PMID- 32475911
OWN - NLM
STAT- MEDLINE
DCOM- 20210121
LR  - 20210121
IS  - 1347-5215 (Electronic)
IS  - 0918-6158 (Linking)
VI  - 43
IP  - 6
DP  - 2020
TI  - beta-Aminoisobutyric Acid Suppresses Atherosclerosis in Apolipoprotein E-Knockout 
      Mice.
PG  - 1016-1019
LID - 10.1248/bpb.b20-00078 [doi]
AB  - Endurance exercise training has been shown to induce peroxisome 
      proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) expression in skeletal 
      muscle. We recently reported that skeletal muscle-specific PGC-1alpha overexpression 
      suppressed atherosclerosis in apolipoprotein E-knockout (ApoE(-/-)) mice. 
      beta-Aminoisobutyric acid (BAIBA) is a PGC-1alpha-dependent myokine secreted from 
      myocytes that affects multiple organs. We have also reported that BAIBA 
      suppresses tumor necrosis factor-alpha-induced vascular cell adhesion molecule-1 
      (VCAM-1) and monocyte chemoattractant protein-1 (MCP-1) gene expression in 
      endothelial cells. In the present study, we hypothesized that BAIBA suppresses 
      atherosclerosis progression, and tested that hypothesis with ApoE(-/-) mice. The 
      mice were administered water containing BAIBA for 14 weeks, and were then 
      sacrificed at 20 weeks of age. Atherosclerotic plaque area, plasma BAIBA 
      concentration, and plasma lipoprotein profiles were assessed. Immunohistochemical 
      analyses of the plaque were performed to assess VCAM-1 and MCP-1 protein 
      expression levels and macrophage infiltration. The results showed that BAIBA 
      administration decreased atherosclerosis plaque area by 30%, concomitant with the 
      elevation of plasma BAIBA levels. On the other hand, plasma lipoprotein profiles 
      were not changed by the administration. Immunohistochemical analyses indicated 
      reductions in VCAM-1, MCP-1, and Mac-2 protein expression levels in the plaque. 
      These results suggest that BAIBA administration suppresses atherosclerosis 
      progression without changing plasma lipoprotein profiles. We propose that the 
      mechanisms of this suppression are reductions in both VCAM-1 and MCP-1 expression 
      as well as macrophage infiltration into the plaque.
FAU - Shimba, Yuki
AU  - Shimba Y
AD  - Laboratory of Nutritional Biochemistry, Graduate School of Nutritional and 
      Environmental Sciences, University of Shizuoka.
FAU - Katayama, Keigo
AU  - Katayama K
AD  - Laboratory of Nutritional Biochemistry, Graduate School of Nutritional and 
      Environmental Sciences, University of Shizuoka.
FAU - Miyoshi, Noriyuki
AU  - Miyoshi N
AD  - Laboratory of Biochemistry, Graduate School of Nutritional and Environmental 
      Sciences, University of Shizuoka.
FAU - Ikeda, Masahiko
AU  - Ikeda M
AD  - Faculty of Social and Environmental Studies, Tokoha University.
FAU - Morita, Akihito
AU  - Morita A
AD  - Laboratory of Nutritional Biochemistry, Graduate School of Nutritional and 
      Environmental Sciences, University of Shizuoka.
FAU - Miura, Shinji
AU  - Miura S
AD  - Laboratory of Nutritional Biochemistry, Graduate School of Nutritional and 
      Environmental Sciences, University of Shizuoka.
LA  - eng
PT  - Journal Article
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (Aminoisobutyric Acids)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Galectin 3)
RN  - 0 (Lipids)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - T68ALE2O9F (3-aminoisobutyric acid)
SB  - IM
MH  - Aminoisobutyric Acids/blood/pharmacokinetics/pharmacology/*therapeutic use
MH  - Animals
MH  - Aortic Valve/drug effects/pathology
MH  - Atherosclerosis/*drug therapy/metabolism/pathology
MH  - Chemokine CCL2/metabolism
MH  - Galectin 3/metabolism
MH  - Lipids/blood
MH  - Mice, Knockout, ApoE
MH  - Vascular Cell Adhesion Molecule-1/metabolism
OTO - NOTNLM
OT  - apolipoprotein E-knockout mouse
OT  - monocyte chemoattractant protein-1
OT  - myokine
OT  - vascular cell adhesion molecule-1
OT  - beta-aminoisobutyric acid
EDAT- 2020/06/02 06:00
MHDA- 2021/01/22 06:00
CRDT- 2020/06/02 06:00
PHST- 2020/06/02 06:00 [entrez]
PHST- 2020/06/02 06:00 [pubmed]
PHST- 2021/01/22 06:00 [medline]
AID - 10.1248/bpb.b20-00078 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 2020;43(6):1016-1019. doi: 10.1248/bpb.b20-00078.