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Daily Oral Administration of Protease-Treated Royal Jelly Protects Against Denervation-Induced Skeletal Muscle Atrophy
Honeybees produce royal jelly (RJ) from their cephalic glands. Royal jelly is a source of nutrition for the queen honey bee throughout its lifespan and is also involved in fertility and longevity. Royal jelly has long been considered beneficial to human health. We recently observed that RJ delayed i...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7600733/ https://www.ncbi.nlm.nih.gov/pubmed/33050588 http://dx.doi.org/10.3390/nu12103089 |
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author | Shirakawa, Tomohiko Miyawaki, Aki Matsubara, Takuma Okumura, Nobuaki Okamoto, Hideto Nakai, Naoya Rojasawasthien, Thira Morikawa, Kazumasa Inoue, Asako Goto, Akino Washio, Ayako Tsujisawa, Toshiyuki Kawamoto, Tatsuo Kokabu, Shoichiro |
author_facet | Shirakawa, Tomohiko Miyawaki, Aki Matsubara, Takuma Okumura, Nobuaki Okamoto, Hideto Nakai, Naoya Rojasawasthien, Thira Morikawa, Kazumasa Inoue, Asako Goto, Akino Washio, Ayako Tsujisawa, Toshiyuki Kawamoto, Tatsuo Kokabu, Shoichiro |
author_sort | Shirakawa, Tomohiko |
collection | PubMed |
description | Honeybees produce royal jelly (RJ) from their cephalic glands. Royal jelly is a source of nutrition for the queen honey bee throughout its lifespan and is also involved in fertility and longevity. Royal jelly has long been considered beneficial to human health. We recently observed that RJ delayed impairment of motor function during aging, affecting muscle fiber size. However, how RJ affects skeletal muscle metabolism and the functional component of RJ is as of yet unidentified. We demonstrate that feeding mice with RJ daily prevents a decrease in myofiber size following denervation without affecting total muscle weight. RJ did not affect atrophy-related genes but stimulated the expression of myogenesis-related genes, including IGF-1 and IGF receptor. Trans-10-hydroxy-2-decenoic acid (10H2DA) and 10-hydroxydecanoic acid (10HDAA), two major fatty acids contained in RJ. After ingestion, 10H2DA and 10HDAA are metabolized into 2-decenedioic acid (2DA) and sebacic acid (SA) respectively. We found that 10H2DA, 10HDAA, 2DA, and SA all regulated myogenesis of C2C12 cells, murine myoblast cells. These novel findings may be useful for potential preventative and therapeutic applications for muscle atrophy disease included in Sarcopenia, an age-related decline in skeletal muscle mass and strength. |
format | Online Article Text |
id | pubmed-7600733 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-76007332020-11-01 Daily Oral Administration of Protease-Treated Royal Jelly Protects Against Denervation-Induced Skeletal Muscle Atrophy Shirakawa, Tomohiko Miyawaki, Aki Matsubara, Takuma Okumura, Nobuaki Okamoto, Hideto Nakai, Naoya Rojasawasthien, Thira Morikawa, Kazumasa Inoue, Asako Goto, Akino Washio, Ayako Tsujisawa, Toshiyuki Kawamoto, Tatsuo Kokabu, Shoichiro Nutrients Article Honeybees produce royal jelly (RJ) from their cephalic glands. Royal jelly is a source of nutrition for the queen honey bee throughout its lifespan and is also involved in fertility and longevity. Royal jelly has long been considered beneficial to human health. We recently observed that RJ delayed impairment of motor function during aging, affecting muscle fiber size. However, how RJ affects skeletal muscle metabolism and the functional component of RJ is as of yet unidentified. We demonstrate that feeding mice with RJ daily prevents a decrease in myofiber size following denervation without affecting total muscle weight. RJ did not affect atrophy-related genes but stimulated the expression of myogenesis-related genes, including IGF-1 and IGF receptor. Trans-10-hydroxy-2-decenoic acid (10H2DA) and 10-hydroxydecanoic acid (10HDAA), two major fatty acids contained in RJ. After ingestion, 10H2DA and 10HDAA are metabolized into 2-decenedioic acid (2DA) and sebacic acid (SA) respectively. We found that 10H2DA, 10HDAA, 2DA, and SA all regulated myogenesis of C2C12 cells, murine myoblast cells. These novel findings may be useful for potential preventative and therapeutic applications for muscle atrophy disease included in Sarcopenia, an age-related decline in skeletal muscle mass and strength. MDPI 2020-10-11 /pmc/articles/PMC7600733/ /pubmed/33050588 http://dx.doi.org/10.3390/nu12103089 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Shirakawa, Tomohiko Miyawaki, Aki Matsubara, Takuma Okumura, Nobuaki Okamoto, Hideto Nakai, Naoya Rojasawasthien, Thira Morikawa, Kazumasa Inoue, Asako Goto, Akino Washio, Ayako Tsujisawa, Toshiyuki Kawamoto, Tatsuo Kokabu, Shoichiro Daily Oral Administration of Protease-Treated Royal Jelly Protects Against Denervation-Induced Skeletal Muscle Atrophy |
title | Daily Oral Administration of Protease-Treated Royal Jelly Protects Against Denervation-Induced Skeletal Muscle Atrophy |
title_full | Daily Oral Administration of Protease-Treated Royal Jelly Protects Against Denervation-Induced Skeletal Muscle Atrophy |
title_fullStr | Daily Oral Administration of Protease-Treated Royal Jelly Protects Against Denervation-Induced Skeletal Muscle Atrophy |
title_full_unstemmed | Daily Oral Administration of Protease-Treated Royal Jelly Protects Against Denervation-Induced Skeletal Muscle Atrophy |
title_short | Daily Oral Administration of Protease-Treated Royal Jelly Protects Against Denervation-Induced Skeletal Muscle Atrophy |
title_sort | daily oral administration of protease-treated royal jelly protects against denervation-induced skeletal muscle atrophy |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7600733/ https://www.ncbi.nlm.nih.gov/pubmed/33050588 http://dx.doi.org/10.3390/nu12103089 |
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