Morphological changes in the heart and aorta of rats with diet-induced metabolic syndrome

Birulina, Yu. G.; Иванов, В. В.; Buyko, E. E.; Bykov, V. V.; Dzyuman, A. N.; Носарев, А. В.; Grigor'eva, A. V.; Гусакова, С. В.

doi:10.20538/1682-0363-2022-3-13-21

Cited by 1 publication

(2 citation statements)

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“…Крыс 3-й группы (n = 12; индуцированный диетой метаболический синдром, МетС) содержали в течение 84 дней на диете с высоким содержанием углево-дов и жиров (высокоуглеводная высокожировая диета (ВУВЖД); питьевая вода была заменена на 20%-й раствор фруктозы. Состав ВУВЖД: белки -16 %, жиры -21 %, углеводы -46 % (в том числе 17 % -фруктоза), холестерин -0,125 %, холиевая кислота -0,5 % [6]. После завершения ВУВЖД животных выдерживали в течение 7 дней на стандартной диете и обычной питьевой воде для исключения завышенных показателей артериального давления (АД) из-за осмотического влияния потребления фруктозы.…”

Section: методыunclassified

“…Полученные результаты позволяют нам говорить о формировании метаболического синдрома. Ранее наблюдали накопление липидов в миокарде и аорте крыс, содержащихся на диете, аналогичной применяемой в нашем исследовании [6]. Однако значимого влияния МетС на размер инфаркта мы не выявили.…”

Section: обсуждение результатовunclassified

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Restoration of adaptive cardioprotection impaired by metabolic syndrome in rats by the PPARα activation

Naryzhnaya,

Derkachev,

Kurbatov

et al. 2024

Acta biomedica scientifica

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Background. It is known that the protective effect of adaptation and conditioning influence is weakened in animals with metabolic syndrome. Metabolic syndrome may be the basis for the failure of cardioprotection in clinical settings.The aim of the study. To identify the relationship between disorder in carbohydrate and lipid metabolism and a decrease in the effectiveness of the infarct-limiting effect of moderate chronic normobaric hypoxia; to check the possibility of correcting reduced cardioprotection by normalizing carbohydrate and lipid metabolism.Methods. The study included 64 Wistar rats. Metabolic syndrome was induced by feeding animals a high-carbohydrate, high-fat diet for 84 days. Chronic normobaric hypoxia was carried out for 21 days in the following mode: 12 % O2 : 0.3 % CO2. Metformin at a dose of 200 mg/kg/day or PPARα agonist WY14643 at a dose of 1 mg/kg/day were added to the drinking water of rats with metabolic syndrome during adaptation period to hypoxia. A 45-minute coronary occlusion and 120-minute reperfusion were performed, and the infarct size was determined. Indicators of lipid and carbohydrate metabolism, leptin, and adiponectin were studied in the blood serum.Results. The infarct-limiting effect of chronic normobaric hypoxia was weakened in animals with metabolic syndrome. Infarct size showed a direct correlation with decreased glucose tolerance and serum triglyceride levels. Using metformin therapy did not lead to the restoration of the infarct-limiting effect of chronic normobaric hypoxia, while the normalization of lipid metabolism with the use of the PPARα agonist WY14643 corrected the impairment of adaptive cardioprotection in rats with metabolic syndrome.Conclusion. The lack of cardioprotection at chronic normobaric hypoxia in rats with metabolic syndrome is associated with impaired carbohydrate and lipid metabolism. The PPARα agonist restores impaired lipid metabolism and adaptive cardioprotection.

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Section: обсуждение результатовunclassified