Research code: مقاله مروری
Ethics code: مقاله مروری
Clinical trials code: مقاله مروری
1- Department of Physical Education and Sports Sciences, science and research Branch, Islamic Azad University, Tehran, Iran
2- Department of Physical Education and Sports Sciences, Borujard Branch, Islamic Azad University, Borujard, Iran
3- Department of Physical Education, Dezfoul Branch, Islamic Azad University, Dezfoul, Iran.
4- Department of Physical Education and Sports Sciences, North Tehran Branch, Islamic Azad University, Tehran, Iran ,peymantahann@gmail.com
2- Department of Physical Education and Sports Sciences, Borujard Branch, Islamic Azad University, Borujard, Iran
3- Department of Physical Education, Dezfoul Branch, Islamic Azad University, Dezfoul, Iran.
4- Department of Physical Education and Sports Sciences, North Tehran Branch, Islamic Azad University, Tehran, Iran ,
Abstract: (126 Views)
Background & Aims: The development of metabolic disorders occurs when physiological metabolic pathways are disrupted due to improper diet, inactivity, and lack of physical activity (1, 2). Genome polymorphisms related to lipid metabolism, glucose uptake, insulin signaling or appetite control are involved in the development of metabolic diseases (3). The liver is a dynamic organ that plays an important role in many physiological processes, including the regulation of systemic lipid and glucose metabolism (4). The liver is a major regulator of systemic metabolism and energy homeostasis of the whole body (4, 5). Inefficient hepatic lipid metabolism is the cause of nonalcoholic fatty liver disease (NAFLD), the most common chronic liver disorder worldwide, and is closely related to insulin resistance and type 2 diabetes. It has been reported that the liver secretes a wide range of proteins, metabolites, and non-coding RNAs (miRNA), and many of these secreted factors have powerful effects on metabolic processes both in the liver and in peripheral tissues (6). Liver-derived proteins known as hepatokines have recently emerged as novel hormones that have dual roles, either exacerbating insulin resistance or ameliorating metabolic variables in the metabolic syndrome (4, 10). The study of hepatokines, as potential biomarkers for metabolic disorders in the liver, is an attractive and relatively simple approach that has attracted the attention of researchers in various fields (10, 11). Recent evidence suggests that exercise can modulate the expression of some hepatokines, suggesting that the liver may also participate in tissue cross-talk during physical activity (12). Fetuins are a family of a large group of proteins (15) that can play a role in metabolic disorders due to their relationship with insulin action (16). The health-promoting effects of physical activity for the prevention and treatment of metabolic disorders are enormous. However, the underlying molecular mechanisms are still not fully understood. Considering that fetuins play a role in metabolic homeostasis and previous researches have reported the relationship between some metabolic disorders and changes in fetuins, the purpose of this research is to review the effect of exercise training on fetuins A and B in metabolic disorders.
Methods: In the current review study, which is a narrative review, the key words of fetoin, metabolic disorders and exercise training were searched without time limit from the Google Scholar search engine and related articles were selected. The articles collected in this review were independently searched and reviewed by the authors, and the selected articles that met the inclusion criteria were selected and included in the study. The inclusion criteria for the study included the use of exercise intervention and examining the variable fetoin A or fetoin B in people with metabolic disorders such as obesity, metabolic syndrome, diabetes, etc. The articles were screened based on PRISMA. In the first step, repeated studies were excluded. In the next step, the title and abstract of the articles were done by all the authors based on the entry and exit conditions, and the articles that were unrelated were removed. In the next step, the selected articles were reviewed by the authors.
Results: Based on the findings of previous researches, it can be said that supervised exercise interventions by reducing fetoins A and B reduce insulin resistance and other metabolic disorders including dyslipidemia as well as hepatic steatosis (4, 23-26). Fetoin-A has been reported to be directly associated with reduced hepatic insulin resistance, insulin-stimulated carbohydrate utilization, and systemic inflammation after exercise in older, obese, prediabetic adults (40). Also, after aerobic exercise interventions, the reduction of fetoin-B is related to the reduction of insulin resistance and improvement of liver function (4). In in vivo and in vitro models, it has been reported that exercise and dietary intervention reduce the formation of fat droplets, decrease hepatic triglyceride in the liver caused by a high-fat diet. Exercise and dietary intervention increase lipophagy by activating AMPK/ULK1 and inhibiting Akt/mTOR/ULK1 pathways, respectively (41). In their study, Zhao et al showed that administration of recombinant fetoin-B exacerbated hepatic fat accumulation induced by free fatty acids (FFAs) or a high-fat diet, in vivo and in vitro. It decreased the level of phosphorylated AMPK and activated the LXR-SREBP1c pathway, which is associated with a decrease in fatty acid oxidation and an increase in lipogenesis. Furthermore, in HepG2 cells exposed to recombinant fetoin B and FFAs, the AMPK agonist downregulated the LXR-SREBP1c pathway and reduced lipid accumulation (42). These results show that fetoin-B, like fetoin-A, plays an important role in the disorder of two metabolic sensors, SIRT1 and AMPK (29). Exercise can significantly affect the PGC-1 α and AMPK-SIRT1 pathway, as it is involved in the regulation of energy metabolism and mitochondrial biogenesis. Exercise is a major energy deprivation process by which many transcription factors are positively regulated (43). These changes can be related to the reduction of fetoins A and B, and as a result, exercise can improve metabolic disorders by modulating fetoins.
