Yüksek fruktozlu diyetle oluşturulan deneysel metabolik sendrom modelinde istemli fiziksel aktivitenin kardiyak yeniden şekillenmedeki rolünün araştırılması
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Dosyalar
Tarih
2023
Yazarlar
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Yayıncı
Trakya Üniversitesi Sağlık Bilimleri Enstitüsü
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Fruktozdan zengin beslenmeye bağlı oluşturulan metabolik sendrom modelinde kardiyak hipertrofiyi etkileyen moleküler mekanizmalar tam olarak bilinmemektedir. Çalışmamızda sıçanlarda fruktozdan zengin beslenmeye bağlı oluşan metabolik sendrom modelinde meydana gelen kardiyak yeniden şekillenmeyi AKT ve ERK yolakları üzerinden araştırmayı ve bu yeniden şekillenmede istemli fiziksel aktivitenin etkilerini belirlemeyi hedefledik. Çalışmamızda Sprague-Dawley ırkı 24 adet erişkin dişi sıçan kontrol, fruktoz, aktivite ve fruktoz+aktivite gruplarına ayrıldı. Fruktoz ve fruktoz+aktivite gruplarının içme sularına 200 g/L dozunda fruktoz eklenerek metabolik sendrom gelişmesi sağlandı. Aynı zaman periyodunda aktivite ve fruktoz+aktivite gruplarındaki sıçanlar istemli fiziksel aktivite yapmaları için aktivite ölçer tekerleklerin bulunduğu kafeslerde tutuldu. Çalışmanın ilk günü, 4. haftası ve 8. haftası olmak üzere üç farklı zamanda kan basıncı ölçümü alındı. Çalışmanın 8. haftasının sonunda tüm sıçanların kan ve sol ventrikül doku örnekleri alındı. Çalışmamızda fruktoz grubunda kontrol grubuna göre HOMA-IR indeksinde, kan trigliserit düzeyinde, sistolik ve diyastolik kan basıncında artış saptandı (tüm gruplar için p<0,05). Sol ventrikül dokusunda kontrol grubuna göre tüm gruplarda AKT protein ifadesinde belirgin bir artış görüldü (p<0,05). Fruktoz grubunda kontrol grubuna göre p-ERK 1/2 ve ERK 1/2 ifadelerinin arttığı, ERK 1/2 ifadesinde meydana gelen artışın fruktoz+aktivite grubunda azaldığı belirlendi (p<0,05). Bu çalışmanın sonuçları, fruktozdan zengin beslenme ile metabolik sendrom oluşturulan sıçanlarda AKT ve ERK yolaklarının aktivitesi ile kardiyak hipertrofinin geliştiğini düşündürmektedir. Çalışmamızda elde edilen bulgular, fruktozdan zengin beslenen sıçanlarda istemli fiziksel aktivitenin patolojik hipertrofi belirteci olan ERK 1/2 yolağını baskıladığını göstermektedir.
The molecular mechanisms affecting cardiac hypertrophy in the metabolic syndrome model created due to a fructose-rich diet are not fully known. In our study, we aimed to investigate the cardiac remodeling that occurs in the metabolic syndrome model caused by a fructose-rich diet in rats through the AKT and ERK pathways and to determine the effects of voluntary physical activity on this remodeling. In our study, 24 adult female Sprague-Dawley rats were divided into control, fructose, activity and fructose+activity groups. The development of metabolic syndrome was achieved by adding 200 g/L fructose to the drinking water of fructose and fructose+activity groups. During the same time period, rats in the activity and fructose+activity groups were kept in cages with activity meter wheels for voluntary physical activity. Blood pressure measurements were taken at three different times, on the first day, 4th week and 8th week of the study. At the end of the 8th week of the study, blood and left ventricular tissue samples were taken from all rats. . In this study, HOMA-IR index, blood triglyceride level, systolic and diastolic blood pressure were increased in the fructose group compared to the control group (for all groups p<0.05). A significant increase in AKT protein expression was observed in all groups compared to the control group in left ventricular tissue (p<0.05). It was determined that p-ERK 1/2 and ERK 1/2 expressions increased in the fructose group compared to the control group, and the increase in ERK 1/2 expression decreased in the fructose+activity group (p<0.05). The results of this study suggest that cardiac hypertrophy develops with the activity of AKT and ERK pathways in rats with metabolic syndrome induced by a fructose-rich diet. The findings of our study show that voluntary physical activity suppresses the ERK 1/2 pathway, which is a marker of pathological hypertrophy, in fructose-rich rats.
The molecular mechanisms affecting cardiac hypertrophy in the metabolic syndrome model created due to a fructose-rich diet are not fully known. In our study, we aimed to investigate the cardiac remodeling that occurs in the metabolic syndrome model caused by a fructose-rich diet in rats through the AKT and ERK pathways and to determine the effects of voluntary physical activity on this remodeling. In our study, 24 adult female Sprague-Dawley rats were divided into control, fructose, activity and fructose+activity groups. The development of metabolic syndrome was achieved by adding 200 g/L fructose to the drinking water of fructose and fructose+activity groups. During the same time period, rats in the activity and fructose+activity groups were kept in cages with activity meter wheels for voluntary physical activity. Blood pressure measurements were taken at three different times, on the first day, 4th week and 8th week of the study. At the end of the 8th week of the study, blood and left ventricular tissue samples were taken from all rats. . In this study, HOMA-IR index, blood triglyceride level, systolic and diastolic blood pressure were increased in the fructose group compared to the control group (for all groups p<0.05). A significant increase in AKT protein expression was observed in all groups compared to the control group in left ventricular tissue (p<0.05). It was determined that p-ERK 1/2 and ERK 1/2 expressions increased in the fructose group compared to the control group, and the increase in ERK 1/2 expression decreased in the fructose+activity group (p<0.05). The results of this study suggest that cardiac hypertrophy develops with the activity of AKT and ERK pathways in rats with metabolic syndrome induced by a fructose-rich diet. The findings of our study show that voluntary physical activity suppresses the ERK 1/2 pathway, which is a marker of pathological hypertrophy, in fructose-rich rats.
Açıklama
Anahtar Kelimeler
AKT, Egzersiz, ERK, Fruktoz, İstemli fiziksel aktivite, Exercise, Fructose, Voluntary physical activity
