Brain-derived neurotrophic factor (BDNF) is a neurotrophic factor that supports neuronal survival, growth, and plasticity, and plays a role in neurotransmission and energy metabolism. It is widely expressed in the central nervous system, gut, and other tissues. BDNF binds to its high-affinity receptor TrkB, activating signaling pathways such as IRS1/2, PI3K, Akt, and MAPK/ERK, which are crucial for cell survival and neuroplasticity. BDNF also regulates glucose and energy metabolism, preventing β-cell exhaustion. Decreased BDNF levels are associated with neurodegenerative diseases such as Parkinson's, Alzheimer's, and Huntington's disease. BDNF may be useful in the prevention and management of several diseases, including diabetes mellitus. BDNF is synthesized in the endoplasmic reticulum and processed through the Golgi apparatus to form the mature 13 kDa BDNF. It has close structural homology with nerve growth factor (NGF) and shares about 50% amino acid identity with NGF, NT-3, and NT-4/5. BDNF has multiple isoforms and is expressed in various brain regions. Its expression is low during fetal development, increases after birth, and then decreases in adults. BDNF exerts its effects through TrkB receptors, which are present in the brain and spinal cord. Activation of TrkB leads to the activation of various signaling pathways, including the Ras/MAPK/ERK, IRS-1/PI3K/AKT, and PLC/DAG/IP3 pathways. These pathways regulate cell survival, neurogenesis, synaptic plasticity, and energy homeostasis. BDNF also interacts with estrogen to induce neuropeptide-Y (NPY), and the trio (BDNF-NPY-estrogen) regulates hippocampal function. BDNF has been implicated in the regulation of food intake and body weight in both experimental animals and humans. BDNF administration decreases non-fasted blood glucose in obese, non-insulin-dependent diabetic mice, and reduces liver glycogen and enzyme activity. BDNF also activates the sympathetic nervous system, regulating energy expenditure in obese diabetic animals. Plasma levels of BDNF are lower in women and decrease with age, and are associated with increased mortality risk. BDNF plays a role in various neurological disorders, including Alzheimer's disease, dementia, and autism. Decreased BDNF levels are associated with cognitive deficits in patients with type 2 diabetes. BDNF is also involved in the pathogenesis of cardiovascular diseases and diabetes mellitus, as it plays a critical role in inflammation, glucose and lipid metabolism. BDNF has a central role in energy homeostasis and is involved in the prevention and management of obesity, type 2 diabetes mellitus, and metabolic syndrome. BDNF may be used as a therapeutic agent in the treatment of these conditionsBrain-derived neurotrophic factor (BDNF) is a neurotrophic factor that supports neuronal survival, growth, and plasticity, and plays a role in neurotransmission and energy metabolism. It is widely expressed in the central nervous system, gut, and other tissues. BDNF binds to its high-affinity receptor TrkB, activating signaling pathways such as IRS1/2, PI3K, Akt, and MAPK/ERK, which are crucial for cell survival and neuroplasticity. BDNF also regulates glucose and energy metabolism, preventing β-cell exhaustion. Decreased BDNF levels are associated with neurodegenerative diseases such as Parkinson's, Alzheimer's, and Huntington's disease. BDNF may be useful in the prevention and management of several diseases, including diabetes mellitus. BDNF is synthesized in the endoplasmic reticulum and processed through the Golgi apparatus to form the mature 13 kDa BDNF. It has close structural homology with nerve growth factor (NGF) and shares about 50% amino acid identity with NGF, NT-3, and NT-4/5. BDNF has multiple isoforms and is expressed in various brain regions. Its expression is low during fetal development, increases after birth, and then decreases in adults. BDNF exerts its effects through TrkB receptors, which are present in the brain and spinal cord. Activation of TrkB leads to the activation of various signaling pathways, including the Ras/MAPK/ERK, IRS-1/PI3K/AKT, and PLC/DAG/IP3 pathways. These pathways regulate cell survival, neurogenesis, synaptic plasticity, and energy homeostasis. BDNF also interacts with estrogen to induce neuropeptide-Y (NPY), and the trio (BDNF-NPY-estrogen) regulates hippocampal function. BDNF has been implicated in the regulation of food intake and body weight in both experimental animals and humans. BDNF administration decreases non-fasted blood glucose in obese, non-insulin-dependent diabetic mice, and reduces liver glycogen and enzyme activity. BDNF also activates the sympathetic nervous system, regulating energy expenditure in obese diabetic animals. Plasma levels of BDNF are lower in women and decrease with age, and are associated with increased mortality risk. BDNF plays a role in various neurological disorders, including Alzheimer's disease, dementia, and autism. Decreased BDNF levels are associated with cognitive deficits in patients with type 2 diabetes. BDNF is also involved in the pathogenesis of cardiovascular diseases and diabetes mellitus, as it plays a critical role in inflammation, glucose and lipid metabolism. BDNF has a central role in energy homeostasis and is involved in the prevention and management of obesity, type 2 diabetes mellitus, and metabolic syndrome. BDNF may be used as a therapeutic agent in the treatment of these conditions