تاثیر چاقی القایی و تمرینات تناوبی شدید بر محور PI3K/AKT1/mTORc1 در بافت قلب موش‌های صحرایی نر نژاد ویستار
محورهای موضوعی : فصلنامه زیست شناسی جانوری
سینا رضازاده
1
(گروه فیزیولوژی ورزشی، واحد اسلامشهر، دانشگاه آزاد اسلامی، تهران، ایران)
ساناز میرزایان شانجانی
2
(گروه فیزیولوژی ورزشی، واحد اسلامشهر، دانشگاه آزاد اسلامی، تهران، ایران)
مجتبی ایزدی
3
(گروه فیزیولوژی ورزشی، واحد ساوه، دانشگاه آزاد اسلامی، ساوه، ایران)
سعید صداقتی
4
(گروه فیزیولوژی ورزشی، واحد اسلامشهر، دانشگاه آزاد اسلامی، تهران، ایران)
یاسر کاظم زاده
5
(گروه فیزیولوژی ورزشی، واحد اسلامشهر، دانشگاه آزاد اسلامی، تهران، ایران)
کلید واژه: چاقی, تمرین تناوبی, بیان ژن, هایپرتروفی فیزیولوژیک قلب,
چکیده مقاله :
مطالعات اپیدمیولوژیکی همواره از چاقی به عنوان پیش زمینه دیابت نوع 2 و بیماری‌های قلبی-عروقی حمایت نموده¬اند. مطالعه حاضر با هدف تعیین اثر تمرینات تناوبی شدید بر بیان برخی ژن‌های موثر در هایپرتروفی فیزیولوژیکی قلبی (PI3K، AKT1و mTORc1) در رت‌های چاق نژاد ویستار انجام گرفت. برای این منظور، از 21 سر رت نر ویستار 10 هفته¬ای (10 ± 220 گرم)، 14 سر پس از القای چاقی توسط 6 هفته رژیم غذایی پر چرب به شیوه تصادفی به گروه‌های هفت¬تایی چاق کنترل و چاق تناوبی تقسیم شدند. هفت سر رت دارای وزن نرمال نیز به عنوان گروه نرمال انتخاب شدند. رت‌های گروه چاق تناوبی یک دوره تمرینات تناوبی 8 هفته‌ای (5 جلسه در هفته) در قالب دویدن¬های تناوبی روی تریدمیل را اجرا نمودند. گروه نرمال و چاق کنترل در برنامه تمرین شرکت نداشتند. 48 ساعت پس از آخرین جلسه تمرین، بیان ژن‌های PI3K، AKT1 و mTORc1 در بافت قلب اندازه¬گیری شد و توسط آزمون آنوای یکسویه و تست تعقیبی توکی بین گروه‌ها مقایسه شد. القای چاقی به کاهش AKT1، PI3K و mTORc1 در بافت قلب در گروه چاق کنترل نسبت به گروه نرمال منجر شد (001/0 = p). در مقایسه با گروه چاق کنترل، تمرینات تناوبی به افزایش بیانPI3K (001/0 = p) و mTORc1 (001/0 = p) منجر شد اما بیان AKT1 در پاسخ به تمرینات تناوبی تغییر معنی‌داری پیدا نکرد (603/0 = p). اجرای تمرینات تناوبی با بهبود بیان ژن‌های موثر بر هایپرتروفی فیزیولوژیکی قلب در رت‌های چاق همراه است. شناخت مکانیسم¬های سلولی مولکولی عهده¬دار این فرآیند نیازمند مطالعات بیشتری است.
Epidemiological studies have always supported obesity as a cause of type 2 diabetes and cardiovascular diseases. The present study was conducted with the aim of determining the effect of intense interval exercise on the expression of some genes effective in physiological cardiac hypertrophy (PI3K, AKT1, mTORc1) in obese Wistar rats. For this purpose, from 21 male Wistar rats aged 10 weeks (220 ± 10 g), 14 after induction of obesity by 6 weeks of high-fat diet (HFD) were randomly divided to control obese (n = 7) or interval obese (n = 7) groups. Also, 7 rats with normal weight were selected as normal group. The interval obese rats were completed 8-weeks interval training (5 times weekly) in the form of interval runs on the treadmill. The control obese and normal groups did not participate in the exercise program. 48 hours after the last training session, the expression of PI3K, AKT1 and mTORc1 genes in heart tissue was measured and compared between groups by one-way ANOVA and Tukey's post hoc test. Induction of obesity led to a significant decrease in PI3K, AKT1 and mTORc1 in the heart tissue in the obese control group compared to the normal group (p = 0.001). Compared to the obese control group, interval training increased the expression of PI3K (p = 0.001) and mTORc1 (p = 0.001), but AKT1 expression did not change significantly in response to interval training (p = 0.603). Interval training is associated with improving the expression of genes affecting the physiological hypertrophy of the heart tissue in obese rats. Knowing the molecular cellular mechanisms responsible for this process requires more studies.
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