PMID- 36638746
OWN - NLM
STAT- MEDLINE
DCOM- 20230213
LR  - 20230302
IS  - 1879-0739 (Electronic)
IS  - 0271-5317 (Linking)
VI  - 110
DP  - 2023 Feb
TI  - Lespedeza bicolor extract supplementation reduced hyperglycemia-induced skeletal 
      muscle damage by regulation of AMPK/SIRT/PGC1alpha-related energy metabolism in type 
      2 diabetic mice.
PG  - 1-13
LID - S0271-5317(22)00150-6 [pii]
LID - 10.1016/j.nutres.2022.12.007 [doi]
AB  - Lespedeza bicolor (LB) is known to have antidiabetic activities; however, the 
      underlying molecular mechanisms of LB in hyperglycemia-induced skeletal muscle 
      damage is unclear. Inflammation and oxidative stress caused by type 2 diabetes 
      mellitus (T2DM) not only contributes to insulin resistance, but also promotes 
      muscle atrophy via decreased muscle protein synthesis and increased protein 
      degradation, leading to frailty and sarcopenia. In this study, we hypothesized 
      that LB extract (LBE) supplementatin has an ameliorative effect on 
      hyperglycemia-induced skeletal muscle damage by activation of 5' adenosine 
      monophosphate-activated protein kinase (AMPK)/sirtuin 
      (SIRT)/proliferator-activated receptor gamma coactivator 1alpha (PGC1alpha)-associated energy 
      metabolism in mice with T2DM. Diabetes was induced by a high-fat diet with a 
      2-time streptozotoxin injection (30 mg/kg body weight) in male C57BL/6J mice. 
      After diabetes was induced (fasting blood glucose level >/=140 mg/dL), the mice 
      were administered with LBE at a low dose (100 mg/kg/d) or high dose (250 mg/kg/d) 
      by gavage for 12 weeks. LBE supplementation ameliorated glucose tolerance and 
      hemoglobin A1c (%) in mice with T2DM. Moreover, LBE supplementation upregulated 
      protein levels of insulin receptor subunit-1 and Akt accompanied by increased 
      translocation of glucose transporter 4 in mice with T2DM. Furthermore, LBE 
      increased mitochondrial biogenesis by activating SIRT1, SIRT3, SIRT4, and 
      peroxisome PGC1alpha in diabetic skeletal muscle. Meanwhile, LBE supplementation 
      reduced oxidative stress and inflammation in mice with T2DM. Taken together, the 
      current study suggested that LBE could be a potential therapeutic to prevent 
      skeletal muscle damage by regulation AMPK/SIRT/PGC1alpha-related energy metabolism in 
      T2DM.
CI  - Copyright (c) 2022 Elsevier Inc. All rights reserved.
FAU - Lee, Heaji
AU  - Lee H
AD  - Department of Food and Nutrition, Kyung Hee University, Seoul 02447, Republic of 
      Korea.
FAU - Kim, Sun Yeou
AU  - Kim SY
AD  - College of Pharmacy, Gachon University, Incheon 21936, Republic of Korea.
FAU - Lim, Yunsook
AU  - Lim Y
AD  - Department of Food and Nutrition, Kyung Hee University, Seoul 02447, Republic of 
      Korea. Electronic address: ylim@khu.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20221222
PL  - United States
TA  - Nutr Res
JT  - Nutrition research (New York, N.Y.)
JID - 8303331
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha)
RN  - 0 (Plant Extracts)
SB  - IM
MH  - Animals
MH  - Male
MH  - Mice
MH  - AMP-Activated Protein Kinases/metabolism
MH  - *Diabetes Mellitus, Experimental/complications/drug therapy
MH  - *Diabetes Mellitus, Type 2/complications/drug therapy/metabolism
MH  - Dietary Supplements
MH  - Energy Metabolism
MH  - *Hyperglycemia/metabolism
MH  - *Lespedeza/chemistry
MH  - Mice, Inbred C57BL
MH  - Muscle, Skeletal
MH  - Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism
MH  - *Plant Extracts/pharmacology
OTO - NOTNLM
OT  - Energy metabolism
OT  - Insulin signaling
OT  - Lespedeza bicolor
OT  - Skeletal muscle
OT  - Type 2 diabetes mellitus
COIS- Declaration of Competing Interest The authors declare that there is no conflict 
      of interest regarding the publication of this paper.
EDAT- 2023/01/14 06:00
MHDA- 2023/02/11 06:00
CRDT- 2023/01/13 18:19
PHST- 2022/03/28 00:00 [received]
PHST- 2022/12/19 00:00 [revised]
PHST- 2022/12/19 00:00 [accepted]
PHST- 2023/01/14 06:00 [pubmed]
PHST- 2023/02/11 06:00 [medline]
PHST- 2023/01/13 18:19 [entrez]
AID - S0271-5317(22)00150-6 [pii]
AID - 10.1016/j.nutres.2022.12.007 [doi]
PST - ppublish
SO  - Nutr Res. 2023 Feb;110:1-13. doi: 10.1016/j.nutres.2022.12.007. Epub 2022 Dec 22.