Papers

Peer-reviewed International journal
2019

Dietary modification reduces serum ANGPTL2 levels and arterial stiffness in overweight and obese men

Journal of Exercise Nutrition and Biochemistry
  • Park J
  • ,
  • Choi Y
  • ,
  • Mizushima R
  • ,
  • Yoshikawa T
  • ,
  • Myoenzono K
  • ,
  • Tagawa K
  • ,
  • Matsui M
  • ,
  • Tanaka K
  • ,
  • Maeda S

Volume
23
Number
3
First page
39
Last page
44
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.20463/jenb.2019.0021

PURPOSE: Weight loss can reduce obesity-induced arterial stiffening that is attributed to decreased inflammation. Angiopoietin-like protein 2 (ANGPTL2) is a pro-inflammatory adipokine that is upregulated in obesity and is important in the progression of atherosclerosis and cardiovascular disease. The purpose of this study is to investigate the effects of dietary modification on circulating ANGPTL2 levels and arterial stiffness in overweight and obese men. METHODS: Twenty-two overweight and obese men (with mean age of 56 ± 2 years and body mass index of 28.6 ± 2.6 kg/m2) completed a 12-week dietary modification program. We measured the arterial compliance and β-stiffness index (as the indices of arterial stiffness) and serum ANGPTL2 levels before and after the program. RESULTS: After the 12-week dietary modification, body mass and daily energy intake were significantly reduced. Arterial compliance was significantly increased and β-stiffness index was significantly decreased after the 12-week dietary modification program. Serum ANGPTL2 levels were significantly decreased. Also, the changes in arterial compliance were negatively correlated with the changes in serum ANGPTL2 levels, whereas the changes in β-stiffness index were positively correlated with the changes in serum ANGPTL2 levels. CONCLUSION: These results suggest that the decrease in circulating ANGPTL2 levels can be attributed to the dietary modification-induced reduction of arterial stiffness in overweight and obese men.

Link information
DOI
https://doi.org/10.20463/jenb.2019.0021
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/31743976
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6823644
ID information
  • DOI : 10.20463/jenb.2019.0021
  • Pubmed ID : 31743976
  • Pubmed Central ID : PMC6823644

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