Type 2 diabetes mellitus (T2DM) is a widespread metabolic condition characterized by elevated glucose levels followed by deficiency in insulin secretion. Metformin notably decreased the incidence of T2DM by 31% and it exerts its effects through various signaling pathways. Databases searched included PubMed, Google Scholar, and Scopus from 2000 to 2024. One of the primary mechanisms involves AMPK activation which causes reduced lipogenesis and improved fatty acid oxidation in the liver and muscles. Key molecules affected by metformin include acetyl-CoA carboxylase (ACC) and sterol regulatory element-binding protein 1c (SREBP-1c), both involved in lipid synthesis regulation. Aerobic exercise has also emerged as a crucial component in managing T2DM due to its improved effects on hyperglycemia and insulin sensitivity. Key signaling pathways affected in T2DM include the PI3K/Akt, AMP-activated protein kinase (AMPK), and MAPK/ERK pathways which play essential roles in regulating glucose homeostasis, glycogenesis, and insulin secretion. When comparing the mechanisms and efficacy of aerobic exercise and metformin, it becomes evident that aerobic exercise primarily enhances physical fitness and metabolic function, while metformin exerts its effects through biochemical pathways involving AMPK activation. Aerobic exercise and metformin are effective for managing T2DM, though they operate through different mechanisms. Regular aerobic exercise improves insulin sensitivity, enhances cardiovascular health, and promotes weight loss, while metformin primarily decreases hepatic gluconeogenesis and enhances insulin secretion. Understanding the intricate signaling pathways affected by metformin and aerobic exercise provides valuable insights into its mechanisms of action and clinical implications for treating diabetic patients effectively.

Type 2 diabetes mellitus (T2DM) is a widespread metabolic condition characterized by elevated glucose levels followed by deficiency in insulin secretion. Metformin notably decreased the incidence of T2DM by 31% and it exerts its effects through various signaling pathways. Databases searched included PubMed, Google Scholar, and Scopus from 2000 to 2024. One of the primary mechanisms involves AMPK activation which causes reduced lipogenesis and improved fatty acid oxidation in the liver and muscles. Key molecules affected by metformin include acetyl-CoA carboxylase (ACC) and sterol regulatory element-binding protein 1c (SREBP-1c), both involved in lipid synthesis regulation. Aerobic exercise has also emerged as a crucial component in managing T2DM due to its improved effects on hyperglycemia and insulin sensitivity. Key signaling pathways affected in T2DM include the PI3K/Akt, AMP-activated protein kinase (AMPK), and MAPK/ERK pathways which play essential roles in regulating glucose homeostasis, glycogenesis, and insulin secretion. When comparing the mechanisms and efficacy of aerobic exercise and metformin, it becomes evident that aerobic exercise primarily enhances physical fitness and metabolic function, while metformin exerts its effects through biochemical pathways involving AMPK activation. Aerobic exercise and metformin are effective for managing T2DM, though they operate through different mechanisms. Regular aerobic exercise improves insulin sensitivity, enhances cardiovascular health, and promotes weight loss, while metformin primarily decreases hepatic gluconeogenesis and enhances insulin secretion. Understanding the intricate signaling pathways affected by metformin and aerobic exercise provides valuable insights into its mechanisms of action and clinical implications for treating diabetic patients effectively.

Type 2 diabetes mellitus (T2DM) is a widespread metabolic condition characterized by elevated glucose levels followed by deficiency in insulin secretion. Metformin notably decreased the incidence of T2DM by 31% and it exerts its effects through various signaling pathways. Databases searched included PubMed, Google Scholar, and Scopus from 2000 to 2024. One of the primary mechanisms involves AMPK activation which causes reduced lipogenesis and improved fatty acid oxidation in the liver and muscles. Key molecules affected by metformin include acetyl-CoA carboxylase (ACC) and sterol regulatory element-binding protein 1c (SREBP-1c), both involved in lipid synthesis regulation. Aerobic exercise has also emerged as a crucial component in managing T2DM due to its improved effects on hyperglycemia and insulin sensitivity. Key signaling pathways affected in T2DM include the PI3K/Akt, AMP-activated protein kinase (AMPK), and MAPK/ERK pathways which play essential roles in regulating glucose homeostasis, glycogenesis, and insulin secretion. When comparing the mechanisms and efficacy of aerobic exercise and metformin, it becomes evident that aerobic exercise primarily enhances physical fitness and metabolic function, while metformin exerts its effects through biochemical pathways involving AMPK activation. Aerobic exercise and metformin are effective for managing T2DM, though they operate through different mechanisms. Regular aerobic exercise improves insulin sensitivity, enhances cardiovascular health, and promotes weight loss, while metformin primarily decreases hepatic gluconeogenesis and enhances insulin secretion. Understanding the intricate signaling pathways affected by metformin and aerobic exercise provides valuable insights into its mechanisms of action and clinical implications for treating diabetic patients effectively.

This study aimed to investigate the activation of the inflammation process, triggered as an immune response to combat the invasion by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 is a highly transmissible and pathogenic coronavirus that emerged in late 2019 and has caused a pandemic of acute respiratory disease, named ‘coronavirus disease 2019’ (COVID-19). Several mechanisms contribute to the reduction in serotonin levels, such as the impaired absorption of dietary tryptophan, hindered serotonin transport via platelets, and increased activity of an enzyme responsible for breaking down serotonin. Individuals seeking treatment for long COVID-19 had lower serotonin levels in their blood than those who had fully recovered from the infection. Furthermore, patients with long COVID-19 also had reduced tryptophan levels. The potential benefits of dietary supplementation with tryptophan or the use of selective serotonin reuptake inhibitors (SSRIs) to improve cognitive impairments and depressive and anxiety disorders in long-term COVID-19 patients. The findings support the immune response’s pivotal role in modulating serotonin levels and further highlight the intricate connection between the immune system and neurotransmitter regulation.

Non-alcoholic fatty liver disease (NAFLD) is a condition in which excess fat builds up in the liver, often related to obesity and insulin resistance, which can lead to inflammation and scarring of the liver tissue. While efforts have been made to develop effective treatments for NAFLD, the need for pharmaceutical interventions remains unmet. Large clinical trials investigating the association between statin use and NAFLD are scarce, leading to contradictory results. Statins play a crucial role in cholesterol synthesis in the liver. Several studies have demonstrated that statins possess anti-inflammatory, anti-thrombotic, and anti-fibrotic properties. These properties make statins potentially useful in preventing the progression of NAFLD from simple steatosis to more severe forms like non-alcoholic steatohepatitis (NASH) and fibrosis. The results indicate that statin use is associated with a lower prevalence of NASH and fibrosis and may have a preventive effect on NAFLD.