Consuming oxidative frying oil impairs cardiac energy production and calcium recycling, causing cardiac hypertrophy, fibrosis and diastolic dysfunction in male Sprague Dawley rats

doi:10.1016/j.jnutbio.2021.108816

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Title:	Consuming oxidative frying oil impairs cardiac energy production and calcium recycling, causing cardiac hypertrophy, fibrosis and diastolic dysfunction in male Sprague Dawley rats
Authors:	Lin, Yu-Shun Chen, Da-Long Shaw, Huey-Mei Wang, Guei-Jane Chao, Pei-Min
Contributors:	China Med Univ, Dept Nutr China Med Univ, Grad Inst Clin Med Sci China Med Univ Hosp, Dept Cardiol Chia Nan Univ Pharm & Sci, Dept Hlth & Nutr China Med Univ, Grad Inst Biomed Sci China Med Univ Hosp, Dept Med Res
Keywords:	Oxidative frying oil Cardiac hypertrophy Cardiac diastolic dysfunction Energy production Calcium cycling Vitamin E
Date:	2021
Issue Date:	2023-11-11 11:48:36 (UTC+8)
Publisher:	ELSEVIER SCIENCE INC
Abstract:	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-alpha-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. (C) 2021 Elsevier Inc. All rights reserved.
Relation:	J NUTR BIOCHEM, v.98
Appears in Collections:	[Dept. of Health and Nutrition (including master's program)] Periodical Articles

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