اساس بیوشیمیایی فوائد روزه

نوع مقاله : مقاله ترویجی

نویسندگان

گروه بیوشیمی، مرکز تحقیقات بیوشیمی و بیوفیزیک، دانشگاه تهران، تهران، ایران.

چکیده

با عنایت به پیشرفت های شگرف اخیر در باره پرخوری و ضد آن یعنی گرسنگی و تاثیرات آنها بر سلامت، درک ما از تاثیر این رفتارها بر سلامتی به مراتب عمیق تر شده است. انسان موجودی است که در طی هزاران سال زندگی به خوبی به گرسنگی خو گرفته است. زیرا بر خلاف روزگار فعلی غذا به وفور و عند المطالبه در دسترس ما نبوده است. بر این اساس تغذیه ممتد و بلاوقفه با عادات چندین هزاران ساله ما در تناقض است. طبیعتا بدن ما با چنین رفتاری سازگار نبوده و منطقی است که انتظار وقوع بیماری های متعدد ناشی از این رفتار را داشته باشیم. بر عکس روزه حالتی است که بدن ما طی ده ها هزار سال با آن سازگار گشته است . مطالعات نشان می دهند که با فاصله انداختن بین دو وعده غذایی که در روزه به بهترین نحو اتفاق می افتد مسیر mTOR٢ غیر فعال شده و متعاقب آن فرایند فیزیولوژیک خود خوری درون سلولی (اتوفاژی) فعال می گردد. خودخوری موجب سالم شدن سلولها، کاهش سرعت پیری و کاهش روند بیماری های تحلیل برنده عصبی می گردد. از طرف دیگر کاهش فعالیت mTOR اثرات مثبت بر سرطان و دیابت نوع ۲ می گذارد. در این نوشتار مکانیسم هایی که از طریق آن روزه می تواند موجب سلامتی ما گردد مورد تفحص قرار گرفته است. 

کلیدواژه‌ها


عنوان مقاله [English]

Biochemical Basis for the Benefits of Fasting

نویسندگان [English]

  • Jamshid Davoodi
  • Azadeh Sarfallah
Department of Biochemistry, Institute of Biochemistry and Biophysics, University of Tehran, Tehran Iran.
چکیده [English]

Given the recent advancements on the effects of food intake on health, our understanding of nutritional behavior on human health has greatly expanded. Our body is adapted to prolonged hunger due to scarcity of food in a great portion of human history. Only in recent years has we had on demand access to food. Accordingly, continuous food consumption goes against the habit of starvation, which our body is accustomed to for tens of thousands of years. It is logical, therefore, to expect various pathological conditions rising from such a change in our feeding habit. On the contrary, fasting during Ramadan appears to be in complete agreement with our habit of prolonged food deprivation and thus should be beneficial to our health. Studies show that by increasing the intervals between two consecutive food intakes, which is best achieved during Ramadan, mammalian Target of Rapamycin pathway is inactivated leading to enhanced autophagy. Reduced mTOR activation slows aging, is beneficial to neurodegenerative conditions, cancer, and type 2 diabetes. This article is aimed at understanding possible mechanisms through which fasting can be beneficial to human health.

کلیدواژه‌ها [English]