Conclusion: In general, this review showed that fetoins A and B are related to metabolic disorders and the levels of these biomarkers increase in the pathogenesis of obesity, metabolic syndrome, non-alcoholic fatty liver, type 2 diabetes, etc., which make these hepatokines It has become suitable biomarkers for investigating metabolic disorders. Also, the research results show the positive effects of exercise on the improvement of metabolic disorders, including the reduction of insulin resistance, and in the intervention research that has been done, it has been shown that the reduction of fetoins is related to the adjustment of metabolic disorders. However, more research is needed to investigate the effect of the type of exercise as well as the volume and intensity of different exercises on these hepatokines.
Methods: In the current review study, which is a narrative review, the key words of fetoin, metabolic disorders and exercise training were searched without time limit from the Google Scholar search engine and related articles were selected. The articles collected in this review were independently searched and reviewed by the authors, and the selected articles that met the inclusion criteria were selected and included in the study. The inclusion criteria for the study included the use of exercise intervention and examining the variable fetoin A or fetoin B in people with metabolic disorders such as obesity, metabolic syndrome, diabetes, etc. The articles were screened based on PRISMA. In the first step, repeated studies were excluded. In the next step, the title and abstract of the articles were done by all the authors based on the entry and exit conditions, and the articles that were unrelated were removed. In the next step, the selected articles were reviewed by the authors.
Results: Based on the findings of previous researches, it can be said that supervised exercise interventions by reducing fetoins A and B reduce insulin resistance and other metabolic disorders including dyslipidemia as well as hepatic steatosis (4, 23-26). Fetoin-A has been reported to be directly associated with reduced hepatic insulin resistance, insulin-stimulated carbohydrate utilization, and systemic inflammation after exercise in older, obese, prediabetic adults (40). Also, after aerobic exercise interventions, the reduction of fetoin-B is related to the reduction of insulin resistance and improvement of liver function (4). In in vivo and in vitro models, it has been reported that exercise and dietary intervention reduce the formation of fat droplets, decrease hepatic triglyceride in the liver caused by a high-fat diet. Exercise and dietary intervention increase lipophagy by activating AMPK/ULK1 and inhibiting Akt/mTOR/ULK1 pathways, respectively (41). In their study, Zhao et al showed that administration of recombinant fetoin-B exacerbated hepatic fat accumulation induced by free fatty acids (FFAs) or a high-fat diet, in vivo and in vitro. It decreased the level of phosphorylated AMPK and activated the LXR-SREBP1c pathway, which is associated with a decrease in fatty acid oxidation and an increase in lipogenesis. Furthermore, in HepG2 cells exposed to recombinant fetoin B and FFAs, the AMPK agonist downregulated the LXR-SREBP1c pathway and reduced lipid accumulation (42). These results show that fetoin-B, like fetoin-A, plays an important role in the disorder of two metabolic sensors, SIRT1 and AMPK (29). Exercise can significantly affect the PGC-1 α and AMPK-SIRT1 pathway, as it is involved in the regulation of energy metabolism and mitochondrial biogenesis. Exercise is a major energy deprivation process by which many transcription factors are positively regulated (43). These changes can be related to the reduction of fetoins A and B, and as a result, exercise can improve metabolic disorders by modulating fetoins.
Conclusion: In general, this review showed that fetoins A and B are related to metabolic disorders and the levels of these biomarkers increase in the pathogenesis of obesity, metabolic syndrome, non-alcoholic fatty liver, type 2 diabetes, etc., which make these hepatokines It has become suitable biomarkers for investigating metabolic disorders. Also, the research results show the positive effects of exercise on the improvement of metabolic disorders, including the reduction of insulin resistance, and in the intervention research that has been done, it has been shown that the reduction of fetoins is related to the adjustment of metabolic disorders. However, more research is needed to investigate the effect of the type of exercise as well as the volume and intensity of different exercises on these hepatokines.
Type of Study: review article |
Subject:
Exercise Physiology
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