Consuming oxidative frying oil impairs cardiac energy production and calcium recycling, causing cardiac hypertrophy, fibrosis and diastolic dysfunction in male Sprague Dawley rats
| Autor: | Huey-Mei Shaw, Guei-Jane Wang, Da-Long Chen, Yu-Shun Lin, Pei-Min Chao |
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| Rok vydání: | 2021 |
| Předmět: |
Male
Cardiac function curve medicine.medical_specialty Endocrinology Diabetes and Metabolism medicine.medical_treatment Clinical Biochemistry Diastole chemistry.chemical_element Blood Pressure Cardiomegaly Oxidative phosphorylation Calcium medicine.disease_cause Biochemistry Antioxidants Rats Sprague-Dawley Fibrosis Internal medicine medicine Animals Vitamin E Cooking Molecular Biology Nutrition and Dietetics Chemistry Myocardium Calcium-Binding Proteins medicine.disease Diet Rats Soybean Oil Phospholamban Oxidative Stress Endocrinology Female Oxidation-Reduction Oxidative stress |
| Zdroj: | The Journal of Nutritional Biochemistry. 98:108816 |
| ISSN: | 0955-2863 |
| DOI: | 10.1016/j.jnutbio.2021.108816 |
| Popis: | With regards to cardiovascular health, frequent consumption of fried foods is discouraged, despite a lack of clear evidence of a direct link between eating oxidative frying oil (OFO) and cardiovascular diseases. In this study, male Sprague Dawley rats were exposed to diets containing fresh or fried soybean oil (groups C and O, respectively) from in utero to 28 weeks of age. A subset of rats in group O was supplemented with vitamin E (500 mg/kg of DL-α-tocopherol acetate; group OE) from 8 week of age onward to mitigate oxidative stress associated with OFO ingestion. Echocardiography, cardiac histology and indices associated with ATP production and calcium cycling in cardiac tissues were measured. Compared to group C, there was cardiac hypertrophy, fibrosis and diastolic dysfunction, in groups O and OE, with no differences between the latter two groups. Although cardiac mRNA levels of genes associated with mitochondrial biogenesis and function were increased, there were lower ATP concentrations and higher transcripts of uncoupling proteins in groups O and OE than in group C. In addition, decreases in phosphorylation of phospholamban and Ca2+/calmodulin-dependent protein kinase II activity, plus increased protein phosphatase 2A activity in groups O and OE, implied calcium cycling required for cardiac function was disrupted by OFO consumption. We concluded that long-term OFO exposure resulted in cardiac hypertrophy, fibrosis and diastolic dysfunction that was not mitigated by vitamin E supplementation. Underlying mechanisms were partly attributed to inefficient energy production via uncoupled phosphorylation and disrupted calcium cycling. |
| Databáze: | OpenAIRE |
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