語系:
繁體中文
English
說明(常見問題)
回圖書館首頁
手機版館藏查詢
登入
回首頁
切換:
標籤
|
MARC模式
|
ISBD
FindBook
Google Book
Amazon
博客來
Essential Amino Acid (EAA) Regulation of Skeletal Muscle Protein Turnover with Age.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Essential Amino Acid (EAA) Regulation of Skeletal Muscle Protein Turnover with Age./
作者:
Komp, Mary.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 2022,
面頁冊數:
93 p.
附註:
Source: Masters Abstracts International, Volume: 84-01.
Contained By:
Masters Abstracts International84-01.
標題:
Food science. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=29207679
ISBN:
9798834076636
Essential Amino Acid (EAA) Regulation of Skeletal Muscle Protein Turnover with Age.
Komp, Mary.
Essential Amino Acid (EAA) Regulation of Skeletal Muscle Protein Turnover with Age.
- Ann Arbor : ProQuest Dissertations & Theses, 2022 - 93 p.
Source: Masters Abstracts International, Volume: 84-01.
Thesis (M.S.)--University of Arkansas, 2022.
This item must not be sold to any third party vendors.
Skeletal muscle (SM) is vital for both long term health and quality of life. Recent research suggests an increase in catabolic signals with age triggers pathologic conditions, such as sarcopenia. Although results from in vitro studies model how EAA can regulate muscle protein synthesis (MPS), the relevance of these models to muscle protein breakdown (MPB) and the presence of physiological EAA concentrations remains to be established. Therefore, the objective of this study was to determine the effects of a low, normal, and supra physiological dose of EAA (0.2, 1.0, and 3.0 x EAA) in a young (passages 2-10) and aging (passages 16-24) C2C12 murine muscle cell model. We hypothesized that increased levels of EAA will increase MPS in aging cells and suppress MPB via mTORC1 when compared to young cells. Myoblasts were seeded (1x105) into 6-well plates and differentiated into myotubes when they reached 80% confluency. Myotubes were serum and AA starved for 24 hours before receiving one of the following treatments: control (CON), 0.2 x EAA, 1.0 x EAA, 3.0 x EAA with or without rapamycin (100 nm; rapamycin (RAP) for 1, 6, and 24 hours. All treatments were performed in triplicate and then each experiment was repeated three times, yielding nine wells per treatment. Phosphorylation for phospho and total protein of p70 S6 kinase 1 (p70S6K1), 4E binding protein 1 (4EBP1), mechanistic target of rapamycin (mTOR), general control nonderepressible 2 (GCN2), eukaryotic initiation factor 2- alpha (eIF2α) and Sestrin 2 (SESN2) was measured using Western Blot analysis. RAP inhibited phosphorylation of MPS markers p70S6K1 and 4EBP1 in all treatments. Whereas the activation of GCN2 in young and old muscle cells is independent of the availability of EAA and mTORC1 activation. The phosphorylation of 4EBP1 increased (p<0.05) following 0.2 x EAA in young cells and 3.0 x EAA in old cells compared to CON. Phosphorylation of p70S6K1 increased (p<0.05) following 0.2, 1.0, and 3.0 x EAA in young cells compared to the CON. In conclusion, we demonstrated EAA can regulate pathways associated with sarcopenia and increase molecular markers related to MPS in young and old muscle cells. Therefore, it can be proposed increasing EAA may be effective for regulating the rate of MPS and MPB via the mTORC1 pathway in both young and aging muscle cells.
ISBN: 9798834076636Subjects--Topical Terms:
3173303
Food science.
Subjects--Index Terms:
Aging
Essential Amino Acid (EAA) Regulation of Skeletal Muscle Protein Turnover with Age.
LDR
:03525nmm a2200397 4500
001
2350939
005
20221028161056.5
008
241004s2022 ||||||||||||||||| ||eng d
020
$a
9798834076636
035
$a
(MiAaPQ)AAI29207679
035
$a
AAI29207679
040
$a
MiAaPQ
$c
MiAaPQ
100
1
$a
Komp, Mary.
