VLDL from Metabolic Syndrome Individuals Enhanced Lipid Accumulation in Atria with Association of Susceptibility to Atrial Fibrillation

Autor: Bin-Nan Wu, Chi Wei, Chu-Huang Chen, Sheng-Hsiung Sheu, Hsiang-Chun Lee, Shyi-Jang Shin, Wen-Ter Lai, Liang-Yin Ke, Yi-Lin Hsiao, Hsin-Ting Lin, Chih-Sheng Chu
Jazyk: angličtina
Rok vydání: 2016
Předmět:
Male
0301 basic medicine
Very low-density lipoprotein
Cardiac output
very-low-density lipoprotein (VLDL)
Apoptosis
Lipoproteins
VLDL
030204 cardiovascular system & hematology
lcsh:Chemistry
Mice
0302 clinical medicine
Diastole
Atrial Fibrillation
Medicine
Cardiac Output
lcsh:QH301-705.5
Spectroscopy
Atrial fibrillation
General Medicine
Stroke volume
Middle Aged
lipotoxicity
Computer Science Applications
atrial fibrillation
metabolic syndrome
Echocardiography
Injections
Intravenous
Female
lipids (amino acids
peptides
and proteins)
Disease Susceptibility
Adult
medicine.medical_specialty
Cardiotonic Agents
Systole
Article
Catalysis
Inorganic Chemistry
03 medical and health sciences
Internal medicine
Animals
Humans
Heart Atria
Physical and Theoretical Chemistry
Molecular Biology
Dyslipidemias
business.industry
Organic Chemistry
Isoproterenol
Stroke Volume
medicine.disease
Mice
Inbred C57BL
030104 developmental biology
Endocrinology
lcsh:Biology (General)
lcsh:QD1-999
Metabolic syndrome
business
Dyslipidemia
Zdroj: International Journal of Molecular Sciences; Volume 17; Issue 1; Pages: 134
International Journal of Molecular Sciences
International Journal of Molecular Sciences, Vol 17, Iss 1, p 134 (2016)
ISSN: 1422-0067
DOI: 10.3390/ijms17010134
Popis: Metabolic syndrome (MetS) represents a cluster of metabolic derangements. Dyslipidemia is an important factor in MetS and is related to atrial fibrillation (AF). We hypothesized that very low density lipoproteins (VLDL) in MetS (MetS-VLDL) may induce atrial dilatation and vulnerability to AF. VLDL was therefore separated from normal (normal-VLDL) and MetS individuals. Wild type C57BL/6 male mice were divided into control, normal-VLDL (nVLDL), and MetS-VLDL (msVLDL) groups. VLDL (15 µg/g) and equivalent volumes of saline were injected via tail vein three times a week for six consecutive weeks. Cardiac chamber size and function were measured by echocardiography. MetS-VLDL significantly caused left atrial dilation (control, n = 10, 1.64 ± 0.23 mm; nVLDL, n = 7, 1.84 ± 0.13 mm; msVLDL, n = 10, 2.18 ± 0.24 mm; p < 0.0001) at week 6, associated with decreased ejection fraction (control, n = 10, 62.5% ± 7.7%, vs. msVLDL, n = 10, 52.9% ± 9.6%; p < 0.05). Isoproterenol-challenge experiment resulted in AF in young msVLDL mice. Unprovoked AF occurred only in elderly msVLDL mice. Immunohistochemistry showed excess lipid accumulation and apoptosis in msVLDL mice atria. These findings suggest a pivotal role of VLDL in AF pathogenesis for MetS individuals.
Databáze: OpenAIRE
Externí odkaz: