Razi Journal of Medical Sciences

fa اثر تمرینات ورزشی بر اختلال عملکرد انسولین مرتبط با چاقی در طول عمر Effect of Exercise Training on Insulin Dysfunction Related to Obesity across the Lifespan فیزیولوژی ورزش Exercise Physiology مروري review article <div style="text-align: justify;">زمینه و هدف: چاقی و مقاومت به انسولین دو اختلال متابولیک می باشند که در کشورهای توسعه یافته و در حال توسعه در حال افزایش هستند. همچنین مقاومت به انسولین به عنوان عامل کلیدی برخی بیماری های مزمن شناخته شده است. هدف تحقیق حاضر خلاصه سازی اثر ورزش به عنوان یک مدخله مرتبط با سبک زندگی در درمان مقاومت به انسولین مرتبط با چاقی در طول عمر می باشد. روش کار: در مطالعه مروری حاضر حاضر کلیدواژه های مرتبط با مطالعه شامل چاقی، انسولین، مقاومت به انسولین، بارداری، نوزادی، شیر مادر، کودکی، نوجوانی، جوانی، سالمندی و یائسگی به تنهایی و با ترکیب با تمرینات ورزشی در پایگاه های داده جستجو شدند و مقالات مرتبط بر اساس عنوان انتخاب شدند و پس از مطالعه اولیه چکیده، مقالات مرتبط برای مرور حاضر استفاده شدند. یافته‌ها: در این مرور به بررسی عوامل چاقی زا و ارتباط آن با مقاومت به انسولین در طول دوره رشد از دوره جنینی، نوزادی، کودکی و نوجوانی تا سالمندی پرداخته شده است و نقش ورزش در طول عمر به عنوان یک مداخله غیردارویی بر مقاومت به انسولین مرتبط با چاقی برجسته شده است. در مجموع نتایج مطالعه ما نشان دهنده اثرات مثبت تمرینات ورزشی بر بهبود مقاوت به انسولین مرتبط با چاقی در سنین مختلف بود. نتیجه‌گیری: انجام تمرینات ورزشی و کنترل وزن مادران قبل و حین و حتی پس از بارداری می تواند با اثرات اپی‌ژنتیکی که دارد نقش پیشگیری کننده برای پیشگیری از چاقی و مقاومت به انسولین کودکان داشته باشد؛ همچنین انجام تمرینات ورزشی منظم یک عامل کلیدی غیردارویی برای بهبود عملکرد انسولین است و توصیه می شود که سبک زندگی فعال با انجام تمرینات ورزشی برای پیشگیری و درمان مقاومت به انسولین در طول عمر استفاده شود. همچنین با توجه به تغییرات ترکیب بدن در بزرگسالی بخصوص در اواخر دوره عمر توصیه می شود که در برنامه های تمرینی سالمندان به حفظ و افزایش توده عضلانی توجه شود که می تواند نشان دهنده اهمیت تمرینات مقاومتی برای پیشگیری و درمان مقاومت به انسولین مرتبط با سارکوپنیا و چاقی سارکوپنیک باشد.   </div> <div style="text-align: justify;">Background & Aims: As obesity reaches epidemic proportions in all ages from childhood, adolescence, youth, middle age and old age, it causes metabolic disorders and chronic diseases during the lifetime of these people (1-3). Convincing evidence has shown that increased adipose tissue mass is not only a consequence of obesity, but also plays an essential role in the development of obesity-related diseases, including insulin resistance (4). Obesity mediates most of its direct medical consequences through the development of insulin resistance. Multiple and complex pathogenic pathways link obesity with the development of insulin resistance, including chronic inflammation, mitochondrial dysfunction (with reactive oxygen species production and endoplasmic reticulum stress), gut microbiota dysbiosis, and fat extracellular matrix remodeling. Furthermore, insulin resistance increases the weight gain associated with secondary hyperinsulinemia, resulting in a vicious cycle of worsening insulin resistance and its metabolic consequences. Finally, insulin resistance underlies other obesity-related diseases. Insulin resistance also underlies many obesity-related malignancies through the effects of compensatory hyperinsulinemia on the relatively intact mitogen-activated protein kinase (MAPK) pathway, which controls the processes of cell growth and mitoses. Furthermore, emerging data in recent decades support an important role of insulin resistance associated with central obesity and type 2 diabetes in the development of cognitive dysfunction, including effects on hippocampal synaptic plasticity (18). Growing evidence suggests that ectopic fat accumulation is more closely related to diabetes physiology than other variables, such as endoplasmic reticulum stress and plasma inflammatory cytokine concentrations. Several animal and epidemiological studies have shown that the accumulation of diacylglycerol in the plasma membrane fractions due to aberrant fat accumulation or reduced fat oxidation is a critical factor in the development of insulin resistance through the activation of novel protein kinase C (nPKC) in liver tissues and skeletal muscles. Based on this pathophysiological mechanism of insulin resistance, suppression of lipid synthesis in the liver and stimulation of fat oxidation in skeletal muscle provide a means to potentially reduce aberrant fat accumulation, improve insulin sensitivity, and ultimately prevent or delay type 2 diabetes. (19). Based on our current knowledge, no research has been found that has comprehensively investigated the effect of exercise training on insulin resistance related to obesity throughout life. Accordingly, the present study aims to review and summarize the effect of exercise training on insulin dysfunction related to obesity. Obesity is lifelong in from fetal period to old age. Methods: In the present review study, which was an narrative review, considering the main purpose of the research, which was to review and summarize the effect of exercise training on obesity-related insulin dysfunction throughout life (from fetal period to old age); Keywords related to the study including obesity, insulin, insulin resistance, pregnancy, infancy, breastfeeding, childhood, adolescence, youth, elderly and menopause alone and in combination with exercise were searched in electronic databases and related articles based on the title were selected and after the initial study of the abstract and removal of unrelated studies or repeated studies, related articles were used for the present review. Results: In this review, obesity-causing factors and its relationship with insulin resistance during the developmental period from fetal, infant, childhood, and adolescence to old age have been investigated, and the role of exercise throughout life as a non-pharmacological intervention on insulin resistance related to Obesity is highlighted. Overall, the results of our study showed the positive effects of exercise on improving insulin resistance associated with obesity at different ages. Conclusion: Although insulin resistance caused by obesity is a metabolic disorder that causes cardiometabolic diseases in obese people under the influence of genetics and environmental factors (19). On the other hand, exercise is a non-pharmacological intervention related to lifestyle that can affect the overall systemic metabolism. In fact, the positive effects of exercise improve the acute insulin function caused by training sessions and chronic adaptation. Exercise challenges the homeostasis of the whole body and affects many cells, tissues and organs through increasing the metabolic activity of skeletal muscles. In addition, the beneficial effects of exercise training are not limited to adaptation in tissues, but rather result from the integration of inter-tissue communication through different signaling molecules, hormones and cytokines secreted by different tissues. According to the current review, epigenetic conditions, including the mother's body composition and mother's metabolic conditions during pregnancy, can cause obesity in babies and metabolic disorders in older children with early planning. Also, obesity and sedentary lifestyle in nursing mothers, affecting the quality of breast milk as the main source of nutrition for the child, are effective factors in the occurrence of metabolic disorders in infants. Based on the findings of the present review, exercise training by pregnant and lactating mothers can improve metabolic health in infants. Also, exercising throughout life from childhood to old age is an effective strategy to reduce insulin resistance related to obesity; which can improve insulin function in obese people even without affecting body composition. However, due to the fact that in adults, muscle mass decreases with age, especially in old age; In training protocols, it is necessary to pay attention to maintaining and increasing muscle mass.</div> چاقی, چاقی سارکوپنیک, تمرینات ورزشی, مقاومت به انسولین, سن Obesity, Sarcopenic obesity, Exercise training, Insulin resistance, Age 1 20 http://rjms.iums.ac.ir/browse.php?a_code=A-10-5175-9&slc_lang=fa&sid=1 Ashkan Gholabi اشکان گلابی 3900319475328460088279 0009-0007-9110-3521 No MSc, Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Guilan, Rasht, Iran کارشناسی ارشد، گروه فیزیولوژی ورزشی، دانشکده تربیت بدنی و علوم ورزشی، دانشگاه گیلان، رشت، ایران Akbar Ghalavand اکبر قلاوند akbarghalavand@gmail.com 3900319475328460088280 3900319475328460088280 Yes PhD in Exercise Physiology, Pediatric Gastroenterology and Hepatology Research Center, Zabol University of Medical Sciences, Zabol, Iran دکتری فیزیولوژی ورزشی، مرکز تحقیقات گوارش و کبد کودکان، دانشگاه علوم پزشکی زابل، زابل، ایران Azin Barmala آذین برملا barmalaazin@yahoo.com 3900319475328460088281 3900319475328460088281 No MSc in Geriatric health, Department of Public Health, Shoushtar Faculty of Medical Sciences, Shoushtar, Iran کارشناسی ارشد سلامت سالمندی، گروه بهداشت عمومی، دانشکده علوم پزشکی شوشتر، شوشتر، ایران Maryam Sadegh Joola مریم صادق ژولا 3900319475328460088282 0009-0007-5988-5383 No PhD, Department of Exercise Physiology, Borujard Branch, Islamic Azad University, Borujard, Iran دکتری، گروه فیزیولوژی ورزشی، واحد بروجرد، دانشگاه آزاد اسلامی، بروجرد، ایران Alinaghi Gholami علی نقی غلامی 3900319475328460088283 3900319475328460088283 No Assistant Professor, Sports Management Department, Payame-Noor University, Tehran, Iran استادیار، گروه مدیریت ورزشی، دانشگاه پیام نور، تهران، ایران