Research code: Review Article

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Abstract:   (194 Views)
Background: 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). It is 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 (from fetal period to old age).
Methods: In the present review study, which was an narative 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.
 
     
Type of Study: review article | Subject: Exercise Physiology

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