widely investigated, the potential activity of Hibiscus sabdariffa Linn. extract (HSE) against FGF21 resistance is unknown. OBJECTIVE: This study aims to determine the effects of HSE on the expression of miR‐34a and FGF21 receptors in white adipose tissue. METHODS: This experimental study used 24 male Sprague‐Dawley rats and divided into four groups: Control (N); diet‐induced‐obesity rats (DIO); DIO rats with HSE 200 mg/kgBW/day and DIO rats with HSE 400 mg/kgBW/day. Rats were fed a high‐fat diet for 17 weeks. HSE was administered daily for 5 weeks. The administration of HSE 400 mg/kgBW/day resulted in the equivalent expression of miR‐34a to that of the control (p > 0.05). RESULTS: FGFR1 receptor expression was also similar to controls (p > 0.05). Beta‐klotho expression was significantly lower than that of control (p < 0.05) but equivalent to that of DIO rats (p < 0.05). CONCLUSIONS: H. sabdariffa has the potential to reduce FGF21 resistance in DIO rats through the suppression of miR‐34a expression and an increase in the number of FGFR1 and beta‐klotho receptors in adipose tissue. John Wiley and Sons Inc. 2021-10-23 /pmc/articles/PMC8788974/ /pubmed/34687158 http://dx.doi.org/10.1002/vms3.653 Text en © 2021 The Authors. Veterinary Medicine and Science published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | RODENTS Kartinah, Neng Tine Komara, Nisa Noviati, Nuraini Diah Dewi, Syarifah Yolanda, Sophie Radhina, Afifa Heriyanto, Heriyanto Sianipar, Imelda Rosalyn Potential of Hibiscus sabdariffa Linn. in managing FGF21 resistance in diet‐induced‐obesity rats via miR‐34a regulation |
title | Potential of Hibiscus sabdariffa Linn. in managing FGF21 resistance in diet‐induced‐obesity rats via miR‐34a regulation |
title_full | Potential of Hibiscus sabdariffa Linn. in managing FGF21 resistance in diet‐induced‐obesity rats via miR‐34a regulation |
title_fullStr | Potential of Hibiscus sabdariffa Linn. in managing FGF21 resistance in diet‐induced‐obesity rats via miR‐34a regulation |
title_full_unstemmed | Potential of Hibiscus sabdariffa Linn. in managing FGF21 resistance in diet‐induced‐obesity rats via miR‐34a regulation |
title_short | Potential of Hibiscus sabdariffa Linn. in managing FGF21 resistance in diet‐induced‐obesity rats via miR‐34a regulation |
title_sort | potential of hibiscus sabdariffa linn. in managing fgf21 resistance in diet‐induced‐obesity rats via mir‐34a regulation |
topic | RODENTS |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8788974/ https://www.ncbi.nlm.nih.gov/pubmed/34687158 http://dx.doi.org/10.1002/vms3.653 |
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