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High‐Saturated Fat High‐Sugar Diet Accelerates Left‐Ventricular Dysfunction Faster than High‐Saturated Fat Diet Alone via Increasing Oxidative Stress and Apoptosis in Obese‐Insulin Resistant Rats
Author(s) -
Apaijai Nattayaporn,
Arinno Apiwan,
Palee Siripong,
Pratchayasakul Wasana,
Kerdphoo Sasiwan,
Jaiwongkam Thidarat,
Chunchai Titikorn,
Chattipakorn Siriporn C,
Chattipakorn Nipon
Publication year - 2019
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201800729
Subject(s) - oxidative stress , medicine , endocrinology , insulin resistance , insulin , apoptosis , diabetes mellitus , saturated fat , oxidative phosphorylation , biology , biochemistry , cholesterol
Scope It has been hypothesized that a high‐saturated‐fat, high‐sugar diet (HFHS) causes worse cardiometabolic dysfunction than a high‐saturated‐fat diet (HFD) due to severe mitochondrial dysfunction, oxidative stress, and apoptosis in obese insulin‐resistant rats. Methods and Results Rats are divided into three groups to receive normal diet (ND), HFD, or HFHS for 24 weeks. Cardiometabolic parameters are determined at baseline and every 4 weeks until the end of the feeding protocol. At week 24, hearts are removed to determine mitochondrial function and dynamics, apoptosis, and insulin signaling. HFD and HFHS rats develop obese insulin‐resistance at week 8. However, fasting plasma glucose level is increased only in HFHS rats. Myocardial insulin signaling is markedly impaired in HFHS rats compared to other groups. Cardiac autonomic imbalance is observed in both HFD and HFHS rats beginning at week 8. However, cardiac dysfunction is observed earlier (week 8) in HFHS rats, and later at week 12 in HFD rats. Moreover, cardiac and mitochondrial oxidative stress levels, and apoptosis are greater in HFHS rats than HFD rats. Conclusion Both HFD and HFHS cause cardiometabolic dysfunction. HFHS causes more severe metabolic disturbance, oxidative stress, and apoptosis than HFD, which leads to an accelerated LV dysfunction in HFHS rats.