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Semaglutide Reverses Ectopic Lipid Accumulation, Impaired Myocardial Perfusion Reserve, and Diastolic Dysfunction in a Mouse Model of Cardiometabolic Heart Disease
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DOI：10.1016/j.jacbts.2026.101554.png)
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Abstract
En 中文
• The GLP-1RA SEMA has been shown to improve symptoms and outcomes of obesity-related cardiovascular disease; yet, the underlying mechanisms remain incompletely understood. • We utilized multiparametric CMR in mice fed an HFHS diet to investigate SEMA’s effects on VAT and cardiovascular function, and to determine whether these effects are independent of changes in dietary intake. • SEMA reversed key features of obesity-induced cardiometabolic heart disease, including ectopic lipid accumulation, CMD, and systolic and diastolic strain impairments, independently of dietary intake.
Keywords:
coronary microvascular dysfunction
epicardial adipose tissue
GLP-1RA
HFpEF
obesity
ASL
arterial spin labeling
CMD
coronary microvascular dysfunction
CMR
cardiac magnetic resonance
DENSE
displacement encoding with stimulated echoes
EAT
epicardial adipose tissue
Ecc
circumferential strain
EDV
end-diastolic volume
EF
ejection fraction
ESV
end-systolic volume
FAC
fatty acid composition
GLP-1RA
glucagon-like peptide-1 receptor agonist
GTT
glucose tolerance testing
HFHS
high-fat, high-sucrose
HFpEF
heart failure with preserved ejection fraction
LV
left ventricle
MBF
myocardial blood flow
MPR
myocardial perfusion reserve
PDFF
proton density fat fraction
PEDSR
peak early diastolic strain rate
PF
pair-fed
PSR
picrosirius red
SAT
subcutaneous adipose tissue
SEMA
semaglutide
SFAi
saturated fatty acid index
VAT
visceral adipose tissue
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