$3
3690477
245
1 0
$a
Essential Amino Acid (EAA) Regulation of Skeletal Muscle Protein Turnover with Age.
260
1
$a
Ann Arbor :
$b
ProQuest Dissertations & Theses,
$c
2022
300
$a
93 p.
500
$a
Source: Masters Abstracts International, Volume: 84-01.
500
$a
Advisor: Baum, Jamie.
502
$a
Thesis (M.S.)--University of Arkansas, 2022.
506
$a
This item must not be sold to any third party vendors.
520
$a
Skeletal muscle (SM) is vital for both long term health and quality of life. Recent research suggests an increase in catabolic signals with age triggers pathologic conditions, such as sarcopenia. Although results from in vitro studies model how EAA can regulate muscle protein synthesis (MPS), the relevance of these models to muscle protein breakdown (MPB) and the presence of physiological EAA concentrations remains to be established. Therefore, the objective of this study was to determine the effects of a low, normal, and supra physiological dose of EAA (0.2, 1.0, and 3.0 x EAA) in a young (passages 2-10) and aging (passages 16-24) C2C12 murine muscle cell model. We hypothesized that increased levels of EAA will increase MPS in aging cells and suppress MPB via mTORC1 when compared to young cells. Myoblasts were seeded (1x105) into 6-well plates and differentiated into myotubes when they reached 80% confluency. Myotubes were serum and AA starved for 24 hours before receiving one of the following treatments: control (CON), 0.2 x EAA, 1.0 x EAA, 3.0 x EAA with or without rapamycin (100 nm; rapamycin (RAP) for 1, 6, and 24 hours. All treatments were performed in triplicate and then each experiment was repeated three times, yielding nine wells per treatment. Phosphorylation for phospho and total protein of p70 S6 kinase 1 (p70S6K1), 4E binding protein 1 (4EBP1), mechanistic target of rapamycin (mTOR), general control nonderepressible 2 (GCN2), eukaryotic initiation factor 2- alpha (eIF2α) and Sestrin 2 (SESN2) was measured using Western Blot analysis. RAP inhibited phosphorylation of MPS markers p70S6K1 and 4EBP1 in all treatments. Whereas the activation of GCN2 in young and old muscle cells is independent of the availability of EAA and mTORC1 activation. The phosphorylation of 4EBP1 increased (p<0.05) following 0.2 x EAA in young cells and 3.0 x EAA in old cells compared to CON. Phosphorylation of p70S6K1 increased (p<0.05) following 0.2, 1.0, and 3.0 x EAA in young cells compared to the CON. In conclusion, we demonstrated EAA can regulate pathways associated with sarcopenia and increase molecular markers related to MPS in young and old muscle cells. Therefore, it can be proposed increasing EAA may be effective for regulating the rate of MPS and MPB via the mTORC1 pathway in both young and aging muscle cells.
590
$a
School code: 0011.
650
4
$a
Food science.
$3
3173303
650
4
$a
Nutrition.
$3
517777
650
4
$a
Molecular biology.
$3
517296
653
$a
Aging
653
$a
Amino acids
653
$a
Essential amino acids
653
$a
Muscles
653
$a
Protein synthesis
653
$a
Sarcopenia
653
$a
Phosphorylation
690
$a
0359
690
$a
0570
690
$a
0307
710
2
$a
University of Arkansas.
$b
Food Science.
$3
3282884
773
0
$t
Masters Abstracts International
$g
84-01.
790
$a
0011
791
$a
M.S.
792
$a
2022
793
$a
English
856
4 0
$u
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=29207679
筆 0 讀者評論
館藏地:
全部
電子資源
出版年:
卷號:
館藏
1 筆 • 頁數 1 •
1
條碼號
典藏地名稱
館藏流通類別
資料類型
索書號
使用類型
借閱狀態
預約狀態
備註欄
附件
W9473377
電子資源
11.線上閱覽_V
電子書
EB
一般使用(Normal)
在架
0
1 筆 • 頁數 1 •
1
多媒體
評論
新增評論
分享你的心得
Export
取書館
處理中
...
變更密碼
登入