  • Benefits of Fasting
  • Health
  • mTOR
  • Autophagy
[1]. Hall, M. N. (2013). " Talks about TORCs: Recent Advances in Target of Rapamycin Signalling", Biochemical Society Transactions, Vol. 41, No. 4. PP. 887–8.
[2]. Sharp, Z. D. Nelson, J. F. and Strong R. (2013). "mTOR, Aging and the Potential for Intervention", Experimental Medicine, Vol. 31, No. 20. PP. 1–12.
[3]. Laplante, M. and Sabatini, D. M. (2012). "mTOR Signaling in Growth Control and Disease",Cell, Vol. 149, No. 2. PP. 274–293.
[4]. Dibble, C. C. and Manning, B. D. (2013). "Signal Integration by mTORC1 Coordinates Nutrient Input with Biosynthetic Output", Nature Cell Biology, Vol. 15, No. 6. PP. 555–64.
[5]. Laplante, M. and Sabatini, D. M. (2009). "mTOR Signaling at a Glance", Journal of Cell Science, Vol. 122, No. 20. PP. 3589–94.
[6]. Shimobayashi, M. and Hall, M. N. (2014). "Making New Contacts: the mTOR Network in Metabolism and Signalling Crosstalk", Nature Reviews Molecular Cell Biololgy, Vol. 15, No. 3. PP. 155–62.
[7]. Alayev, A. and Holz, M. K. (2013). "mTOR Signaling for Biological Control and Cancer", Journal of Cell Physiology, Vol. 228, No. 8. PP. 1658–64.
[8].Zoncu, R., Efeyan, A. and Sabatini, D. M. (2011). "mTOR: from Growth Signal Integration to Cancer,Diabetes and Ageing", Nature Reviews Molecular Cell Biololgy, Vol. 12, No. 1. PP. 21–35.
[9].Dann, S. G., Selvaraj, A., and Thomas, G. (2007)."mTOR Complex1-S6K1 Signaling: at the Crossroads of Obesity, Diabetes and Cancer", Trends in Molecular Medicine, Vol. 13, No. 6, PP. 252–9.
[10].Dunlop, E. A and Tee, A. R. (2014)."mTOR and Autophagy: A Dynamic Relationship Governed by Nutrients and Energy", Seminars in Cell and Developmental Biology, PP. 1–9.
[11].Ravikumar, B., Sarkar, S. Davies, J. E., Futter, M., Garcia-arencibia, M., Green-thompson, Z. W., Jimenezsanchez, M., Korolchuk, V. I., Lichtenberg, M., Luo, S., Massey, D. C. O., Menzies, F. M., Moreau, K., Narayanan, U., Renna, M., Siddiqi, F. H., Underwood, B. R., Winslow, A. R., and Rubinsztein, D. C. (2010)."Regulation of Mammalian Autophagy in Physiology and Pathophysiology", Physiology Reviews, Vol. 90, PP. 1383–1435.
[12].Jung, C. H., Ro, S.-H., Cao, Otto, J. N. M. and Kim, D.-H. (2010 )."mTOR Regulation of Autophagy", FEBS Letters, Vol. 584, No. 7. PP. 1287–95.
[13].Jewell,J. L., Russell, R. C. and Guan, K.-L. (2013)."AminoAcidSignalling Upstream of Mtor", Nature Reviews Molecular Cell Biololgy, Vol. 14, No. 3. PP. 133–9.
[14].Nixon, R.A. (2013). "The Role of Autophagy in Neurodegenerative Disease", Nature Medicine, Vol. 19. PP. 983–97.
[15].Wong, M. (2012)."Mammalian Target of Rapamycin (mTOR) Pathways in Neurological Diseases", Biomedical Journal, Vol.36, No.2. PP. 40–50.
[16].Saxena, A. and Sampson, J. R. (2014). "Phenotypes Associated with Inherited and Developmental Somatic Mutations in Genes Encoding mTOR Pathway Components", Seminars in Cell and Developmental Biology. Vol. 36, PP. 140–6.
[17].Cornu, M., Albert, V. and Hall, M. N. (2013)."mTOR in Aging, Metabolism, and Cancer", Current Opinion in Genetics and Development, Vol. 23, No. 1. PP. 53–62.
[18].Leontieva,O. V, Paszkiewicz, G. M. and Blagosklonny, M. V. (2012). "Mechanistic or Mammalian Target of Rapamycin (mTOR) may Determine Robustness in Young male Mice at the Cost of Accelerated Aging", Aging, Vol. 4, No. 12. PP. 899–916.
[19].Blagosklonny, M. V (2010 ). "Calorie Restriction, Decelerating mTOR-Driven Aging from Cells to Organisma (including humans)", Landes Biosciences, Vol. 9, No. 4. PP. 683–688.
[20].Tor, R. O. S. and Blagosklonny, M. V (2008). "Aging ROS or TOR", Landes Biosciences, Vol. 7, No. 21. PP. 3344–3354.
[21]. Harrison, D. E., Strong, R., Sharp, Z. D., Nelson, J. F., Clinton, M. Flurkey, K., Nadon, N. L., Wilkinson, J. E., Frenkel, K., Christy, S., Pahor, M., Javors, M. A., Fernandez, E. and Miller, R. A. (2009)."Rapamycin Fed Late in Life Extends Lifespan in Genetically Heterogeneous Mice". Nature, Vol. 460, No. 7253. PP. 392–395.