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The effect of high-calorie meal consumption on oxidative stress and endothelial dysfunction in healthy male adults
S. Kackov, AM. Simundic, N. Nikolac, I. Celap, L. Dukic, D. Ruzic, M. Bilusic
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- apolipoproteiny A genetika MeSH
- cévní endotel patofyziologie MeSH
- dietní tuky metabolismus MeSH
- dospělí MeSH
- energetický příjem MeSH
- hypertriglyceridemie patofyziologie MeSH
- jednonukleotidový polymorfismus genetika MeSH
- lidé středního věku MeSH
- lidé MeSH
- oxidační stres * MeSH
- postprandiální období * MeSH
- referenční hodnoty MeSH
- senioři MeSH
- triglyceridy krev MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Several authors have reported the association of postprandial hypertriglyceridemia with oxidative stress, systemic inflammation and endothelial dysfunction. Our aim was to investigate the effect of high-calorie meal on blood markers of oxidative stress and endothelial dysfunction and the association of APOA5 -1131T/C and -250G/A hepatic lipase (HL) polymorphisms with postprandial triglyceride response. This study included 102 healthy male volunteers. All participants consumed a high-calorie meal (823 calories, 50 g fat, 28 g protein, 60 g carbohydrates). Total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, hsCRP, TAS and ICAM-1 were measured at fasting state and postprandially. APOA5 -1131T/C and -250G/A HL polymorphisms were also determined. Postprandial triglycerides were significantly increased (1.4 (1.1-2.1) vs. 2.4 (1.9-3.3) mmol/l, P<0.001). Average triglyceride increase was 1.0+/-0.7 mmol/l (65 %). Concentration of triglycerides, HDL-cholesterol, LDL-cholesterol, TAS and ICAM-1 differed significantly between the fasting state and postprandial measurements (P<0.001). However, those differences were within the limits of analytical imprecision. Other parameters did not change 3 h after the meal. Triglycerides response did not differ respective to the APOA5 and HL polymorphisms. Family history of hypertension and acute myocardial infarction were associated with higher postprandial triglyceride concentrations. Postprandial hypertriglyceridemia is not associated with increased concentrations of hsCRP, TAS and ICAM-1. Furthermore, APOA5 -1131T/C and -250G/A HL polymorphisms are not associated with different postprandial triglyceride response.
Medical Biochemistry Laboratory Policlinic Bonifarm Zagreb Croatia
University Department of Chemistry Sisters of Mercy University Hospital Center Zagreb Croatia
Citace poskytuje Crossref.org
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- $a Several authors have reported the association of postprandial hypertriglyceridemia with oxidative stress, systemic inflammation and endothelial dysfunction. Our aim was to investigate the effect of high-calorie meal on blood markers of oxidative stress and endothelial dysfunction and the association of APOA5 -1131T/C and -250G/A hepatic lipase (HL) polymorphisms with postprandial triglyceride response. This study included 102 healthy male volunteers. All participants consumed a high-calorie meal (823 calories, 50 g fat, 28 g protein, 60 g carbohydrates). Total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, hsCRP, TAS and ICAM-1 were measured at fasting state and postprandially. APOA5 -1131T/C and -250G/A HL polymorphisms were also determined. Postprandial triglycerides were significantly increased (1.4 (1.1-2.1) vs. 2.4 (1.9-3.3) mmol/l, P<0.001). Average triglyceride increase was 1.0+/-0.7 mmol/l (65 %). Concentration of triglycerides, HDL-cholesterol, LDL-cholesterol, TAS and ICAM-1 differed significantly between the fasting state and postprandial measurements (P<0.001). However, those differences were within the limits of analytical imprecision. Other parameters did not change 3 h after the meal. Triglycerides response did not differ respective to the APOA5 and HL polymorphisms. Family history of hypertension and acute myocardial infarction were associated with higher postprandial triglyceride concentrations. Postprandial hypertriglyceridemia is not associated with increased concentrations of hsCRP, TAS and ICAM-1. Furthermore, APOA5 -1131T/C and -250G/A HL polymorphisms are not associated with different postprandial triglyceride response.
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