scholarly journals Brain-derived Neurotrophic Factor Regulates Energy Expenditure Through the Central Nervous System in Obese Diabetic Mice

2001 ◽  
Vol 2 (3) ◽  
pp. 201-209 ◽  
Author(s):  
Takeshi Nonomura ◽  
Atsushi Tsuchida ◽  
Michiko Ono-Kishino ◽  
Tsutomu Nakagawa ◽  
Mutsuo Taiji ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Blood Glucose ◽  
Energy Expenditure ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Central Administration ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
The Central Nervous System

It has been previously demonstrated that brain-derived neurotrophic factor (BDNF) regulates glucose metabolism and energy expenditure in rodent diabetic models such as C57BL/KsJ-leprdb/leprdb(db/db) mice. Central administration of BDNF has been found to reduce blood glucose indb/dbmice, suggesting that BDNF acts through the central nervous system. In the present study we have expanded these investigations to explore the effect of central administration of BDNF on energy metabolism. Intracerebroventricular administration of BDNF lowered blood glucose and increased pancreatic insulin content ofdb/dbmice compared with vehicle-treated pellet pair-feddb/dbmice. While body temperatures of the pellet pair-feddb/dbmice given vehicle were reduced because of restricted food supply in this pair-feeding condition, BDNF treatment remarkably alleviated the reduction of body temperature suggesting the enhancement of thermogenesis. BDNF enhanced norepinephrine turnover and increased uncoupling protein-1 mRNA expression in the interscapular brown adipose tissue. Our evidence indicates that BDNF activates the sympathetic nervous systemviathe central nervous system and regulates energy expenditure in obese diabetic animals.

scholarly journals Brain-derived neurotrophic factor as a potential therapeutic tool in the treatment of nervous system disorders

2020 ◽  
Vol 74 ◽  
pp. 517-531
Author(s):  
Wioletta Kazana ◽  
Agnieszka Zabłocka
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurotrophic Factor ◽  
Intracellular Transport ◽  
Brain Derived Neurotrophic Factor ◽  
Nerve Cells ◽  
The Body ◽  
Bdnf Level ◽  
The Central Nervous System ◽  
The Brain

Brain-derived neurotrophic factor (BDNF) plays an important role in the proper functioning of the nervous system. It regulates the growth and survival of nerve cells, and is crucial in processes related to the memory, learning and synaptic plasticity. Abnormalities related to the distribution and secretion of BDNF protein accompany many diseases of the nervous system, in the course of which a significant decrease in BDNF level in the brain is observed. Impairments of BDNF transport may occur, for example, in the event of a single nucleotide polymorphism in the Bdnf (Val66Met) coding gene or due to the dysfunctions of the proteins involved in intracellular transport, such as huntingtin (HTT), huntingtin-associated protein 1 (HAP1), carboxypeptidase E (CPE) or sortilin 1 (SORT1). One of the therapeutic goals in the treatment of diseases of the central nervous system may be the regulation of expression and secretion of BDNF protein by nerve cells. Potential therapeutic strategies are based on direct injection of the protein into the specific region of the brain, the use of viral vectors expressing the Bdnf gene, transplantation of BDNF-producing cells, the use of substances of natural origin that stimulate the cells of the central nervous system for BDNF production, or the use of molecules activating the main receptor for BDNF – tyrosine receptor kinase B (TrkB). In addition, an appropriate lifestyle that promotes physical activity helps to increase BDNF level in the body. This paper summarizes the current knowledge about the biological role of BDNF protein and proteins involved in intracellular transport of this neurotrophin. Moreover, it presents contemporary research trends to develop therapeutic methods, leading to an increase in the level of BDNF protein in the brain.

scholarly journals The Role of Brain-Derived Neurotrophic Factor in Epileptogenesis: an Update

2021 ◽  
Vol 12 ◽  
Author(s):  
Xinyi Wang ◽  
Zhe Hu ◽  
Kai Zhong
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurotrophic Factor ◽  
Neurological Diseases ◽  
Brain Derived Neurotrophic Factor ◽  
The World ◽  
The Central Nervous System ◽  
Spontaneous Recurrent Seizures ◽  
New Evidence

Epilepsy, which is characterized by spontaneous recurrent seizures, is one of the most common and serious chronic neurological diseases in the world. 30% patients failed to control seizures with multiple anti-seizure epileptic drugs, leading to serious outcomes. The pathogenesis of epilepsy is very complex and remains unclear. Brain-derived neurotrophic factor (BDNF), as a member of the neurotrophic factor family, is considered to play an important role in the survival, growth and differentiation of neurons during the development of the central nervous system. Recent years, a series of studies have reported that BDNF can maintain the function of the nervous system and promotes the regeneration of neurons after injury, which is believed to be closely related to epileptogenesis. However, two controversial views (BDNF inhibits or promotes epileptogenesis) still exist. Thus, this mini-review focuses on updating the new evidence of the role of BDNF in epileptogenesis and discussing the possibility of BDNF as an underlying target for the treatment of epilepsy.

scholarly journals The thermogenic effect of nesfatin-1 requires recruitment of the melanocortin system

2017 ◽  
Vol 235 (2) ◽  
pp. 111-122 ◽  
Author(s):  
Riccardo Dore ◽  
Luka Levata ◽  
Sogol Gachkar ◽  
Olaf Jöhren ◽  
Jens Mittag ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Heat Loss ◽  
Central Administration ◽  
Melanocortin System ◽  
Direct Calorimetry ◽  
Iodothyronine Deiodinase ◽  
Interscapular Brown Adipose Tissue ◽  
Peripheral Tissues ◽  
Dry Heat ◽  
Brown Adipose

Nesfatin-1 is a bioactive polypeptide expressed both in the brain and peripheral tissues and involved in the control of energy balance by reducing food intake. Central administration of nesfatin-1 significantly increases energy expenditure, as demonstrated by a higher dry heat loss; yet, the mechanisms underlying the thermogenic effect of central nesfatin-1 remain unknown. Therefore, in this study, we sought to investigate whether the increase in energy expenditure induced by nesfatin-1 is mediated by the central melanocortin pathway, which was previously reported to mediate central nesfatin-1´s effects on feeding and numerous other physiological functions. With the application of direct calorimetry, we found that intracerebroventricular nesfatin-1 (25 pmol) treatment increased dry heat loss and that this effect was fully blocked by simultaneous administration of an equimolar dose of the melanocortin 3/4 receptor antagonist, SHU9119. Interestingly, the nesfatin-1-induced increase in dry heat loss was positively correlated with body weight loss. In addition, as assessed with thermal imaging, intracerebroventricular nesfatin-1 (100 pmol) increased interscapular brown adipose tissue (iBAT) as well as tail temperature, suggesting increased heat production in the iBAT and heat dissipation over the tail surface. Finally, nesfatin-1 upregulated pro-opiomelanocortin and melanocortin 3 receptor mRNA expression in the hypothalamus, accompanied by a significant increase in iodothyronine deiodinase 2 and by a nonsignificant increase in uncoupling protein 1 and peroxisome proliferator-activated receptor gamma coactivator-1 alpha mRNA in the iBAT. Overall, we clearly demonstrate that nesfatin-1 requires the activation of the central melanocortin system to increase iBAT thermogenesis and, in turn, overall energy expenditure.

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